---
_id: '12120'
abstract:
- lang: eng
text: Plant root architecture flexibly adapts to changing nitrate (NO3−) availability
in the soil; however, the underlying molecular mechanism of this adaptive development
remains under-studied. To explore the regulation of NO3−-mediated root growth,
we screened for low-nitrate-resistant mutant (lonr) and identified mutants that
were defective in the NAC transcription factor NAC075 (lonr1) as being less sensitive
to low NO3− in terms of primary root growth. We show that NAC075 is a mobile transcription
factor relocating from the root stele tissues to the endodermis based on NO3−
availability. Under low-NO3− availability, the kinase CBL-interacting protein
kinase 1 (CIPK1) is activated, and it phosphorylates NAC075, restricting its movement
from the stele, which leads to the transcriptional regulation of downstream target
WRKY53, consequently leading to adapted root architecture. Our work thus identifies
an adaptive mechanism involving translocation of transcription factor based on
nutrient availability and leading to cell-specific reprogramming of plant root
growth.
acknowledgement: The authors are grateful to Jörg Kudla, Ying Miao, Yu Zheng, Gang
Li, and Jun Zheng for providing published materials and to Wenkun Zhou and Caifu
Jiang for helpful discussions. This work was supported by grants from the National
Key Research and Development Program of China (2021YFF1000500), the National Natural
Science Foundation of China (32170265 and 32022007), the Beijing Municipal Natural
Science Foundation (5192011), and the Chinese Universities Scientific Fund (2022TC153).
article_processing_charge: No
article_type: original
author:
- first_name: Huixin
full_name: Xiao, Huixin
last_name: Xiao
- first_name: Yumei
full_name: Hu, Yumei
last_name: Hu
- first_name: Yaping
full_name: Wang, Yaping
last_name: Wang
- first_name: Jinkui
full_name: Cheng, Jinkui
last_name: Cheng
- first_name: Jinyi
full_name: Wang, Jinyi
last_name: Wang
- first_name: Guojingwei
full_name: Chen, Guojingwei
last_name: Chen
- first_name: Qian
full_name: Li, Qian
last_name: Li
- first_name: Shuwei
full_name: Wang, Shuwei
last_name: Wang
- first_name: Yalu
full_name: Wang, Yalu
last_name: Wang
- first_name: Shao-Shuai
full_name: Wang, Shao-Shuai
last_name: Wang
- first_name: Yi
full_name: Wang, Yi
last_name: Wang
- first_name: Wei
full_name: Xuan, Wei
last_name: Xuan
- first_name: Zhen
full_name: Li, Zhen
last_name: Li
- first_name: Yan
full_name: Guo, Yan
last_name: Guo
- first_name: Zhizhong
full_name: Gong, Zhizhong
last_name: Gong
- first_name: Jiří
full_name: Friml, Jiří
id: 4159519E-F248-11E8-B48F-1D18A9856A87
last_name: Friml
orcid: 0000-0002-8302-7596
- first_name: Jing
full_name: Zhang, Jing
last_name: Zhang
citation:
ama: Xiao H, Hu Y, Wang Y, et al. Nitrate availability controls translocation of
the transcription factor NAC075 for cell-type-specific reprogramming of root growth.
Developmental Cell. 2022;57(23):2638-2651.e6. doi:10.1016/j.devcel.2022.11.006
apa: Xiao, H., Hu, Y., Wang, Y., Cheng, J., Wang, J., Chen, G., … Zhang, J. (2022).
Nitrate availability controls translocation of the transcription factor NAC075
for cell-type-specific reprogramming of root growth. Developmental Cell.
Elsevier. https://doi.org/10.1016/j.devcel.2022.11.006
chicago: Xiao, Huixin, Yumei Hu, Yaping Wang, Jinkui Cheng, Jinyi Wang, Guojingwei
Chen, Qian Li, et al. “Nitrate Availability Controls Translocation of the Transcription
Factor NAC075 for Cell-Type-Specific Reprogramming of Root Growth.” Developmental
Cell. Elsevier, 2022. https://doi.org/10.1016/j.devcel.2022.11.006.
ieee: H. Xiao et al., “Nitrate availability controls translocation of the
transcription factor NAC075 for cell-type-specific reprogramming of root growth,”
Developmental Cell, vol. 57, no. 23. Elsevier, p. 2638–2651.e6, 2022.
ista: Xiao H, Hu Y, Wang Y, Cheng J, Wang J, Chen G, Li Q, Wang S, Wang Y, Wang
S-S, Wang Y, Xuan W, Li Z, Guo Y, Gong Z, Friml J, Zhang J. 2022. Nitrate availability
controls translocation of the transcription factor NAC075 for cell-type-specific
reprogramming of root growth. Developmental Cell. 57(23), 2638–2651.e6.
mla: Xiao, Huixin, et al. “Nitrate Availability Controls Translocation of the Transcription
Factor NAC075 for Cell-Type-Specific Reprogramming of Root Growth.” Developmental
Cell, vol. 57, no. 23, Elsevier, 2022, p. 2638–2651.e6, doi:10.1016/j.devcel.2022.11.006.
short: H. Xiao, Y. Hu, Y. Wang, J. Cheng, J. Wang, G. Chen, Q. Li, S. Wang, Y. Wang,
S.-S. Wang, Y. Wang, W. Xuan, Z. Li, Y. Guo, Z. Gong, J. Friml, J. Zhang, Developmental
Cell 57 (2022) 2638–2651.e6.
date_created: 2023-01-12T11:57:00Z
date_published: 2022-12-05T00:00:00Z
date_updated: 2023-10-04T08:23:20Z
day: '05'
department:
- _id: JiFr
doi: 10.1016/j.devcel.2022.11.006
external_id:
isi:
- '000919603800005'
pmid:
- '36473460'
intvolume: ' 57'
isi: 1
issue: '23'
keyword:
- Developmental Biology
- Cell Biology
- General Biochemistry
- Genetics and Molecular Biology
- Molecular Biology
language:
- iso: eng
month: '12'
oa_version: None
page: 2638-2651.e6
pmid: 1
publication: Developmental Cell
publication_identifier:
issn:
- 1534-5807
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Nitrate availability controls translocation of the transcription factor NAC075
for cell-type-specific reprogramming of root growth
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 57
year: '2022'
...
---
_id: '12121'
abstract:
- lang: eng
text: Autophagosomes are double-membraned vesicles that traffic harmful or unwanted
cellular macromolecules to the vacuole for recycling. Although autophagosome biogenesis
has been extensively studied, autophagosome maturation, i.e., delivery and fusion
with the vacuole, remains largely unknown in plants. Here, we have identified
an autophagy adaptor, CFS1, that directly interacts with the autophagosome marker
ATG8 and localizes on both membranes of the autophagosome. Autophagosomes form
normally in Arabidopsis thaliana cfs1 mutants, but their delivery to the vacuole
is disrupted. CFS1’s function is evolutionarily conserved in plants, as it also
localizes to the autophagosomes and plays a role in autophagic flux in the liverwort
Marchantia polymorpha. CFS1 regulates autophagic flux by bridging autophagosomes
with the multivesicular body-localized ESCRT-I component VPS23A, leading to the
formation of amphisomes. Similar to CFS1-ATG8 interaction, disrupting the CFS1-VPS23A
interaction blocks autophagic flux and renders plants sensitive to nitrogen starvation.
Altogether, our results reveal a conserved vacuolar sorting hub that regulates
autophagic flux in plants.
acknowledgement: "We thank Suayip Ustün, Karin Schumacher, Erika Isono, Gerd Juergens,
Takashi Ueda, Daniel Hofius, and Liwen Jiang for sharing published materials.\r\nWe
acknowledge funding from Austrian Academy of Sciences, Austrian Science Fund (FWF,
P 32355, P 34944), Austrian Science Fund (FWF-SFB F79), Vienna Science and Technology\r\nFund
(WWTF, LS17-047) to Y. Dagdas; Austrian Academy of Sciences DOC Fellowship to J.
Zhao, Marie Curie VIP2 Fellowship to J.C. De La Concepcion and M. Clavel; Hong Kong
Research Grant Council (GRF14121019, 14113921, AoE/M-05/12, C4002-17G) to B.-H.
Kang. We thank Vienna Biocenter Core Facilities (VBCF) Protein Chemistry, Biooptics,
Plant Sciences, Molecular Biology, and Protein Technologies. We thank J. Matthew
Watson\r\nand members of the Dagdas lab for the critical reading and editing of
the manuscript."
article_number: e202203139
article_processing_charge: No
article_type: original
author:
- first_name: Jierui
full_name: Zhao, Jierui
last_name: Zhao
- first_name: Mai Thu
full_name: Bui, Mai Thu
last_name: Bui
- first_name: Juncai
full_name: Ma, Juncai
last_name: Ma
- first_name: Fabian
full_name: Künzl, Fabian
last_name: Künzl
- first_name: Lorenzo
full_name: Picchianti, Lorenzo
last_name: Picchianti
- first_name: Juan Carlos
full_name: De La Concepcion, Juan Carlos
last_name: De La Concepcion
- first_name: Yixuan
full_name: Chen, Yixuan
last_name: Chen
- first_name: Sofia
full_name: Petsangouraki, Sofia
last_name: Petsangouraki
- first_name: Azadeh
full_name: Mohseni, Azadeh
last_name: Mohseni
- first_name: Marta
full_name: García-Leon, Marta
last_name: García-Leon
- first_name: Marta Salas
full_name: Gomez, Marta Salas
last_name: Gomez
- first_name: Caterina
full_name: Giannini, Caterina
id: e3fdddd5-f6e0-11ea-865d-ca99ee6367f4
last_name: Giannini
- first_name: Dubois
full_name: Gwennogan, Dubois
last_name: Gwennogan
- first_name: Roksolana
full_name: Kobylinska, Roksolana
last_name: Kobylinska
- first_name: Marion
full_name: Clavel, Marion
last_name: Clavel
- first_name: Swen
full_name: Schellmann, Swen
last_name: Schellmann
- first_name: Yvon
full_name: Jaillais, Yvon
last_name: Jaillais
- first_name: Jiří
full_name: Friml, Jiří
id: 4159519E-F248-11E8-B48F-1D18A9856A87
last_name: Friml
orcid: 0000-0002-8302-7596
- first_name: Byung-Ho
full_name: Kang, Byung-Ho
last_name: Kang
- first_name: Yasin
full_name: Dagdas, Yasin
last_name: Dagdas
citation:
ama: Zhao J, Bui MT, Ma J, et al. Plant autophagosomes mature into amphisomes prior
to their delivery to the central vacuole. Journal of Cell Biology. 2022;221(12).
doi:10.1083/jcb.202203139
apa: Zhao, J., Bui, M. T., Ma, J., Künzl, F., Picchianti, L., De La Concepcion,
J. C., … Dagdas, Y. (2022). Plant autophagosomes mature into amphisomes prior
to their delivery to the central vacuole. Journal of Cell Biology. Rockefeller
University Press. https://doi.org/10.1083/jcb.202203139
chicago: Zhao, Jierui, Mai Thu Bui, Juncai Ma, Fabian Künzl, Lorenzo Picchianti,
Juan Carlos De La Concepcion, Yixuan Chen, et al. “Plant Autophagosomes Mature
into Amphisomes Prior to Their Delivery to the Central Vacuole.” Journal of
Cell Biology. Rockefeller University Press, 2022. https://doi.org/10.1083/jcb.202203139.
ieee: J. Zhao et al., “Plant autophagosomes mature into amphisomes prior
to their delivery to the central vacuole,” Journal of Cell Biology, vol.
221, no. 12. Rockefeller University Press, 2022.
ista: Zhao J, Bui MT, Ma J, Künzl F, Picchianti L, De La Concepcion JC, Chen Y,
Petsangouraki S, Mohseni A, García-Leon M, Gomez MS, Giannini C, Gwennogan D,
Kobylinska R, Clavel M, Schellmann S, Jaillais Y, Friml J, Kang B-H, Dagdas Y.
2022. Plant autophagosomes mature into amphisomes prior to their delivery to the
central vacuole. Journal of Cell Biology. 221(12), e202203139.
mla: Zhao, Jierui, et al. “Plant Autophagosomes Mature into Amphisomes Prior to
Their Delivery to the Central Vacuole.” Journal of Cell Biology, vol. 221,
no. 12, e202203139, Rockefeller University Press, 2022, doi:10.1083/jcb.202203139.
short: J. Zhao, M.T. Bui, J. Ma, F. Künzl, L. Picchianti, J.C. De La Concepcion,
Y. Chen, S. Petsangouraki, A. Mohseni, M. García-Leon, M.S. Gomez, C. Giannini,
D. Gwennogan, R. Kobylinska, M. Clavel, S. Schellmann, Y. Jaillais, J. Friml,
B.-H. Kang, Y. Dagdas, Journal of Cell Biology 221 (2022).
date_created: 2023-01-12T11:57:10Z
date_published: 2022-12-01T00:00:00Z
date_updated: 2023-08-03T14:20:15Z
day: '01'
ddc:
- '580'
department:
- _id: JiFr
doi: 10.1083/jcb.202203139
external_id:
isi:
- '000932958800001'
pmid:
- '36260289'
file:
- access_level: open_access
checksum: 050b5cc4b25e6b94fe3e3cbfe0f5c06b
content_type: application/pdf
creator: dernst
date_created: 2023-01-23T10:30:11Z
date_updated: 2023-01-23T10:30:11Z
file_id: '12342'
file_name: 2022_JCB_Zhao.pdf
file_size: 10365777
relation: main_file
success: 1
file_date_updated: 2023-01-23T10:30:11Z
has_accepted_license: '1'
intvolume: ' 221'
isi: 1
issue: '12'
keyword:
- Cell Biology
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
pmid: 1
publication: Journal of Cell Biology
publication_identifier:
eissn:
- 1540-8140
issn:
- 0021-9525
publication_status: published
publisher: Rockefeller University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Plant autophagosomes mature into amphisomes prior to their delivery to the
central vacuole
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 221
year: '2022'
...
---
_id: '12122'
abstract:
- lang: eng
text: Centrosomes play a crucial role during immune cell interactions and initiation
of the immune response. In proliferating cells, centrosome numbers are tightly
controlled and generally limited to one in G1 and two prior to mitosis. Defects
in regulating centrosome numbers have been associated with cell transformation
and tumorigenesis. Here, we report the emergence of extra centrosomes in leukocytes
during immune activation. Upon antigen encounter, dendritic cells pass through
incomplete mitosis and arrest in the subsequent G1 phase leading to tetraploid
cells with accumulated centrosomes. In addition, cell stimulation increases expression
of polo-like kinase 2, resulting in diploid cells with two centrosomes in G1-arrested
cells. During cell migration, centrosomes tightly cluster and act as functional
microtubule-organizing centers allowing for increased persistent locomotion along
gradients of chemotactic cues. Moreover, dendritic cells with extra centrosomes
display enhanced secretion of inflammatory cytokines and optimized T cell responses.
Together, these results demonstrate a previously unappreciated role of extra centrosomes
for regular cell and tissue homeostasis.
acknowledgement: "We thank Markéta Dalecká and Irena Krejzová for their support with
FIB-SEM imaging, the Imaging Methods Core Facility at BIOCEV supported by the Ministry
of Education, Youth and Sports Czech Republic (Large RI Project LM2018129 Czech-BioImaging),
and European Regional Development Fund (project No. CZ.02.1.01/0.0/0.0/18_046/0016045)
for their support with obtaining imaging data presented in this paper. The authors
further thank Andreas Villunger, Florian Gärtner, Frank Bradke, and Sarah Förster
for helpful discussions; Andy Zielinski for help with statistics; and Björn Weiershausen
for assisting with figure illustration.\r\n\r\nThis work was funded by a fellowship
of the Ministry of Innovation, Science and Research of North-Rhine-Westphalia (AZ:
421-8.03.03.02-137069) to E. Kiermaier and the Deutsche Forschungsgemeinschaft (German
Research Foundation) under Germany’s Excellence Strategy – EXC 2151 – 390873048.
R. Hauschild was funded by grant number 2020-225401 from the Chan Zuckerberg Initiative
Donor-Advised Fund, an advised fund of Silicon Valley Community Foundation. M. Hons
is supported by Czech Science Foundation GACR 20-24603Y and Charles University PRIMUS/20/MED/013."
article_number: e202107134
article_processing_charge: No
article_type: original
author:
- first_name: Ann-Kathrin
full_name: Weier, Ann-Kathrin
last_name: Weier
- first_name: Mirka
full_name: Homrich, Mirka
last_name: Homrich
- first_name: Stephanie
full_name: Ebbinghaus, Stephanie
last_name: Ebbinghaus
- first_name: Pavel
full_name: Juda, Pavel
last_name: Juda
- first_name: Eliška
full_name: Miková, Eliška
last_name: Miková
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Lili
full_name: Zhang, Lili
last_name: Zhang
- first_name: Thomas
full_name: Quast, Thomas
last_name: Quast
- first_name: Elvira
full_name: Mass, Elvira
last_name: Mass
- first_name: Andreas
full_name: Schlitzer, Andreas
last_name: Schlitzer
- first_name: Waldemar
full_name: Kolanus, Waldemar
last_name: Kolanus
- first_name: Sven
full_name: Burgdorf, Sven
last_name: Burgdorf
- first_name: Oliver J.
full_name: Gruß, Oliver J.
last_name: Gruß
- first_name: Miroslav
full_name: Hons, Miroslav
last_name: Hons
- first_name: Stefan
full_name: Wieser, Stefan
last_name: Wieser
- first_name: Eva
full_name: Kiermaier, Eva
last_name: Kiermaier
citation:
ama: Weier A-K, Homrich M, Ebbinghaus S, et al. Multiple centrosomes enhance migration
and immune cell effector functions of mature dendritic cells. Journal of Cell
Biology. 2022;221(12). doi:10.1083/jcb.202107134
apa: Weier, A.-K., Homrich, M., Ebbinghaus, S., Juda, P., Miková, E., Hauschild,
R., … Kiermaier, E. (2022). Multiple centrosomes enhance migration and immune
cell effector functions of mature dendritic cells. Journal of Cell Biology.
Rockefeller University Press. https://doi.org/10.1083/jcb.202107134
chicago: Weier, Ann-Kathrin, Mirka Homrich, Stephanie Ebbinghaus, Pavel Juda, Eliška
Miková, Robert Hauschild, Lili Zhang, et al. “Multiple Centrosomes Enhance Migration
and Immune Cell Effector Functions of Mature Dendritic Cells.” Journal of Cell
Biology. Rockefeller University Press, 2022. https://doi.org/10.1083/jcb.202107134.
ieee: A.-K. Weier et al., “Multiple centrosomes enhance migration and immune
cell effector functions of mature dendritic cells,” Journal of Cell Biology,
vol. 221, no. 12. Rockefeller University Press, 2022.
ista: Weier A-K, Homrich M, Ebbinghaus S, Juda P, Miková E, Hauschild R, Zhang L,
Quast T, Mass E, Schlitzer A, Kolanus W, Burgdorf S, Gruß OJ, Hons M, Wieser S,
Kiermaier E. 2022. Multiple centrosomes enhance migration and immune cell effector
functions of mature dendritic cells. Journal of Cell Biology. 221(12), e202107134.
mla: Weier, Ann-Kathrin, et al. “Multiple Centrosomes Enhance Migration and Immune
Cell Effector Functions of Mature Dendritic Cells.” Journal of Cell Biology,
vol. 221, no. 12, e202107134, Rockefeller University Press, 2022, doi:10.1083/jcb.202107134.
short: A.-K. Weier, M. Homrich, S. Ebbinghaus, P. Juda, E. Miková, R. Hauschild,
L. Zhang, T. Quast, E. Mass, A. Schlitzer, W. Kolanus, S. Burgdorf, O.J. Gruß,
M. Hons, S. Wieser, E. Kiermaier, Journal of Cell Biology 221 (2022).
date_created: 2023-01-12T12:01:09Z
date_published: 2022-12-05T00:00:00Z
date_updated: 2023-08-16T11:29:12Z
day: '05'
ddc:
- '570'
department:
- _id: Bio
doi: 10.1083/jcb.202107134
external_id:
isi:
- '000932941400001'
pmid:
- '36214847 '
file:
- access_level: open_access
checksum: 0c9af38f82af30c6ce528f2caece4246
content_type: application/pdf
creator: dernst
date_created: 2023-08-16T11:24:53Z
date_updated: 2023-08-16T11:24:53Z
file_id: '14065'
file_name: 2023_JCB_Weier.pdf
file_size: 11090179
relation: main_file
success: 1
file_date_updated: 2023-08-16T11:24:53Z
has_accepted_license: '1'
intvolume: ' 221'
isi: 1
issue: '12'
keyword:
- Cell Biology
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: c08e9ad1-5a5b-11eb-8a69-9d1cf3b07473
grant_number: CZI01
name: Tools for automation and feedback microscopy
publication: Journal of Cell Biology
publication_identifier:
eissn:
- 1540-8140
issn:
- 0021-9525
publication_status: published
publisher: Rockefeller University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Multiple centrosomes enhance migration and immune cell effector functions of
mature dendritic cells
tmp:
image: /images/cc_by_nc_sa.png
legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC
BY-NC-SA 4.0)
short: CC BY-NC-SA (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 221
year: '2022'
...
---
_id: '12130'
abstract:
- lang: eng
text: Germline determination is essential for species survival and evolution in
multicellular organisms. In most flowering plants, formation of the female germline
is initiated with specification of one megaspore mother cell (MMC) in each ovule;
however, the molecular mechanism underlying this key event remains unclear. Here
we report that spatially restricted auxin signaling promotes MMC fate in Arabidopsis.
Our results show that the microRNA160 (miR160) targeted gene ARF17 (AUXIN RESPONSE
FACTOR17) is required for promoting MMC specification by genetically interacting
with the SPL/NZZ (SPOROCYTELESS/NOZZLE) gene. Alterations of auxin signaling cause
formation of supernumerary MMCs in an ARF17- and SPL/NZZ-dependent manner. Furthermore,
miR160 and ARF17 are indispensable for attaining a normal auxin maximum at the
ovule apex via modulating the expression domain of PIN1 (PIN-FORMED1) auxin transporter.
Our findings elucidate the mechanism by which auxin signaling promotes the acquisition
of female germline cell fate in plants.
acknowledgement: "We thank A. Cheung,W. Lukowitz, V.Walbot, D.Weijers, and R. Yadegari
for critically reading the manuscript; E. Xiong and G. Zhang for preparing some
experiments, T. Schuck, J. Gonnering, and P. Engevold for plant care, the Arabidopsis
Biological Resource Center (ABRC) for ARF10,ARF16, ARF17, EMS1,MIR160a BAC clones
and cDNAs, the SALK_090804 seed, T. Nakagawa for pGBW vectors, Y. Zhao for the YUC1
cDNA, Q. Chen for the pHEE401E vector, R. Yadegari for pAT5G01860::n1GFP, pAT5G45980:n1GFP,
pAT5G50490::n1GFP, pAT5G56200:n1GFP vectors, and D.Weijers for the pGreenII KAN
SV40-3×GFP and R2D2 vectors, W. Yang for the splmutant, Y. Qin for the pKNU::KNU-VENUS
vector and seed, G. Tang for the STTM160/160-48 vector, and L. Colombo for pPIN1::PIN1-GFP
spl and pin1-5 seeds. This work was supported by the US National Science Foundation
(NSF)-Israel Binational Science Foundation (BSF) research grant to D.Z. (IOS-1322796)
and T.A. (2012756). D.Z. also\r\ngratefully acknowledges supports of the Shaw Scientist
Award from the Greater Milwaukee Foundation, USDA National Institute of Food and
Agriculture (NIFA, 2022-67013-36294), the UWM Discovery and Innovation Grant, the
Bradley Catalyst Award from the UWM Research\r\nFoundation, and WiSys and UW System
Applied Research Funding Programs."
article_number: '6960'
article_processing_charge: No
article_type: original
author:
- first_name: Jian
full_name: Huang, Jian
last_name: Huang
- first_name: Lei
full_name: Zhao, Lei
last_name: Zhao
- first_name: Shikha
full_name: Malik, Shikha
last_name: Malik
- first_name: Benjamin R.
full_name: Gentile, Benjamin R.
last_name: Gentile
- first_name: Va
full_name: Xiong, Va
last_name: Xiong
- first_name: Tzahi
full_name: Arazi, Tzahi
last_name: Arazi
- first_name: Heather A.
full_name: Owen, Heather A.
last_name: Owen
- first_name: Jiří
full_name: Friml, Jiří
id: 4159519E-F248-11E8-B48F-1D18A9856A87
last_name: Friml
orcid: 0000-0002-8302-7596
- first_name: Dazhong
full_name: Zhao, Dazhong
last_name: Zhao
citation:
ama: Huang J, Zhao L, Malik S, et al. Specification of female germline by microRNA
orchestrated auxin signaling in Arabidopsis. Nature Communications. 2022;13.
doi:10.1038/s41467-022-34723-6
apa: Huang, J., Zhao, L., Malik, S., Gentile, B. R., Xiong, V., Arazi, T., … Zhao,
D. (2022). Specification of female germline by microRNA orchestrated auxin signaling
in Arabidopsis. Nature Communications. Springer Nature. https://doi.org/10.1038/s41467-022-34723-6
chicago: Huang, Jian, Lei Zhao, Shikha Malik, Benjamin R. Gentile, Va Xiong, Tzahi
Arazi, Heather A. Owen, Jiří Friml, and Dazhong Zhao. “Specification of Female
Germline by MicroRNA Orchestrated Auxin Signaling in Arabidopsis.” Nature Communications.
Springer Nature, 2022. https://doi.org/10.1038/s41467-022-34723-6.
ieee: J. Huang et al., “Specification of female germline by microRNA orchestrated
auxin signaling in Arabidopsis,” Nature Communications, vol. 13. Springer
Nature, 2022.
ista: Huang J, Zhao L, Malik S, Gentile BR, Xiong V, Arazi T, Owen HA, Friml J,
Zhao D. 2022. Specification of female germline by microRNA orchestrated auxin
signaling in Arabidopsis. Nature Communications. 13, 6960.
mla: Huang, Jian, et al. “Specification of Female Germline by MicroRNA Orchestrated
Auxin Signaling in Arabidopsis.” Nature Communications, vol. 13, 6960,
Springer Nature, 2022, doi:10.1038/s41467-022-34723-6.
short: J. Huang, L. Zhao, S. Malik, B.R. Gentile, V. Xiong, T. Arazi, H.A. Owen,
J. Friml, D. Zhao, Nature Communications 13 (2022).
date_created: 2023-01-12T12:02:41Z
date_published: 2022-11-15T00:00:00Z
date_updated: 2023-08-04T08:52:01Z
day: '15'
ddc:
- '580'
department:
- _id: JiFr
doi: 10.1038/s41467-022-34723-6
external_id:
isi:
- '000884426700001'
pmid:
- '36379956'
file:
- access_level: open_access
checksum: 233922a7b9507d9d48591e6799e4526e
content_type: application/pdf
creator: dernst
date_created: 2023-01-23T11:17:33Z
date_updated: 2023-01-23T11:17:33Z
file_id: '12346'
file_name: 2022_NatureCommunications_Huang.pdf
file_size: 3375249
relation: main_file
success: 1
file_date_updated: 2023-01-23T11:17:33Z
has_accepted_license: '1'
intvolume: ' 13'
isi: 1
keyword:
- General Physics and Astronomy
- General Biochemistry
- Genetics and Molecular Biology
- General Chemistry
- Multidisciplinary
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
pmid: 1
publication: Nature Communications
publication_identifier:
issn:
- 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Specification of female germline by microRNA orchestrated auxin signaling in
Arabidopsis
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 13
year: '2022'
...
---
_id: '12143'
abstract:
- lang: eng
text: MicroRNA (miRNA) and RNA interference (RNAi) pathways rely on small RNAs produced
by Dicer endonucleases. Mammalian Dicer primarily supports the essential gene-regulating
miRNA pathway, but how it is specifically adapted to miRNA biogenesis is unknown.
We show that the adaptation entails a unique structural role of Dicer’s DExD/H
helicase domain. Although mice tolerate loss of its putative ATPase function,
the complete absence of the domain is lethal because it assures high-fidelity
miRNA biogenesis. Structures of murine Dicer⋅miRNA precursor complexes revealed
that the DExD/H domain has a helicase-unrelated structural function. It locks
Dicer in a closed state, which facilitates miRNA precursor selection. Transition
to a cleavage-competent open state is stimulated by Dicer-binding protein TARBP2.
Absence of the DExD/H domain or its mutations unlocks the closed state, reduces
substrate selectivity, and activates RNAi. Thus, the DExD/H domain structurally
contributes to mammalian miRNA biogenesis and underlies mechanistical partitioning
of miRNA and RNAi pathways.
acknowledged_ssus:
- _id: EM-Fac
acknowledgement: We thank Kristian Vlahovicek (University of Zagreb) for support of
bioinformatics analyses and Vladimir Benes (EMBL Sequencing Facility) and Genomics
and Bioinformatics Core Facility at the Institute of Molecular Genetics for help
with RNA sequencing. The main funding was provided by the Czech Science Foundation
(EXPRO grant 20-03950X to P.S. and 22-19896S to R. Stefl). Early stages of the work
were supported by European Research Council grants under the European Union’s Horizon
2020 Research and Innovation Programme (grants 647403 to P.S. and 649030 to R. Stefl).
V.B., D.F.J., and F.H. were in part supported by PhD student fellowships from the
Charles University; this work will be in part fulfilling requirements for a PhD
degree as “school work.” Funding of D.Z. included the OP RDE project “Internal Grant
Agency of Masaryk University” no. CZ.02.2.69/0.0/0.0/19_073/0016943. The Ministry
of Education, Youth, and Sports of the Czech Republic (MEYS CR) provided institutional
support for CEITEC 2020 project LQ1601. For technical support, we acknowledge EMBL
Monterotondo’s genome engineering and transgenic core facilities, the Czech Centre
for Phenogenomics at the Institute of Molecular Genetics (supported by RVO 68378050
from the Czech Academy of Sciences and LM2018126 and CZ.02.1.01/0.0/0.0/18_046/0015861
CCP Infrastructure Upgrade II from MEYS CR), the Cryo-EM and Proteomics Core Facilities
(CEITEC, Masaryk University) supported by the CIISB research infrastructure (LM2018127
from MEYS CR), and support from the Scientific Service Units of ISTA through resources
from the Electron Microscopy Facility. Computational resources included e-Infrastruktura
CZ (LM2018140) and ELIXIR-CZ (LM2018131) projects by MEYS CR and the Croatian National
Centres of Research Excellence in Personalized Healthcare (#KK.01.1.1.01.0010) and
Data Science and Advanced Cooperative Systems (#KK.01.1.1.01.0009) projects funded
by the European Structural and Investment Funds grants.
article_processing_charge: No
article_type: original
author:
- first_name: David
full_name: Zapletal, David
last_name: Zapletal
- first_name: Eliska
full_name: Taborska, Eliska
last_name: Taborska
- first_name: Josef
full_name: Pasulka, Josef
last_name: Pasulka
- first_name: Radek
full_name: Malik, Radek
last_name: Malik
- first_name: Karel
full_name: Kubicek, Karel
last_name: Kubicek
- first_name: Martina
full_name: Zanova, Martina
last_name: Zanova
- first_name: Christian
full_name: Much, Christian
last_name: Much
- first_name: Marek
full_name: Sebesta, Marek
last_name: Sebesta
- first_name: Valeria
full_name: Buccheri, Valeria
last_name: Buccheri
- first_name: Filip
full_name: Horvat, Filip
last_name: Horvat
- first_name: Irena
full_name: Jenickova, Irena
last_name: Jenickova
- first_name: Michaela
full_name: Prochazkova, Michaela
last_name: Prochazkova
- first_name: Jan
full_name: Prochazka, Jan
last_name: Prochazka
- first_name: Matyas
full_name: Pinkas, Matyas
last_name: Pinkas
- first_name: Jiri
full_name: Novacek, Jiri
last_name: Novacek
- first_name: Diego F.
full_name: Joseph, Diego F.
last_name: Joseph
- first_name: Radislav
full_name: Sedlacek, Radislav
last_name: Sedlacek
- first_name: Carrie A
full_name: Bernecky, Carrie A
id: 2CB9DFE2-F248-11E8-B48F-1D18A9856A87
last_name: Bernecky
orcid: 0000-0003-0893-7036
- first_name: Dónal
full_name: O’Carroll, Dónal
last_name: O’Carroll
- first_name: Richard
full_name: Stefl, Richard
last_name: Stefl
- first_name: Petr
full_name: Svoboda, Petr
last_name: Svoboda
citation:
ama: Zapletal D, Taborska E, Pasulka J, et al. Structural and functional basis of
mammalian microRNA biogenesis by Dicer. Molecular Cell. 2022;82(21):4064-4079.e13.
doi:10.1016/j.molcel.2022.10.010
apa: Zapletal, D., Taborska, E., Pasulka, J., Malik, R., Kubicek, K., Zanova, M.,
… Svoboda, P. (2022). Structural and functional basis of mammalian microRNA biogenesis
by Dicer. Molecular Cell. Elsevier. https://doi.org/10.1016/j.molcel.2022.10.010
chicago: Zapletal, David, Eliska Taborska, Josef Pasulka, Radek Malik, Karel Kubicek,
Martina Zanova, Christian Much, et al. “Structural and Functional Basis of Mammalian
MicroRNA Biogenesis by Dicer.” Molecular Cell. Elsevier, 2022. https://doi.org/10.1016/j.molcel.2022.10.010.
ieee: D. Zapletal et al., “Structural and functional basis of mammalian microRNA
biogenesis by Dicer,” Molecular Cell, vol. 82, no. 21. Elsevier, p. 4064–4079.e13,
2022.
ista: Zapletal D, Taborska E, Pasulka J, Malik R, Kubicek K, Zanova M, Much C, Sebesta
M, Buccheri V, Horvat F, Jenickova I, Prochazkova M, Prochazka J, Pinkas M, Novacek
J, Joseph DF, Sedlacek R, Bernecky C, O’Carroll D, Stefl R, Svoboda P. 2022. Structural
and functional basis of mammalian microRNA biogenesis by Dicer. Molecular Cell.
82(21), 4064–4079.e13.
mla: Zapletal, David, et al. “Structural and Functional Basis of Mammalian MicroRNA
Biogenesis by Dicer.” Molecular Cell, vol. 82, no. 21, Elsevier, 2022,
p. 4064–4079.e13, doi:10.1016/j.molcel.2022.10.010.
short: D. Zapletal, E. Taborska, J. Pasulka, R. Malik, K. Kubicek, M. Zanova, C.
Much, M. Sebesta, V. Buccheri, F. Horvat, I. Jenickova, M. Prochazkova, J. Prochazka,
M. Pinkas, J. Novacek, D.F. Joseph, R. Sedlacek, C. Bernecky, D. O’Carroll, R.
Stefl, P. Svoboda, Molecular Cell 82 (2022) 4064–4079.e13.
date_created: 2023-01-12T12:05:36Z
date_published: 2022-11-03T00:00:00Z
date_updated: 2023-08-04T08:57:17Z
day: '03'
ddc:
- '570'
department:
- _id: CaBe
doi: 10.1016/j.molcel.2022.10.010
external_id:
isi:
- '000898565300011'
pmid:
- '36332606'
file:
- access_level: open_access
checksum: 999e443b54e4fdaa2542ca5a97619731
content_type: application/pdf
creator: dernst
date_created: 2023-01-24T09:29:02Z
date_updated: 2023-01-24T09:29:02Z
file_id: '12354'
file_name: 2022_MolecularCell_Zapletal.pdf
file_size: 7368534
relation: main_file
success: 1
file_date_updated: 2023-01-24T09:29:02Z
has_accepted_license: '1'
intvolume: ' 82'
isi: 1
issue: '21'
keyword:
- Cell Biology
- Molecular Biology
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
page: 4064-4079.e13
pmid: 1
publication: Molecular Cell
publication_identifier:
issn:
- 1097-2765
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Structural and functional basis of mammalian microRNA biogenesis by Dicer
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 82
year: '2022'
...
---
_id: '12585'
abstract:
- lang: eng
text: Glaciers in High Mountain Asia generate meltwater that supports the water
needs of 250 million people, but current knowledge of annual accumulation and
ablation is limited to sparse field measurements biased in location and glacier
size. Here, we present altitudinally-resolved specific mass balances (surface,
internal, and basal combined) for 5527 glaciers in High Mountain Asia for 2000–2016,
derived by correcting observed glacier thinning patterns for mass redistribution
due to ice flow. We find that 41% of glaciers accumulated mass over less than
20% of their area, and only 60% ± 10% of regional annual ablation was compensated
by accumulation. Even without 21st century warming, 21% ± 1% of ice volume will
be lost by 2100 due to current climatic-geometric imbalance, representing a reduction
in glacier ablation into rivers of 28% ± 1%. The ablation of glaciers in the Himalayas
and Tien Shan was mostly unsustainable and ice volume in these regions will reduce
by at least 30% by 2100. The most important and vulnerable glacier-fed river basins
(Amu Darya, Indus, Syr Darya, Tarim Interior) were supplied with >50% sustainable
glacier ablation but will see long-term reductions in ice mass and glacier meltwater
supply regardless of the Karakoram Anomaly.
article_number: '2868'
article_processing_charge: No
article_type: original
author:
- first_name: Evan
full_name: Miles, Evan
last_name: Miles
- first_name: Michael
full_name: McCarthy, Michael
last_name: McCarthy
- first_name: Amaury
full_name: Dehecq, Amaury
last_name: Dehecq
- first_name: Marin
full_name: Kneib, Marin
last_name: Kneib
- first_name: Stefan
full_name: Fugger, Stefan
last_name: Fugger
- first_name: Francesca
full_name: Pellicciotti, Francesca
id: b28f055a-81ea-11ed-b70c-a9fe7f7b0e70
last_name: Pellicciotti
citation:
ama: Miles E, McCarthy M, Dehecq A, Kneib M, Fugger S, Pellicciotti F. Health and
sustainability of glaciers in High Mountain Asia. Nature Communications.
2021;12. doi:10.1038/s41467-021-23073-4
apa: Miles, E., McCarthy, M., Dehecq, A., Kneib, M., Fugger, S., & Pellicciotti,
F. (2021). Health and sustainability of glaciers in High Mountain Asia. Nature
Communications. Springer Nature. https://doi.org/10.1038/s41467-021-23073-4
chicago: Miles, Evan, Michael McCarthy, Amaury Dehecq, Marin Kneib, Stefan Fugger,
and Francesca Pellicciotti. “Health and Sustainability of Glaciers in High Mountain
Asia.” Nature Communications. Springer Nature, 2021. https://doi.org/10.1038/s41467-021-23073-4.
ieee: E. Miles, M. McCarthy, A. Dehecq, M. Kneib, S. Fugger, and F. Pellicciotti,
“Health and sustainability of glaciers in High Mountain Asia,” Nature Communications,
vol. 12. Springer Nature, 2021.
ista: Miles E, McCarthy M, Dehecq A, Kneib M, Fugger S, Pellicciotti F. 2021. Health
and sustainability of glaciers in High Mountain Asia. Nature Communications. 12,
2868.
mla: Miles, Evan, et al. “Health and Sustainability of Glaciers in High Mountain
Asia.” Nature Communications, vol. 12, 2868, Springer Nature, 2021, doi:10.1038/s41467-021-23073-4.
short: E. Miles, M. McCarthy, A. Dehecq, M. Kneib, S. Fugger, F. Pellicciotti, Nature
Communications 12 (2021).
date_created: 2023-02-20T08:11:29Z
date_published: 2021-05-17T00:00:00Z
date_updated: 2023-02-28T13:21:51Z
day: '17'
doi: 10.1038/s41467-021-23073-4
extern: '1'
intvolume: ' 12'
keyword:
- General Physics and Astronomy
- General Biochemistry
- Genetics and Molecular Biology
- General Chemistry
- Multidisciplinary
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1038/s41467-021-23073-4
month: '05'
oa: 1
oa_version: Published Version
publication: Nature Communications
publication_identifier:
issn:
- 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Health and sustainability of glaciers in High Mountain Asia
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 12
year: '2021'
...
---
_id: '8966'
abstract:
- lang: eng
text: During development, a single cell is transformed into a highly complex organism
through progressive cell division, specification and rearrangement. An important
prerequisite for the emergence of patterns within the developing organism is to
establish asymmetries at various scales, ranging from individual cells to the
entire embryo, eventually giving rise to the different body structures. This becomes
especially apparent during gastrulation, when the earliest major lineage restriction
events lead to the formation of the different germ layers. Traditionally, the
unfolding of the developmental program from symmetry breaking to germ layer formation
has been studied by dissecting the contributions of different signaling pathways
and cellular rearrangements in the in vivo context of intact embryos. Recent efforts,
using the intrinsic capacity of embryonic stem cells to self-assemble and generate
embryo-like structures de novo, have opened new avenues for understanding the
many ways by which an embryo can be built and the influence of extrinsic factors
therein. Here, we discuss and compare divergent and conserved strategies leading
to germ layer formation in embryos as compared to in vitro systems, their upstream
molecular cascades and the role of extrinsic factors in this process.
acknowledgement: We thank Nicoletta Petridou, Diana Pinheiro, Cornelia Schwayer and
Stefania Tavano for feedback on the manuscript. Research in the Heisenberg lab is
supported by an ERC Advanced Grant (MECSPEC 742573) to C.-P.H. A.S. is a recipient
of a DOC Fellowship of the Austrian Academy of Science.
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Alexandra
full_name: Schauer, Alexandra
id: 30A536BA-F248-11E8-B48F-1D18A9856A87
last_name: Schauer
orcid: 0000-0001-7659-9142
- first_name: Carl-Philipp J
full_name: Heisenberg, Carl-Philipp J
id: 39427864-F248-11E8-B48F-1D18A9856A87
last_name: Heisenberg
orcid: 0000-0002-0912-4566
citation:
ama: Schauer A, Heisenberg C-PJ. Reassembling gastrulation. Developmental Biology.
2021;474:71-81. doi:10.1016/j.ydbio.2020.12.014
apa: Schauer, A., & Heisenberg, C.-P. J. (2021). Reassembling gastrulation.
Developmental Biology. Elsevier. https://doi.org/10.1016/j.ydbio.2020.12.014
chicago: Schauer, Alexandra, and Carl-Philipp J Heisenberg. “Reassembling Gastrulation.”
Developmental Biology. Elsevier, 2021. https://doi.org/10.1016/j.ydbio.2020.12.014.
ieee: A. Schauer and C.-P. J. Heisenberg, “Reassembling gastrulation,” Developmental
Biology, vol. 474. Elsevier, pp. 71–81, 2021.
ista: Schauer A, Heisenberg C-PJ. 2021. Reassembling gastrulation. Developmental
Biology. 474, 71–81.
mla: Schauer, Alexandra, and Carl-Philipp J. Heisenberg. “Reassembling Gastrulation.”
Developmental Biology, vol. 474, Elsevier, 2021, pp. 71–81, doi:10.1016/j.ydbio.2020.12.014.
short: A. Schauer, C.-P.J. Heisenberg, Developmental Biology 474 (2021) 71–81.
date_created: 2020-12-22T09:53:34Z
date_published: 2021-06-01T00:00:00Z
date_updated: 2023-08-07T13:30:01Z
day: '01'
ddc:
- '570'
department:
- _id: CaHe
doi: 10.1016/j.ydbio.2020.12.014
ec_funded: 1
external_id:
isi:
- '000639461800008'
file:
- access_level: open_access
checksum: fa2a5731fd16ab171b029f32f031c440
content_type: application/pdf
creator: kschuh
date_created: 2021-08-11T10:28:06Z
date_updated: 2021-08-11T10:28:06Z
file_id: '9880'
file_name: 2021_DevBiology_Schauer.pdf
file_size: 1440321
relation: main_file
success: 1
file_date_updated: 2021-08-11T10:28:06Z
has_accepted_license: '1'
intvolume: ' 474'
isi: 1
keyword:
- Developmental Biology
- Cell Biology
- Molecular Biology
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
page: 71-81
project:
- _id: 260F1432-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '742573'
name: Interaction and feedback between cell mechanics and fate specification in
vertebrate gastrulation
- _id: 26B1E39C-B435-11E9-9278-68D0E5697425
grant_number: '25239'
name: 'Mesendoderm specification in zebrafish: The role of extraembryonic tissues'
publication: Developmental Biology
publication_identifier:
issn:
- 0012-1606
publication_status: published
publisher: Elsevier
quality_controlled: '1'
related_material:
record:
- id: '12891'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Reassembling gastrulation
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 474
year: '2021'
...
---
_id: '8997'
abstract:
- lang: eng
text: Phenomenological relations such as Ohm’s or Fourier’s law have a venerable
history in physics but are still scarce in biology. This situation restrains predictive
theory. Here, we build on bacterial “growth laws,” which capture physiological
feedback between translation and cell growth, to construct a minimal biophysical
model for the combined action of ribosome-targeting antibiotics. Our model predicts
drug interactions like antagonism or synergy solely from responses to individual
drugs. We provide analytical results for limiting cases, which agree well with
numerical results. We systematically refine the model by including direct physical
interactions of different antibiotics on the ribosome. In a limiting case, our
model provides a mechanistic underpinning for recent predictions of higher-order
interactions that were derived using entropy maximization. We further refine the
model to include the effects of antibiotics that mimic starvation and the presence
of resistance genes. We describe the impact of a starvation-mimicking antibiotic
on drug interactions analytically and verify it experimentally. Our extended model
suggests a change in the type of drug interaction that depends on the strength
of resistance, which challenges established rescaling paradigms. We experimentally
show that the presence of unregulated resistance genes can lead to altered drug
interaction, which agrees with the prediction of the model. While minimal, the
model is readily adaptable and opens the door to predicting interactions of second
and higher-order in a broad range of biological systems.
acknowledgement: 'This work was supported in part by Tum stipend of Knafelj foundation
(to B.K.), Austrian Science Fund (FWF) standalone grants P 27201-B22 (to T.B.) and
P 28844(to G.T.), HFSP program Grant RGP0042/2013 (to T.B.), German Research Foundation
(DFG) individual grant BO 3502/2-1 (to T.B.), and German Research Foundation (DFG)
Collaborative Research Centre (SFB) 1310 (to T.B.). '
article_number: e1008529
article_processing_charge: Yes
article_type: original
author:
- first_name: Bor
full_name: Kavcic, Bor
id: 350F91D2-F248-11E8-B48F-1D18A9856A87
last_name: Kavcic
orcid: 0000-0001-6041-254X
- first_name: Gašper
full_name: Tkačik, Gašper
id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
last_name: Tkačik
orcid: 0000-0002-6699-1455
- first_name: Tobias
full_name: Bollenbach, Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
citation:
ama: Kavcic B, Tkačik G, Bollenbach MT. Minimal biophysical model of combined antibiotic
action. PLOS Computational Biology. 2021;17. doi:10.1371/journal.pcbi.1008529
apa: Kavcic, B., Tkačik, G., & Bollenbach, M. T. (2021). Minimal biophysical
model of combined antibiotic action. PLOS Computational Biology. Public
Library of Science. https://doi.org/10.1371/journal.pcbi.1008529
chicago: Kavcic, Bor, Gašper Tkačik, and Mark Tobias Bollenbach. “Minimal Biophysical
Model of Combined Antibiotic Action.” PLOS Computational Biology. Public
Library of Science, 2021. https://doi.org/10.1371/journal.pcbi.1008529.
ieee: B. Kavcic, G. Tkačik, and M. T. Bollenbach, “Minimal biophysical model of
combined antibiotic action,” PLOS Computational Biology, vol. 17. Public
Library of Science, 2021.
ista: Kavcic B, Tkačik G, Bollenbach MT. 2021. Minimal biophysical model of combined
antibiotic action. PLOS Computational Biology. 17, e1008529.
mla: Kavcic, Bor, et al. “Minimal Biophysical Model of Combined Antibiotic Action.”
PLOS Computational Biology, vol. 17, e1008529, Public Library of Science,
2021, doi:10.1371/journal.pcbi.1008529.
short: B. Kavcic, G. Tkačik, M.T. Bollenbach, PLOS Computational Biology 17 (2021).
date_created: 2021-01-08T07:16:18Z
date_published: 2021-01-07T00:00:00Z
date_updated: 2024-02-21T12:41:41Z
day: '07'
ddc:
- '570'
department:
- _id: GaTk
doi: 10.1371/journal.pcbi.1008529
external_id:
isi:
- '000608045000010'
file:
- access_level: open_access
checksum: e29f2b42651bef8e034781de8781ffac
content_type: application/pdf
creator: dernst
date_created: 2021-02-04T12:30:48Z
date_updated: 2021-02-04T12:30:48Z
file_id: '9092'
file_name: 2021_PlosComBio_Kavcic.pdf
file_size: 3690053
relation: main_file
success: 1
file_date_updated: 2021-02-04T12:30:48Z
has_accepted_license: '1'
intvolume: ' 17'
isi: 1
keyword:
- Modelling and Simulation
- Genetics
- Molecular Biology
- Antibiotics
- Drug interactions
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
project:
- _id: 25E9AF9E-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P27201-B22
name: Revealing the mechanisms underlying drug interactions
- _id: 254E9036-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P28844-B27
name: Biophysics of information processing in gene regulation
publication: PLOS Computational Biology
publication_identifier:
issn:
- 1553-7358
publication_status: published
publisher: Public Library of Science
quality_controlled: '1'
related_material:
record:
- id: '7673'
relation: earlier_version
status: public
- id: '8930'
relation: research_data
status: public
status: public
title: Minimal biophysical model of combined antibiotic action
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 17
year: '2021'
...
---
_id: '9188'
abstract:
- lang: eng
text: Genomic imprinting is an epigenetic mechanism that results in parental allele-specific
expression of ~1% of all genes in mouse and human. Imprinted genes are key developmental
regulators and play pivotal roles in many biological processes such as nutrient
transfer from the mother to offspring and neuronal development. Imprinted genes
are also involved in human disease, including neurodevelopmental disorders, and
often occur in clusters that are regulated by a common imprint control region
(ICR). In extra-embryonic tissues ICRs can act over large distances, with the
largest surrounding Igf2r spanning over 10 million base-pairs. Besides classical
imprinted expression that shows near exclusive maternal or paternal expression,
widespread biased imprinted expression has been identified mainly in brain. In
this review we discuss recent developments mapping cell type specific imprinted
expression in extra-embryonic tissues and neocortex in the mouse. We highlight
the advantages of using an inducible uniparental chromosome disomy (UPD) system
to generate cells carrying either two maternal or two paternal copies of a specific
chromosome to analyze the functional consequences of genomic imprinting. Mosaic
Analysis with Double Markers (MADM) allows fluorescent labeling and concomitant
induction of UPD sparsely in specific cell types, and thus to over-express or
suppress all imprinted genes on that chromosome. To illustrate the utility of
this technique, we explain how MADM-induced UPD revealed new insights about the
function of the well-studied Cdkn1c imprinted gene, and how MADM-induced UPDs
led to identification of highly cell type specific phenotypes related to perturbed
imprinted expression in the mouse neocortex. Finally, we give an outlook on how
MADM could be used to probe cell type specific imprinted expression in other tissues
in mouse, particularly in extra-embryonic tissues.
acknowledgement: We thank Melissa Stouffer for critically reading the manuscript.
This work was supported by IST Austria institutional funds; NÖ Forschung und Bildung
n[f + b] life science call grant (C13-002) to S.H. and the European Research Council
(ERC) under the European Union's Horizon 2020 research and innovation program (grant
agreement 725780 LinPro) to S.H.
article_number: '104986'
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
- first_name: Quanah
full_name: Hudson, Quanah
last_name: Hudson
- first_name: Susanne
full_name: Laukoter, Susanne
id: 2D6B7A9A-F248-11E8-B48F-1D18A9856A87
last_name: Laukoter
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Pauler F, Hudson Q, Laukoter S, Hippenmeyer S. Inducible uniparental chromosome
disomy to probe genomic imprinting at single-cell level in brain and beyond. Neurochemistry
International. 2021;145(5). doi:10.1016/j.neuint.2021.104986
apa: Pauler, F., Hudson, Q., Laukoter, S., & Hippenmeyer, S. (2021). Inducible
uniparental chromosome disomy to probe genomic imprinting at single-cell level
in brain and beyond. Neurochemistry International. Elsevier. https://doi.org/10.1016/j.neuint.2021.104986
chicago: Pauler, Florian, Quanah Hudson, Susanne Laukoter, and Simon Hippenmeyer.
“Inducible Uniparental Chromosome Disomy to Probe Genomic Imprinting at Single-Cell
Level in Brain and Beyond.” Neurochemistry International. Elsevier, 2021.
https://doi.org/10.1016/j.neuint.2021.104986.
ieee: F. Pauler, Q. Hudson, S. Laukoter, and S. Hippenmeyer, “Inducible uniparental
chromosome disomy to probe genomic imprinting at single-cell level in brain and
beyond,” Neurochemistry International, vol. 145, no. 5. Elsevier, 2021.
ista: Pauler F, Hudson Q, Laukoter S, Hippenmeyer S. 2021. Inducible uniparental
chromosome disomy to probe genomic imprinting at single-cell level in brain and
beyond. Neurochemistry International. 145(5), 104986.
mla: Pauler, Florian, et al. “Inducible Uniparental Chromosome Disomy to Probe Genomic
Imprinting at Single-Cell Level in Brain and Beyond.” Neurochemistry International,
vol. 145, no. 5, 104986, Elsevier, 2021, doi:10.1016/j.neuint.2021.104986.
short: F. Pauler, Q. Hudson, S. Laukoter, S. Hippenmeyer, Neurochemistry International
145 (2021).
date_created: 2021-02-23T12:31:43Z
date_published: 2021-05-01T00:00:00Z
date_updated: 2023-08-07T13:48:26Z
day: '01'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1016/j.neuint.2021.104986
ec_funded: 1
external_id:
isi:
- '000635575000005'
pmid:
- '33600873'
file:
- access_level: open_access
checksum: c6d7a40089cd29e289f9b22e75768304
content_type: application/pdf
creator: kschuh
date_created: 2021-08-11T12:30:38Z
date_updated: 2021-08-11T12:30:38Z
file_id: '9883'
file_name: 2021_NCI_Pauler.pdf
file_size: 7083499
relation: main_file
success: 1
file_date_updated: 2021-08-11T12:30:38Z
has_accepted_license: '1'
intvolume: ' 145'
isi: 1
issue: '5'
keyword:
- Cell Biology
- Cellular and Molecular Neuroscience
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
- _id: 25D92700-B435-11E9-9278-68D0E5697425
grant_number: LS13-002
name: Mapping Cell-Type Specificity of the Genomic Imprintome in the Brain
publication: Neurochemistry International
publication_identifier:
issn:
- 0197-0186
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Inducible uniparental chromosome disomy to probe genomic imprinting at single-cell
level in brain and beyond
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 145
year: '2021'
...
---
_id: '9283'
abstract:
- lang: eng
text: Gene expression levels are influenced by multiple coexisting molecular mechanisms.
Some of these interactions such as those of transcription factors and promoters
have been studied extensively. However, predicting phenotypes of gene regulatory
networks (GRNs) remains a major challenge. Here, we use a well-defined synthetic
GRN to study in Escherichia coli how network phenotypes depend on local genetic
context, i.e. the genetic neighborhood of a transcription factor and its relative
position. We show that one GRN with fixed topology can display not only quantitatively
but also qualitatively different phenotypes, depending solely on the local genetic
context of its components. Transcriptional read-through is the main molecular
mechanism that places one transcriptional unit (TU) within two separate regulons
without the need for complex regulatory sequences. We propose that relative order
of individual TUs, with its potential for combinatorial complexity, plays an important
role in shaping phenotypes of GRNs.
acknowledgement: "We thank J Bollback, L Hurst, M Lagator, C Nizak, O Rivoire, M Savageau,
G Tkacik, and B Vicozo\r\nfor helpful discussions; A Dolinar and A Greshnova for
technical assistance; T Bollenbach for supplying the strain JW0336; C Rusnac, and
members of the Guet lab for comments. The research leading to these results has
received funding from the People Programme (Marie Curie Actions) of the European
Union’s Seventh Framework Programme (FP7/2007-2013) under REA grant agreement n˚\r\n628377
(ANS) and an Austrian Science Fund (FWF) grant n˚ I 3901-B32 (CCG)."
article_number: e65993
article_processing_charge: Yes
article_type: original
author:
- first_name: Anna A
full_name: Nagy-Staron, Anna A
id: 3ABC5BA6-F248-11E8-B48F-1D18A9856A87
last_name: Nagy-Staron
orcid: 0000-0002-1391-8377
- first_name: Kathrin
full_name: Tomasek, Kathrin
id: 3AEC8556-F248-11E8-B48F-1D18A9856A87
last_name: Tomasek
orcid: 0000-0003-3768-877X
- first_name: Caroline
full_name: Caruso Carter, Caroline
last_name: Caruso Carter
- first_name: Elisabeth
full_name: Sonnleitner, Elisabeth
last_name: Sonnleitner
- first_name: Bor
full_name: Kavcic, Bor
id: 350F91D2-F248-11E8-B48F-1D18A9856A87
last_name: Kavcic
orcid: 0000-0001-6041-254X
- first_name: Tiago
full_name: Paixão, Tiago
last_name: Paixão
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
citation:
ama: Nagy-Staron AA, Tomasek K, Caruso Carter C, et al. Local genetic context shapes
the function of a gene regulatory network. eLife. 2021;10. doi:10.7554/elife.65993
apa: Nagy-Staron, A. A., Tomasek, K., Caruso Carter, C., Sonnleitner, E., Kavcic,
B., Paixão, T., & Guet, C. C. (2021). Local genetic context shapes the function
of a gene regulatory network. ELife. eLife Sciences Publications. https://doi.org/10.7554/elife.65993
chicago: Nagy-Staron, Anna A, Kathrin Tomasek, Caroline Caruso Carter, Elisabeth
Sonnleitner, Bor Kavcic, Tiago Paixão, and Calin C Guet. “Local Genetic Context
Shapes the Function of a Gene Regulatory Network.” ELife. eLife Sciences
Publications, 2021. https://doi.org/10.7554/elife.65993.
ieee: A. A. Nagy-Staron et al., “Local genetic context shapes the function
of a gene regulatory network,” eLife, vol. 10. eLife Sciences Publications,
2021.
ista: Nagy-Staron AA, Tomasek K, Caruso Carter C, Sonnleitner E, Kavcic B, Paixão
T, Guet CC. 2021. Local genetic context shapes the function of a gene regulatory
network. eLife. 10, e65993.
mla: Nagy-Staron, Anna A., et al. “Local Genetic Context Shapes the Function of
a Gene Regulatory Network.” ELife, vol. 10, e65993, eLife Sciences Publications,
2021, doi:10.7554/elife.65993.
short: A.A. Nagy-Staron, K. Tomasek, C. Caruso Carter, E. Sonnleitner, B. Kavcic,
T. Paixão, C.C. Guet, ELife 10 (2021).
date_created: 2021-03-23T10:11:46Z
date_published: 2021-03-08T00:00:00Z
date_updated: 2024-02-21T12:41:57Z
day: '08'
ddc:
- '570'
department:
- _id: GaTk
- _id: CaGu
doi: 10.7554/elife.65993
ec_funded: 1
external_id:
isi:
- '000631050900001'
file:
- access_level: open_access
checksum: 3c2f44058c2dd45a5a1027f09d263f8e
content_type: application/pdf
creator: bkavcic
date_created: 2021-03-23T10:12:58Z
date_updated: 2021-03-23T10:12:58Z
file_id: '9284'
file_name: elife-65993-v2.pdf
file_size: 1390469
relation: main_file
success: 1
file_date_updated: 2021-03-23T10:12:58Z
has_accepted_license: '1'
intvolume: ' 10'
isi: 1
keyword:
- Genetics and Molecular Biology
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
project:
- _id: 2517526A-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '628377'
name: 'The Systems Biology of Transcriptional Read-Through in Bacteria: from Synthetic
Networks to Genomic Studies'
- _id: 268BFA92-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: I03901
name: 'CyberCircuits: Cybergenetic circuits to test composability of gene networks'
publication: eLife
publication_identifier:
issn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
related_material:
record:
- id: '8951'
relation: research_data
status: public
status: public
title: Local genetic context shapes the function of a gene regulatory network
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 10
year: '2021'
...
---
_id: '9387'
abstract:
- lang: eng
text: We report the complete analysis of a deterministic model of deleterious mutations
and negative selection against them at two haploid loci without recombination.
As long as mutation is a weaker force than selection, mutant alleles remain rare
at the only stable equilibrium, and otherwise, a variety of dynamics are possible.
If the mutation-free genotype is absent, generally the only stable equilibrium
is the one that corresponds to fixation of the mutant allele at the locus where
it is less deleterious. This result suggests that fixation of a deleterious allele
that follows a click of the Muller’s ratchet is governed by natural selection,
instead of random drift.
acknowledgement: This work was supported by the Russian Science Foundation grant N
16-14-10173.
article_number: '110729'
article_processing_charge: No
article_type: original
author:
- first_name: Kseniia
full_name: Khudiakova, Kseniia
id: 4E6DC800-AE37-11E9-AC72-31CAE5697425
last_name: Khudiakova
orcid: 0000-0002-6246-1465
- first_name: Tatiana Yu.
full_name: Neretina, Tatiana Yu.
last_name: Neretina
- first_name: Alexey S.
full_name: Kondrashov, Alexey S.
last_name: Kondrashov
citation:
ama: Khudiakova K, Neretina TY, Kondrashov AS. Two linked loci under mutation-selection
balance and Muller’s ratchet. Journal of Theoretical Biology. 2021;524.
doi:10.1016/j.jtbi.2021.110729
apa: Khudiakova, K., Neretina, T. Y., & Kondrashov, A. S. (2021). Two linked
loci under mutation-selection balance and Muller’s ratchet. Journal of Theoretical
Biology. Elsevier . https://doi.org/10.1016/j.jtbi.2021.110729
chicago: Khudiakova, Kseniia, Tatiana Yu. Neretina, and Alexey S. Kondrashov. “Two
Linked Loci under Mutation-Selection Balance and Muller’s Ratchet.” Journal
of Theoretical Biology. Elsevier , 2021. https://doi.org/10.1016/j.jtbi.2021.110729.
ieee: K. Khudiakova, T. Y. Neretina, and A. S. Kondrashov, “Two linked loci under
mutation-selection balance and Muller’s ratchet,” Journal of Theoretical Biology,
vol. 524. Elsevier , 2021.
ista: Khudiakova K, Neretina TY, Kondrashov AS. 2021. Two linked loci under mutation-selection
balance and Muller’s ratchet. Journal of Theoretical Biology. 524, 110729.
mla: Khudiakova, Kseniia, et al. “Two Linked Loci under Mutation-Selection Balance
and Muller’s Ratchet.” Journal of Theoretical Biology, vol. 524, 110729,
Elsevier , 2021, doi:10.1016/j.jtbi.2021.110729.
short: K. Khudiakova, T.Y. Neretina, A.S. Kondrashov, Journal of Theoretical Biology
524 (2021).
date_created: 2021-05-12T05:58:42Z
date_published: 2021-04-24T00:00:00Z
date_updated: 2023-08-08T13:32:40Z
day: '24'
department:
- _id: GradSch
doi: 10.1016/j.jtbi.2021.110729
external_id:
isi:
- '000659161500002'
intvolume: ' 524'
isi: 1
keyword:
- General Biochemistry
- Genetics and Molecular Biology
- Modelling and Simulation
- Statistics and Probability
- General Immunology and Microbiology
- Applied Mathematics
- General Agricultural and Biological Sciences
- General Medicine
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.biorxiv.org/content/10.1101/477489v1
month: '04'
oa: 1
oa_version: Preprint
publication: Journal of Theoretical Biology
publication_identifier:
issn:
- 0022-5193
publication_status: published
publisher: 'Elsevier '
quality_controlled: '1'
status: public
title: Two linked loci under mutation-selection balance and Muller’s ratchet
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 524
year: '2021'
...
---
_id: '13356'
abstract:
- lang: eng
text: 'Self-assembly of nanoparticles can be mediated by polymers, but has so far
led almost exclusively to nanoparticle aggregates that are amorphous. Here, we
employed Coulombic interactions to generate a range of composite materials from
mixtures of charged nanoparticles and oppositely charged polymers. The assembly
behavior of these nanoparticle/polymer composites depends on their order of addition:
polymers added to nanoparticles give rise to stable aggregates, but nanoparticles
added to polymers disassemble the initially formed aggregates. The amorphous aggregates
were transformed into crystalline ones by transiently increasing the ionic strength
of the solution. The morphology of the resulting crystals depended on the length
of the polymer: short polymer chains mediated the self-assembly of nanoparticles
into strongly faceted crystals, whereas long chains led to pseudospherical nanoparticle/polymer
assemblies, within which the crystalline order of nanoparticles was retained.'
article_processing_charge: No
article_type: original
author:
- first_name: Tong
full_name: Bian, Tong
last_name: Bian
- first_name: Rafal
full_name: Klajn, Rafal
id: 8e84690e-1e48-11ed-a02b-a1e6fb8bb53b
last_name: Klajn
citation:
ama: Bian T, Klajn R. Morphology control in crystalline nanoparticle–polymer aggregates.
Annals of the New York Academy of Sciences. 2021;1505(1):191-201. doi:10.1111/nyas.14674
apa: Bian, T., & Klajn, R. (2021). Morphology control in crystalline nanoparticle–polymer
aggregates. Annals of the New York Academy of Sciences. Wiley. https://doi.org/10.1111/nyas.14674
chicago: Bian, Tong, and Rafal Klajn. “Morphology Control in Crystalline Nanoparticle–Polymer
Aggregates.” Annals of the New York Academy of Sciences. Wiley, 2021. https://doi.org/10.1111/nyas.14674.
ieee: T. Bian and R. Klajn, “Morphology control in crystalline nanoparticle–polymer
aggregates,” Annals of the New York Academy of Sciences, vol. 1505, no.
1. Wiley, pp. 191–201, 2021.
ista: Bian T, Klajn R. 2021. Morphology control in crystalline nanoparticle–polymer
aggregates. Annals of the New York Academy of Sciences. 1505(1), 191–201.
mla: Bian, Tong, and Rafal Klajn. “Morphology Control in Crystalline Nanoparticle–Polymer
Aggregates.” Annals of the New York Academy of Sciences, vol. 1505, no.
1, Wiley, 2021, pp. 191–201, doi:10.1111/nyas.14674.
short: T. Bian, R. Klajn, Annals of the New York Academy of Sciences 1505 (2021)
191–201.
date_created: 2023-08-01T09:33:39Z
date_published: 2021-12-01T00:00:00Z
date_updated: 2023-08-07T10:01:10Z
day: '01'
ddc:
- '540'
doi: 10.1111/nyas.14674
extern: '1'
external_id:
pmid:
- '34427923'
intvolume: ' 1505'
issue: '1'
keyword:
- History and Philosophy of Science
- General Biochemistry
- Genetics and Molecular Biology
- General Neuroscience
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1111/nyas.14674
month: '12'
oa: 1
oa_version: Published Version
page: 191-201
pmid: 1
publication: Annals of the New York Academy of Sciences
publication_identifier:
eissn:
- 1749-6632
issn:
- 0077-8923
publication_status: published
publisher: Wiley
quality_controlled: '1'
scopus_import: '1'
status: public
title: Morphology control in crystalline nanoparticle–polymer aggregates
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 1505
year: '2021'
...
---
_id: '10163'
abstract:
- lang: eng
text: The C-terminal domain (CTD) of the largest subunit of RNA polymerase II (Pol
II) is a regulatory hub for transcription and RNA processing. Here, we identify
PHD-finger protein 3 (PHF3) as a regulator of transcription and mRNA stability
that docks onto Pol II CTD through its SPOC domain. We characterize SPOC as a
CTD reader domain that preferentially binds two phosphorylated Serine-2 marks
in adjacent CTD repeats. PHF3 drives liquid-liquid phase separation of phosphorylated
Pol II, colocalizes with Pol II clusters and tracks with Pol II across the length
of genes. PHF3 knock-out or SPOC deletion in human cells results in increased
Pol II stalling, reduced elongation rate and an increase in mRNA stability, with
marked derepression of neuronal genes. Key neuronal genes are aberrantly expressed
in Phf3 knock-out mouse embryonic stem cells, resulting in impaired neuronal differentiation.
Our data suggest that PHF3 acts as a prominent effector of neuronal gene regulation
by bridging transcription with mRNA decay.
acknowledgement: 'D.S. thanks Claudine Kraft, Renée Schroeder, Verena Jantsch, Franz
Klein and Peter Schlögelhofer for support. We thank Anita Testa Salmazo for help
with purifying Pol II; Matthias Geyer and Robert Düster for sharing DYRK1A kinase;
Felix Hartmann and Clemens Plaschka for help with mass photometry; Goran Kokic for
design of the arrest assay sequences; Petra van der Lelij for help with generating
mESC KO; Maximilian Freilinger for help with the purification of mEGFP-CTD; Stefan
Ameres, Nina Fasching and Brian Reichholf for advice on SLAM-seq and for sharing
reagents; Laura Gallego Valle for advice regarding LLPS assays; Krzysztof Chylinski
for advice regarding CRISPR/Cas9 methodology; VBCF Protein Technologies facility
for purifying PHF3 and providing gRNAs and Cas9; VBCF NGS facility for sequencing;
Monoclonal antibody facility at the Helmholtz center for Pol II antibodies; Friedrich
Propst and Elzbieta Kowalska for advice and for sharing materials; Egon Ogris for
sharing materials; Martin Eilers for recommending a ChIP-grade TFIIS antibody; Susanne
Opravil, Otto Hudecz, Markus Hartl and Natascha Hartl for mass spectrometry analysis;
staff of the X-ray beamlines at the ESRF in Grenoble for their excellent support;
Christa Bücker, Anton Meinhart, Clemens Plaschka and members of the Slade lab for
critical comments on the manuscript; Life Science Editors for editing assistance.
M.B. and D.S. acknowledge support by the FWF-funded DK ‘Chromosome Dynamics’. T.K.
is a recipient of the DOC fellowship from the Austrian Academy of Sciences. U.S.
is supported by the L’Oreal for Women in Science Austria Fellowship and the Austrian
Science Fund (FWF T 795-B30). M.L is supported by the Vienna Science and Technology
Fund (WWTF, VRG14-006). R.S. is supported by the Czech Science Foundation (15-17670 S
and 21-24460 S), Ministry of Education, Youths and Sports of the Czech Republic
(CEITEC 2020 project (LQ1601)), and the European Research Council (ERC) under the
European Union’s Horizon 2020 research and innovation programme (Grant agreement
no. 649030); this publication reflects only the author’s view and the Research Executive
Agency is not responsible for any use that may be made of the information it contains.
M.S. is supported by the Czech Science Foundation (GJ20-21581Y). K.D.C. research
is supported by the Austrian Science Fund (FWF) Projects I525 and I1593, P22276,
P19060, and W1221, Federal Ministry of Economy, Family and Youth through the initiative
‘Laura Bassi Centres of Expertise’, funding from the Centre of Optimized Structural
Studies No. 253275, the Wellcome Trust Collaborative Award (201543/Z/16), COST action
BM1405 Non-globular proteins - from sequence to structure, function and application
in molecular physiopathology (NGP-NET), the Vienna Science and Technology Fund (WWTF
LS17-008), and by the University of Vienna. This project was funded by the MFPL
start-up grant, the Vienna Science and Technology Fund (WWTF LS14-001), and the
Austrian Science Fund (P31546-B28 and W1258 “DK: Integrative Structural Biology”)
to D.S.'
article_number: '6078'
article_processing_charge: No
article_type: original
author:
- first_name: Lisa-Marie
full_name: Appel, Lisa-Marie
last_name: Appel
- first_name: Vedran
full_name: Franke, Vedran
last_name: Franke
- first_name: Melania
full_name: Bruno, Melania
last_name: Bruno
- first_name: Irina
full_name: Grishkovskaya, Irina
last_name: Grishkovskaya
- first_name: Aiste
full_name: Kasiliauskaite, Aiste
last_name: Kasiliauskaite
- first_name: Tanja
full_name: Kaufmann, Tanja
last_name: Kaufmann
- first_name: Ursula E.
full_name: Schoeberl, Ursula E.
last_name: Schoeberl
- first_name: Martin G.
full_name: Puchinger, Martin G.
last_name: Puchinger
- first_name: Sebastian
full_name: Kostrhon, Sebastian
last_name: Kostrhon
- first_name: Carmen
full_name: Ebenwaldner, Carmen
last_name: Ebenwaldner
- first_name: Marek
full_name: Sebesta, Marek
last_name: Sebesta
- first_name: Etienne
full_name: Beltzung, Etienne
last_name: Beltzung
- first_name: Karl
full_name: Mechtler, Karl
last_name: Mechtler
- first_name: Gen
full_name: Lin, Gen
last_name: Lin
- first_name: Anna
full_name: Vlasova, Anna
last_name: Vlasova
- first_name: Martin
full_name: Leeb, Martin
last_name: Leeb
- first_name: Rushad
full_name: Pavri, Rushad
last_name: Pavri
- first_name: Alexander
full_name: Stark, Alexander
last_name: Stark
- first_name: Altuna
full_name: Akalin, Altuna
last_name: Akalin
- first_name: Richard
full_name: Stefl, Richard
last_name: Stefl
- first_name: Carrie A
full_name: Bernecky, Carrie A
id: 2CB9DFE2-F248-11E8-B48F-1D18A9856A87
last_name: Bernecky
orcid: 0000-0003-0893-7036
- first_name: Kristina
full_name: Djinovic-Carugo, Kristina
last_name: Djinovic-Carugo
- first_name: Dea
full_name: Slade, Dea
last_name: Slade
citation:
ama: Appel L-M, Franke V, Bruno M, et al. PHF3 regulates neuronal gene expression
through the Pol II CTD reader domain SPOC. Nature Communications. 2021;12(1).
doi:10.1038/s41467-021-26360-2
apa: Appel, L.-M., Franke, V., Bruno, M., Grishkovskaya, I., Kasiliauskaite, A.,
Kaufmann, T., … Slade, D. (2021). PHF3 regulates neuronal gene expression through
the Pol II CTD reader domain SPOC. Nature Communications. Springer Nature.
https://doi.org/10.1038/s41467-021-26360-2
chicago: Appel, Lisa-Marie, Vedran Franke, Melania Bruno, Irina Grishkovskaya, Aiste
Kasiliauskaite, Tanja Kaufmann, Ursula E. Schoeberl, et al. “PHF3 Regulates Neuronal
Gene Expression through the Pol II CTD Reader Domain SPOC.” Nature Communications.
Springer Nature, 2021. https://doi.org/10.1038/s41467-021-26360-2.
ieee: L.-M. Appel et al., “PHF3 regulates neuronal gene expression through
the Pol II CTD reader domain SPOC,” Nature Communications, vol. 12, no.
1. Springer Nature, 2021.
ista: Appel L-M, Franke V, Bruno M, Grishkovskaya I, Kasiliauskaite A, Kaufmann
T, Schoeberl UE, Puchinger MG, Kostrhon S, Ebenwaldner C, Sebesta M, Beltzung
E, Mechtler K, Lin G, Vlasova A, Leeb M, Pavri R, Stark A, Akalin A, Stefl R,
Bernecky C, Djinovic-Carugo K, Slade D. 2021. PHF3 regulates neuronal gene expression
through the Pol II CTD reader domain SPOC. Nature Communications. 12(1), 6078.
mla: Appel, Lisa-Marie, et al. “PHF3 Regulates Neuronal Gene Expression through
the Pol II CTD Reader Domain SPOC.” Nature Communications, vol. 12, no.
1, 6078, Springer Nature, 2021, doi:10.1038/s41467-021-26360-2.
short: L.-M. Appel, V. Franke, M. Bruno, I. Grishkovskaya, A. Kasiliauskaite, T.
Kaufmann, U.E. Schoeberl, M.G. Puchinger, S. Kostrhon, C. Ebenwaldner, M. Sebesta,
E. Beltzung, K. Mechtler, G. Lin, A. Vlasova, M. Leeb, R. Pavri, A. Stark, A.
Akalin, R. Stefl, C. Bernecky, K. Djinovic-Carugo, D. Slade, Nature Communications
12 (2021).
date_created: 2021-10-20T14:40:32Z
date_published: 2021-10-19T00:00:00Z
date_updated: 2023-08-14T08:02:31Z
day: '19'
ddc:
- '610'
department:
- _id: CaBe
doi: 10.1038/s41467-021-26360-2
external_id:
isi:
- '000709050300001'
file:
- access_level: open_access
checksum: d99fcd51aebde19c21314e3de0148007
content_type: application/pdf
creator: cchlebak
date_created: 2021-10-21T13:51:49Z
date_updated: 2021-10-21T13:51:49Z
file_id: '10169'
file_name: 2021_NatComm_Appel.pdf
file_size: 5111706
relation: main_file
success: 1
file_date_updated: 2021-10-21T13:51:49Z
has_accepted_license: '1'
intvolume: ' 12'
isi: 1
issue: '1'
keyword:
- general physics and astronomy
- general biochemistry
- genetics and molecular biology
- general chemistry
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
publication: Nature Communications
publication_identifier:
eissn:
- 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
link:
- description: 'Preprint '
relation: earlier_version
url: https://www.biorxiv.org/content/10.1101/2020.02.11.943159
status: public
title: PHF3 regulates neuronal gene expression through the Pol II CTD reader domain
SPOC
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 12
year: '2021'
...
---
_id: '10290'
abstract:
- lang: eng
text: A precise quantitative description of the ultrastructural characteristics
underlying biological mechanisms is often key to their understanding. This is
particularly true for dynamic extra- and intracellular filamentous assemblies,
playing a role in cell motility, cell integrity, cytokinesis, tissue formation
and maintenance. For example, genetic manipulation or modulation of actin regulatory
proteins frequently manifests in changes of the morphology, dynamics, and ultrastructural
architecture of actin filament-rich cell peripheral structures, such as lamellipodia
or filopodia. However, the observed ultrastructural effects often remain subtle
and require sufficiently large datasets for appropriate quantitative analysis.
The acquisition of such large datasets has been enabled by recent advances in
high-throughput cryo-electron tomography (cryo-ET) methods. This also necessitates
the development of complementary approaches to maximize the extraction of relevant
biological information. We have developed a computational toolbox for the semi-automatic
quantification of segmented and vectorized filamentous networks from pre-processed
cryo-electron tomograms, facilitating the analysis and cross-comparison of multiple
experimental conditions. GUI-based components simplify the processing of data
and allow users to obtain a large number of ultrastructural parameters describing
filamentous assemblies. We demonstrate the feasibility of this workflow by analyzing
cryo-ET data of untreated and chemically perturbed branched actin filament networks
and that of parallel actin filament arrays. In principle, the computational toolbox
presented here is applicable for data analysis comprising any type of filaments
in regular (i.e. parallel) or random arrangement. We show that it can ease the
identification of key differences between experimental groups and facilitate the
in-depth analysis of ultrastructural data in a time-efficient manner.
acknowledged_ssus:
- _id: ScienComp
- _id: LifeSc
- _id: Bio
- _id: EM-Fac
acknowledgement: 'This research was supported by the Scientific Service Units (SSUs)
of IST Austria through resources provided by Scientific Computing (SciComp), the
Life Science Facility (LSF), the BioImaging Facility (BIF), and the Electron Microscopy
Facility (EMF). We also thank Victor-Valentin Hodirnau for help with cryo-ET data
acquisition. The authors acknowledge support from IST Austria and from the Austrian
Science Fund (FWF): M02495 to G.D. and Austrian Science Fund (FWF): P33367 to F.K.M.S.'
article_number: '107808'
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Georgi A
full_name: Dimchev, Georgi A
id: 38C393BE-F248-11E8-B48F-1D18A9856A87
last_name: Dimchev
orcid: 0000-0001-8370-6161
- first_name: Behnam
full_name: Amiri, Behnam
last_name: Amiri
- first_name: Florian
full_name: Fäßler, Florian
id: 404F5528-F248-11E8-B48F-1D18A9856A87
last_name: Fäßler
orcid: 0000-0001-7149-769X
- first_name: Martin
full_name: Falcke, Martin
last_name: Falcke
- first_name: Florian KM
full_name: Schur, Florian KM
id: 48AD8942-F248-11E8-B48F-1D18A9856A87
last_name: Schur
orcid: 0000-0003-4790-8078
citation:
ama: Dimchev GA, Amiri B, Fäßler F, Falcke M, Schur FK. Computational toolbox for
ultrastructural quantitative analysis of filament networks in cryo-ET data. Journal
of Structural Biology. 2021;213(4). doi:10.1016/j.jsb.2021.107808
apa: Dimchev, G. A., Amiri, B., Fäßler, F., Falcke, M., & Schur, F. K. (2021).
Computational toolbox for ultrastructural quantitative analysis of filament networks
in cryo-ET data. Journal of Structural Biology. Elsevier . https://doi.org/10.1016/j.jsb.2021.107808
chicago: Dimchev, Georgi A, Behnam Amiri, Florian Fäßler, Martin Falcke, and Florian
KM Schur. “Computational Toolbox for Ultrastructural Quantitative Analysis of
Filament Networks in Cryo-ET Data.” Journal of Structural Biology. Elsevier
, 2021. https://doi.org/10.1016/j.jsb.2021.107808.
ieee: G. A. Dimchev, B. Amiri, F. Fäßler, M. Falcke, and F. K. Schur, “Computational
toolbox for ultrastructural quantitative analysis of filament networks in cryo-ET
data,” Journal of Structural Biology, vol. 213, no. 4. Elsevier , 2021.
ista: Dimchev GA, Amiri B, Fäßler F, Falcke M, Schur FK. 2021. Computational toolbox
for ultrastructural quantitative analysis of filament networks in cryo-ET data.
Journal of Structural Biology. 213(4), 107808.
mla: Dimchev, Georgi A., et al. “Computational Toolbox for Ultrastructural Quantitative
Analysis of Filament Networks in Cryo-ET Data.” Journal of Structural Biology,
vol. 213, no. 4, 107808, Elsevier , 2021, doi:10.1016/j.jsb.2021.107808.
short: G.A. Dimchev, B. Amiri, F. Fäßler, M. Falcke, F.K. Schur, Journal of Structural
Biology 213 (2021).
date_created: 2021-11-15T12:21:42Z
date_published: 2021-11-03T00:00:00Z
date_updated: 2023-11-21T08:36:02Z
day: '03'
ddc:
- '572'
department:
- _id: FlSc
doi: 10.1016/j.jsb.2021.107808
external_id:
isi:
- '000720259500002'
file:
- access_level: open_access
checksum: 6b209e4d44775d4e02b50f78982c15fa
content_type: application/pdf
creator: cchlebak
date_created: 2021-11-15T13:11:27Z
date_updated: 2021-11-15T13:11:27Z
file_id: '10291'
file_name: 2021_JournalStructBiol_Dimchev.pdf
file_size: 16818304
relation: main_file
success: 1
file_date_updated: 2021-11-15T13:11:27Z
has_accepted_license: '1'
intvolume: ' 213'
isi: 1
issue: '4'
keyword:
- Structural Biology
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
project:
- _id: 9B954C5C-BA93-11EA-9121-9846C619BF3A
grant_number: P33367
name: Structure and isoform diversity of the Arp2/3 complex
- _id: 2674F658-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: M02495
name: Protein structure and function in filopodia across scales
publication: Journal of Structural Biology
publication_identifier:
issn:
- 1047-8477
publication_status: published
publisher: 'Elsevier '
quality_controlled: '1'
related_material:
record:
- id: '14502'
relation: software
status: public
scopus_import: '1'
status: public
title: Computational toolbox for ultrastructural quantitative analysis of filament
networks in cryo-ET data
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 213
year: '2021'
...
---
_id: '10301'
abstract:
- lang: eng
text: De novo protein synthesis is required for synapse modifications underlying
stable memory encoding. Yet neurons are highly compartmentalized cells and how
protein synthesis can be regulated at the synapse level is unknown. Here, we characterize
neuronal signaling complexes formed by the postsynaptic scaffold GIT1, the mechanistic
target of rapamycin (mTOR) kinase, and Raptor that couple synaptic stimuli to
mTOR-dependent protein synthesis; and identify NMDA receptors containing GluN3A
subunits as key negative regulators of GIT1 binding to mTOR. Disruption of GIT1/mTOR
complexes by enhancing GluN3A expression or silencing GIT1 inhibits synaptic mTOR
activation and restricts the mTOR-dependent translation of specific activity-regulated
mRNAs. Conversely, GluN3A removal enables complex formation, potentiates mTOR-dependent
protein synthesis, and facilitates the consolidation of associative and spatial
memories in mice. The memory enhancement becomes evident with light or spaced
training, can be achieved by selectively deleting GluN3A from excitatory neurons
during adulthood, and does not compromise other aspects of cognition such as memory
flexibility or extinction. Our findings provide mechanistic insight into synaptic
translational control and reveal a potentially selective target for cognitive
enhancement.
acknowledgement: We thank Stuart Lipton and Nobuki Nakanishi for providing the Grin3a
knockout mice, Beverly Davidson for the AAV-caRheb, Jose Esteban for help with behavioral
and biochemical experiments, and Noelia Campillo, Rebeca Martínez-Turrillas, and
Ana Navarro for expert technical help. Work was funded by the UTE project CIMA;
fellowships from the Fundación Tatiana Pérez de Guzmán el Bueno, FEBS, and IBRO
(to M.J.C.D.), Generalitat Valenciana (to O.E.-Z.), Juan de la Cierva (to L.G.R.),
FPI-MINECO (to E.R.V., to S.N.) and Intertalentum postdoctoral program (to V.B.);
ANR (GluBrain3A) and ERC Advanced Grants (#693021) (to P.P.); Ramón y Cajal program
RYC2014-15784, RETOS-MINECO SAF2016-76565-R, ERANET-Neuron JTC 2019 ISCIII AC19/00077
FEDER funds (to R.A.); RETOS-MINECO SAF2017-87928-R (to A.B.); an NIH grant (NS76637)
and UTHSC College of Medicine funds (to S.J.T.); and NARSAD Independent Investigator
Award and grants from the MINECO (CSD2008-00005, SAF2013-48983R, SAF2016-80895-R),
Generalitat Valenciana (PROMETEO 2019/020)(to I.P.O.) and Severo-Ochoa Excellence
Awards (SEV-2013-0317, SEV-2017-0723).
article_number: e71575
article_processing_charge: No
article_type: original
author:
- first_name: María J
full_name: Conde-Dusman, María J
last_name: Conde-Dusman
- first_name: Partha N
full_name: Dey, Partha N
last_name: Dey
- first_name: Óscar
full_name: Elía-Zudaire, Óscar
last_name: Elía-Zudaire
- first_name: Luis E
full_name: Garcia Rabaneda, Luis E
id: 33D1B084-F248-11E8-B48F-1D18A9856A87
last_name: Garcia Rabaneda
- first_name: Carmen
full_name: García-Lira, Carmen
last_name: García-Lira
- first_name: Teddy
full_name: Grand, Teddy
last_name: Grand
- first_name: Victor
full_name: Briz, Victor
last_name: Briz
- first_name: Eric R
full_name: Velasco, Eric R
last_name: Velasco
- first_name: Raül
full_name: Andero Galí, Raül
last_name: Andero Galí
- first_name: Sergio
full_name: Niñerola, Sergio
last_name: Niñerola
- first_name: Angel
full_name: Barco, Angel
last_name: Barco
- first_name: Pierre
full_name: Paoletti, Pierre
last_name: Paoletti
- first_name: John F
full_name: Wesseling, John F
last_name: Wesseling
- first_name: Fabrizio
full_name: Gardoni, Fabrizio
last_name: Gardoni
- first_name: Steven J
full_name: Tavalin, Steven J
last_name: Tavalin
- first_name: Isabel
full_name: Perez-Otaño, Isabel
last_name: Perez-Otaño
citation:
ama: Conde-Dusman MJ, Dey PN, Elía-Zudaire Ó, et al. Control of protein synthesis
and memory by GluN3A-NMDA receptors through inhibition of GIT1/mTORC1 assembly.
eLife. 2021;10. doi:10.7554/elife.71575
apa: Conde-Dusman, M. J., Dey, P. N., Elía-Zudaire, Ó., Garcia Rabaneda, L. E.,
García-Lira, C., Grand, T., … Perez-Otaño, I. (2021). Control of protein synthesis
and memory by GluN3A-NMDA receptors through inhibition of GIT1/mTORC1 assembly.
ELife. eLife Sciences Publications. https://doi.org/10.7554/elife.71575
chicago: Conde-Dusman, María J, Partha N Dey, Óscar Elía-Zudaire, Luis E Garcia
Rabaneda, Carmen García-Lira, Teddy Grand, Victor Briz, et al. “Control of Protein
Synthesis and Memory by GluN3A-NMDA Receptors through Inhibition of GIT1/MTORC1
Assembly.” ELife. eLife Sciences Publications, 2021. https://doi.org/10.7554/elife.71575.
ieee: M. J. Conde-Dusman et al., “Control of protein synthesis and memory
by GluN3A-NMDA receptors through inhibition of GIT1/mTORC1 assembly,” eLife,
vol. 10. eLife Sciences Publications, 2021.
ista: Conde-Dusman MJ, Dey PN, Elía-Zudaire Ó, Garcia Rabaneda LE, García-Lira C,
Grand T, Briz V, Velasco ER, Andero Galí R, Niñerola S, Barco A, Paoletti P, Wesseling
JF, Gardoni F, Tavalin SJ, Perez-Otaño I. 2021. Control of protein synthesis and
memory by GluN3A-NMDA receptors through inhibition of GIT1/mTORC1 assembly. eLife.
10, e71575.
mla: Conde-Dusman, María J., et al. “Control of Protein Synthesis and Memory by
GluN3A-NMDA Receptors through Inhibition of GIT1/MTORC1 Assembly.” ELife,
vol. 10, e71575, eLife Sciences Publications, 2021, doi:10.7554/elife.71575.
short: M.J. Conde-Dusman, P.N. Dey, Ó. Elía-Zudaire, L.E. Garcia Rabaneda, C. García-Lira,
T. Grand, V. Briz, E.R. Velasco, R. Andero Galí, S. Niñerola, A. Barco, P. Paoletti,
J.F. Wesseling, F. Gardoni, S.J. Tavalin, I. Perez-Otaño, ELife 10 (2021).
date_created: 2021-11-18T06:59:45Z
date_published: 2021-11-17T00:00:00Z
date_updated: 2023-08-14T11:50:50Z
day: '17'
ddc:
- '570'
department:
- _id: GaNo
doi: 10.7554/elife.71575
external_id:
isi:
- '000720945900001'
file:
- access_level: open_access
checksum: 59318e9e41507cec83c2f4070e6ad540
content_type: application/pdf
creator: lgarciar
date_created: 2021-11-18T07:02:02Z
date_updated: 2021-11-18T07:02:02Z
file_id: '10302'
file_name: elife-71575-v1.pdf
file_size: 2477302
relation: main_file
success: 1
file_date_updated: 2021-11-18T07:02:02Z
has_accepted_license: '1'
intvolume: ' 10'
isi: 1
keyword:
- general immunology and microbiology
- general biochemistry
- genetics and molecular biology
- general medicine
- general neuroscience
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
publication: eLife
publication_identifier:
issn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
status: public
title: Control of protein synthesis and memory by GluN3A-NMDA receptors through inhibition
of GIT1/mTORC1 assembly
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 10
year: '2021'
...
---
_id: '10310'
abstract:
- lang: eng
text: A high-resolution structure of trimeric cyanobacterial Photosystem I (PSI)
from Thermosynechococcus elongatus was reported as the first atomic model of PSI
almost 20 years ago. However, the monomeric PSI structure has not yet been reported
despite long-standing interest in its structure and extensive spectroscopic characterization
of the loss of red chlorophylls upon monomerization. Here, we describe the structure
of monomeric PSI from Thermosynechococcus elongatus BP-1. Comparison with the
trimer structure gave detailed insights into monomerization-induced changes in
both the central trimerization domain and the peripheral regions of the complex.
Monomerization-induced loss of red chlorophylls is assigned to a cluster of chlorophylls
adjacent to PsaX. Based on our findings, we propose a role of PsaX in the stabilization
of red chlorophylls and that lipids of the surrounding membrane present a major
source of thermal energy for uphill excitation energy transfer from red chlorophylls
to P700.
acknowledgement: We are grateful for additional support and valuable scientific input
for this project by Yuko Misumi, Jiannan Li, Hisako Kubota-Kawai, Takeshi Kawabata,
Mian Wu, Eiki Yamashita, Atsushi Nakagawa, Volker Hartmann, Melanie Völkel and Matthias
Rögner. Parts of this research were funded by the German Research Council (DFG)
within the framework of GRK 2341 (Microbial Substrate Conversion) to M.M.N., the
Platform Project for Supporting Drug Discovery and Life Science Research [Basis
for Supporting Innovative Drug Discovery and Life Science Research (BINDS)] from
AMED under grant number JP20am0101117 (K.N.), JP16K07266 to Atsunori Oshima and
C.G., a Grants-in-Aid for Scientific Research under grant number JP 25000013 (K.N.),
17H03647 (C.G.) and 16H06560 (G.K.) from MEXT-KAKENHI, the International Joint Research
Promotion Program from Osaka University to M.M.N., C.G. and G.K., and the Cyclic
Innovation for Clinical Empowerment (CiCLE) Grant Number JP17pc0101020 from AMED
to K.N. and G.K.
article_number: '304'
article_processing_charge: No
article_type: original
author:
- first_name: Mehmet Orkun
full_name: Çoruh, Mehmet Orkun
id: d25163e5-8d53-11eb-a251-e6dd8ea1b8ef
last_name: Çoruh
orcid: 0000-0002-3219-2022
- first_name: Anna
full_name: Frank, Anna
last_name: Frank
- first_name: Hideaki
full_name: Tanaka, Hideaki
last_name: Tanaka
- first_name: Akihiro
full_name: Kawamoto, Akihiro
last_name: Kawamoto
- first_name: Eithar
full_name: El-Mohsnawy, Eithar
last_name: El-Mohsnawy
- first_name: Takayuki
full_name: Kato, Takayuki
last_name: Kato
- first_name: Keiichi
full_name: Namba, Keiichi
last_name: Namba
- first_name: Christoph
full_name: Gerle, Christoph
last_name: Gerle
- first_name: Marc M.
full_name: Nowaczyk, Marc M.
last_name: Nowaczyk
- first_name: Genji
full_name: Kurisu, Genji
last_name: Kurisu
citation:
ama: Çoruh MO, Frank A, Tanaka H, et al. Cryo-EM structure of a functional monomeric
Photosystem I from Thermosynechococcus elongatus reveals red chlorophyll cluster.
Communications Biology. 2021;4(1). doi:10.1038/s42003-021-01808-9
apa: Çoruh, M. O., Frank, A., Tanaka, H., Kawamoto, A., El-Mohsnawy, E., Kato, T.,
… Kurisu, G. (2021). Cryo-EM structure of a functional monomeric Photosystem I
from Thermosynechococcus elongatus reveals red chlorophyll cluster. Communications
Biology. Springer . https://doi.org/10.1038/s42003-021-01808-9
chicago: Çoruh, Mehmet Orkun, Anna Frank, Hideaki Tanaka, Akihiro Kawamoto, Eithar
El-Mohsnawy, Takayuki Kato, Keiichi Namba, Christoph Gerle, Marc M. Nowaczyk,
and Genji Kurisu. “Cryo-EM Structure of a Functional Monomeric Photosystem I from
Thermosynechococcus Elongatus Reveals Red Chlorophyll Cluster.” Communications
Biology. Springer , 2021. https://doi.org/10.1038/s42003-021-01808-9.
ieee: M. O. Çoruh et al., “Cryo-EM structure of a functional monomeric Photosystem
I from Thermosynechococcus elongatus reveals red chlorophyll cluster,” Communications
Biology, vol. 4, no. 1. Springer , 2021.
ista: Çoruh MO, Frank A, Tanaka H, Kawamoto A, El-Mohsnawy E, Kato T, Namba K, Gerle
C, Nowaczyk MM, Kurisu G. 2021. Cryo-EM structure of a functional monomeric Photosystem
I from Thermosynechococcus elongatus reveals red chlorophyll cluster. Communications
Biology. 4(1), 304.
mla: Çoruh, Mehmet Orkun, et al. “Cryo-EM Structure of a Functional Monomeric Photosystem
I from Thermosynechococcus Elongatus Reveals Red Chlorophyll Cluster.” Communications
Biology, vol. 4, no. 1, 304, Springer , 2021, doi:10.1038/s42003-021-01808-9.
short: M.O. Çoruh, A. Frank, H. Tanaka, A. Kawamoto, E. El-Mohsnawy, T. Kato, K.
Namba, C. Gerle, M.M. Nowaczyk, G. Kurisu, Communications Biology 4 (2021).
date_created: 2021-11-19T11:37:29Z
date_published: 2021-03-08T00:00:00Z
date_updated: 2023-08-14T11:51:19Z
day: '08'
ddc:
- '570'
department:
- _id: LeSa
doi: 10.1038/s42003-021-01808-9
external_id:
isi:
- '000627440700001'
pmid:
- '33686186'
file:
- access_level: open_access
checksum: 8ffd39f2bba7152a2441802ff313bf0b
content_type: application/pdf
creator: cchlebak
date_created: 2021-11-19T15:09:18Z
date_updated: 2021-11-19T15:09:18Z
file_id: '10318'
file_name: 2021_CommBio_Çoruh.pdf
file_size: 6030261
relation: main_file
success: 1
file_date_updated: 2021-11-19T15:09:18Z
has_accepted_license: '1'
intvolume: ' 4'
isi: 1
issue: '1'
keyword:
- general agricultural and biological Sciences
- general biochemistry
- genetics and molecular biology
- medicine (miscellaneous)
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
pmid: 1
publication: Communications Biology
publication_identifier:
issn:
- 2399-3642
publication_status: published
publisher: 'Springer '
quality_controlled: '1'
scopus_import: '1'
status: public
title: Cryo-EM structure of a functional monomeric Photosystem I from Thermosynechococcus
elongatus reveals red chlorophyll cluster
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 4
year: '2021'
...
---
_id: '10337'
abstract:
- lang: eng
text: The T cell receptor (TCR) pathway receives, processes, and amplifies the signal
from pathogenic antigens to the activation of T cells. Although major components
in this pathway have been identified, the knowledge on how individual components
cooperate to effectively transduce signals remains limited. Phase separation emerges
as a biophysical principle in organizing signaling molecules into liquid-like
condensates. Here, we report that phospholipase Cγ1 (PLCγ1) promotes phase separation
of LAT, a key adaptor protein in the TCR pathway. PLCγ1 directly cross-links LAT
through its two SH2 domains. PLCγ1 also protects LAT from dephosphorylation by
the phosphatase CD45 and promotes LAT-dependent ERK activation and SLP76 phosphorylation.
Intriguingly, a nonmonotonic effect of PLCγ1 on LAT clustering was discovered.
Computer simulations, based on patchy particles, revealed how the cluster size
is regulated by protein compositions. Together, these results define a critical
function of PLCγ1 in promoting phase separation of the LAT complex and TCR signal
transduction.
acknowledgement: Charles H. Hood Foundation (NO AWARD) ; Rally Foundation (NO AWARD)
article_number: e202009154
article_processing_charge: No
article_type: original
author:
- first_name: Longhui
full_name: Zeng, Longhui
last_name: Zeng
- first_name: Ivan
full_name: Palaia, Ivan
last_name: Palaia
- first_name: Anđela
full_name: Šarić, Anđela
id: bf63d406-f056-11eb-b41d-f263a6566d8b
last_name: Šarić
orcid: 0000-0002-7854-2139
- first_name: Xiaolei
full_name: Su, Xiaolei
last_name: Su
citation:
ama: Zeng L, Palaia I, Šarić A, Su X. PLCγ1 promotes phase separation of T cell
signaling components. Journal of Cell Biology. 2021;220(6). doi:10.1083/jcb.202009154
apa: Zeng, L., Palaia, I., Šarić, A., & Su, X. (2021). PLCγ1 promotes phase
separation of T cell signaling components. Journal of Cell Biology. Rockefeller
University Press. https://doi.org/10.1083/jcb.202009154
chicago: Zeng, Longhui, Ivan Palaia, Anđela Šarić, and Xiaolei Su. “PLCγ1 Promotes
Phase Separation of T Cell Signaling Components.” Journal of Cell Biology.
Rockefeller University Press, 2021. https://doi.org/10.1083/jcb.202009154.
ieee: L. Zeng, I. Palaia, A. Šarić, and X. Su, “PLCγ1 promotes phase separation
of T cell signaling components,” Journal of Cell Biology, vol. 220, no.
6. Rockefeller University Press, 2021.
ista: Zeng L, Palaia I, Šarić A, Su X. 2021. PLCγ1 promotes phase separation of
T cell signaling components. Journal of Cell Biology. 220(6), e202009154.
mla: Zeng, Longhui, et al. “PLCγ1 Promotes Phase Separation of T Cell Signaling
Components.” Journal of Cell Biology, vol. 220, no. 6, e202009154, Rockefeller
University Press, 2021, doi:10.1083/jcb.202009154.
short: L. Zeng, I. Palaia, A. Šarić, X. Su, Journal of Cell Biology 220 (2021).
date_created: 2021-11-25T15:21:30Z
date_published: 2021-04-30T00:00:00Z
date_updated: 2021-11-25T15:33:08Z
day: '30'
doi: 10.1083/jcb.202009154
extern: '1'
external_id:
pmid:
- '33929486'
intvolume: ' 220'
issue: '6'
keyword:
- cell biology
language:
- iso: eng
month: '04'
oa_version: None
pmid: 1
publication: Journal of Cell Biology
publication_identifier:
eissn:
- 1540-8140
issn:
- 0021-9525
publication_status: published
publisher: Rockefeller University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: PLCγ1 promotes phase separation of T cell signaling components
tmp:
image: /images/cc_by_nc_sa.png
legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC
BY-NC-SA 4.0)
short: CC BY-NC-SA (4.0)
type: journal_article
user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9
volume: 220
year: '2021'
...
---
_id: '10533'
abstract:
- lang: eng
text: Flowering plants utilize small RNA molecules to guide DNA methyltransferases
to genomic sequences. This RNA-directed DNA methylation (RdDM) pathway preferentially
targets euchromatic transposable elements. However, RdDM is thought to be recruited
by methylation of histone H3 at lysine 9 (H3K9me), a hallmark of heterochromatin.
How RdDM is targeted to euchromatin despite an affinity for H3K9me is unclear.
Here we show that loss of histone H1 enhances heterochromatic RdDM, preferentially
at nucleosome linker DNA. Surprisingly, this does not require SHH1, the RdDM component
that binds H3K9me. Furthermore, H3K9me is dispensable for RdDM, as is CG DNA methylation.
Instead, we find that non-CG methylation is specifically associated with small
RNA biogenesis, and without H1 small RNA production quantitatively expands to
non-CG methylated loci. Our results demonstrate that H1 enforces the separation
of euchromatic and heterochromatic DNA methylation pathways by excluding the small
RNA-generating branch of RdDM from non-CG methylated heterochromatin.
acknowledgement: We thank X Feng for helpful comments on the manuscript. This work
was supported by a European Research Council grant MaintainMeth (725746) to DZ.
article_number: e72676
article_processing_charge: No
article_type: original
author:
- first_name: Jaemyung
full_name: Choi, Jaemyung
last_name: Choi
- first_name: David B
full_name: Lyons, David B
last_name: Lyons
- first_name: Daniel
full_name: Zilberman, Daniel
id: 6973db13-dd5f-11ea-814e-b3e5455e9ed1
last_name: Zilberman
orcid: 0000-0002-0123-8649
citation:
ama: Choi J, Lyons DB, Zilberman D. Histone H1 prevents non-CG methylation-mediated
small RNA biogenesis in Arabidopsis heterochromatin. eLife. 2021;10. doi:10.7554/elife.72676
apa: Choi, J., Lyons, D. B., & Zilberman, D. (2021). Histone H1 prevents non-CG
methylation-mediated small RNA biogenesis in Arabidopsis heterochromatin. ELife.
eLife Sciences Publications. https://doi.org/10.7554/elife.72676
chicago: Choi, Jaemyung, David B Lyons, and Daniel Zilberman. “Histone H1 Prevents
Non-CG Methylation-Mediated Small RNA Biogenesis in Arabidopsis Heterochromatin.”
ELife. eLife Sciences Publications, 2021. https://doi.org/10.7554/elife.72676.
ieee: J. Choi, D. B. Lyons, and D. Zilberman, “Histone H1 prevents non-CG methylation-mediated
small RNA biogenesis in Arabidopsis heterochromatin,” eLife, vol. 10. eLife
Sciences Publications, 2021.
ista: Choi J, Lyons DB, Zilberman D. 2021. Histone H1 prevents non-CG methylation-mediated
small RNA biogenesis in Arabidopsis heterochromatin. eLife. 10, e72676.
mla: Choi, Jaemyung, et al. “Histone H1 Prevents Non-CG Methylation-Mediated Small
RNA Biogenesis in Arabidopsis Heterochromatin.” ELife, vol. 10, e72676,
eLife Sciences Publications, 2021, doi:10.7554/elife.72676.
short: J. Choi, D.B. Lyons, D. Zilberman, ELife 10 (2021).
date_created: 2021-12-10T13:12:08Z
date_published: 2021-12-01T00:00:00Z
date_updated: 2023-08-17T06:21:08Z
day: '01'
ddc:
- '570'
department:
- _id: DaZi
doi: 10.7554/elife.72676
ec_funded: 1
external_id:
isi:
- '000754832000001'
pmid:
- '34850679'
file:
- access_level: open_access
checksum: 22ed4c55fb550f6da02ae55c359be651
content_type: application/pdf
creator: dernst
date_created: 2022-05-16T10:42:22Z
date_updated: 2022-05-16T10:42:22Z
file_id: '11384'
file_name: 2021_eLife_Choi.pdf
file_size: 2715200
relation: main_file
success: 1
file_date_updated: 2022-05-16T10:42:22Z
has_accepted_license: '1'
intvolume: ' 10'
isi: 1
keyword:
- genetics and molecular biology
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 62935a00-2b32-11ec-9570-eff30fa39068
call_identifier: H2020
grant_number: '725746'
name: Quantitative analysis of DNA methylation maintenance with chromatin
publication: eLife
publication_identifier:
issn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Histone H1 prevents non-CG methylation-mediated small RNA biogenesis in Arabidopsis
heterochromatin
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 10
year: '2021'
...
---
_id: '9429'
abstract:
- lang: eng
text: De novo loss of function mutations in the ubiquitin ligase-encoding gene Cullin3
lead to autism spectrum disorder (ASD). In mouse, constitutive haploinsufficiency
leads to motor coordination deficits as well as ASD-relevant social and cognitive
impairments. However, induction of Cul3 haploinsufficiency later in life does
not lead to ASD-relevant behaviors, pointing to an important role of Cul3 during
a critical developmental window. Here we show that Cul3 is essential to regulate
neuronal migration and, therefore, constitutive Cul3 heterozygous mutant mice
display cortical lamination abnormalities. At the molecular level, we found that
Cul3 controls neuronal migration by tightly regulating the amount of Plastin3
(Pls3), a previously unrecognized player of neural migration. Furthermore, we
found that Pls3 cell-autonomously regulates cell migration by regulating actin
cytoskeleton organization, and its levels are inversely proportional to neural
migration speed. Finally, we provide evidence that cellular phenotypes associated
with autism-linked gene haploinsufficiency can be rescued by transcriptional activation
of the intact allele in vitro, offering a proof of concept for a potential therapeutic
approach for ASDs.
acknowledged_ssus:
- _id: PreCl
acknowledgement: We thank A. Coll Manzano, F. Freeman, M. Ladron de Guevara, and A.
Ç. Yahya for technical assistance, S. Deixler, A. Lepold, and A. Schlerka for the
management of our animal colony, as well as M. Schunn and the Preclinical Facility
team for technical assistance. We thank K. Heesom and her team at the University
of Bristol Proteomics Facility for the proteomics sample preparation, data generation,
and analysis support. We thank Y. B. Simon for kindly providing the plasmid for
lentiviral labeling. Further, we thank M. Sixt for his advice regarding cell migration
and the fruitful discussions. This work was supported by the ISTPlus postdoctoral
fellowship (Grant Agreement No. 754411) to B.B., by the European Union’s Horizon
2020 research and innovation program (ERC) grant 715508 (REVERSEAUTISM), and by
the Austrian Science Fund (FWF) to G.N. (DK W1232-B24 and SFB F7807-B) and to J.G.D
(I3600-B27).
article_number: '3058'
article_processing_charge: No
article_type: original
author:
- first_name: Jasmin
full_name: Morandell, Jasmin
id: 4739D480-F248-11E8-B48F-1D18A9856A87
last_name: Morandell
- first_name: Lena A
full_name: Schwarz, Lena A
id: 29A8453C-F248-11E8-B48F-1D18A9856A87
last_name: Schwarz
- first_name: Bernadette
full_name: Basilico, Bernadette
id: 36035796-5ACA-11E9-A75E-7AF2E5697425
last_name: Basilico
orcid: 0000-0003-1843-3173
- first_name: Saren
full_name: Tasciyan, Saren
id: 4323B49C-F248-11E8-B48F-1D18A9856A87
last_name: Tasciyan
orcid: 0000-0003-1671-393X
- first_name: Georgi A
full_name: Dimchev, Georgi A
id: 38C393BE-F248-11E8-B48F-1D18A9856A87
last_name: Dimchev
orcid: 0000-0001-8370-6161
- first_name: Armel
full_name: Nicolas, Armel
id: 2A103192-F248-11E8-B48F-1D18A9856A87
last_name: Nicolas
- first_name: Christoph M
full_name: Sommer, Christoph M
id: 4DF26D8C-F248-11E8-B48F-1D18A9856A87
last_name: Sommer
orcid: 0000-0003-1216-9105
- first_name: Caroline
full_name: Kreuzinger, Caroline
id: 382077BA-F248-11E8-B48F-1D18A9856A87
last_name: Kreuzinger
- first_name: Christoph
full_name: Dotter, Christoph
id: 4C66542E-F248-11E8-B48F-1D18A9856A87
last_name: Dotter
orcid: 0000-0002-9033-9096
- first_name: Lisa
full_name: Knaus, Lisa
id: 3B2ABCF4-F248-11E8-B48F-1D18A9856A87
last_name: Knaus
- first_name: Zoe
full_name: Dobler, Zoe
id: D23090A2-9057-11EA-883A-A8396FC7A38F
last_name: Dobler
- first_name: Emanuele
full_name: Cacci, Emanuele
last_name: Cacci
- first_name: Florian KM
full_name: Schur, Florian KM
id: 48AD8942-F248-11E8-B48F-1D18A9856A87
last_name: Schur
orcid: 0000-0003-4790-8078
- first_name: Johann G
full_name: Danzl, Johann G
id: 42EFD3B6-F248-11E8-B48F-1D18A9856A87
last_name: Danzl
orcid: 0000-0001-8559-3973
- first_name: Gaia
full_name: Novarino, Gaia
id: 3E57A680-F248-11E8-B48F-1D18A9856A87
last_name: Novarino
orcid: 0000-0002-7673-7178
citation:
ama: Morandell J, Schwarz LA, Basilico B, et al. Cul3 regulates cytoskeleton protein
homeostasis and cell migration during a critical window of brain development.
Nature Communications. 2021;12(1). doi:10.1038/s41467-021-23123-x
apa: Morandell, J., Schwarz, L. A., Basilico, B., Tasciyan, S., Dimchev, G. A.,
Nicolas, A., … Novarino, G. (2021). Cul3 regulates cytoskeleton protein homeostasis
and cell migration during a critical window of brain development. Nature Communications.
Springer Nature. https://doi.org/10.1038/s41467-021-23123-x
chicago: Morandell, Jasmin, Lena A Schwarz, Bernadette Basilico, Saren Tasciyan,
Georgi A Dimchev, Armel Nicolas, Christoph M Sommer, et al. “Cul3 Regulates Cytoskeleton
Protein Homeostasis and Cell Migration during a Critical Window of Brain Development.”
Nature Communications. Springer Nature, 2021. https://doi.org/10.1038/s41467-021-23123-x.
ieee: J. Morandell et al., “Cul3 regulates cytoskeleton protein homeostasis
and cell migration during a critical window of brain development,” Nature Communications,
vol. 12, no. 1. Springer Nature, 2021.
ista: Morandell J, Schwarz LA, Basilico B, Tasciyan S, Dimchev GA, Nicolas A, Sommer
CM, Kreuzinger C, Dotter C, Knaus L, Dobler Z, Cacci E, Schur FK, Danzl JG, Novarino
G. 2021. Cul3 regulates cytoskeleton protein homeostasis and cell migration during
a critical window of brain development. Nature Communications. 12(1), 3058.
mla: Morandell, Jasmin, et al. “Cul3 Regulates Cytoskeleton Protein Homeostasis
and Cell Migration during a Critical Window of Brain Development.” Nature Communications,
vol. 12, no. 1, 3058, Springer Nature, 2021, doi:10.1038/s41467-021-23123-x.
short: J. Morandell, L.A. Schwarz, B. Basilico, S. Tasciyan, G.A. Dimchev, A. Nicolas,
C.M. Sommer, C. Kreuzinger, C. Dotter, L. Knaus, Z. Dobler, E. Cacci, F.K. Schur,
J.G. Danzl, G. Novarino, Nature Communications 12 (2021).
date_created: 2021-05-28T11:49:46Z
date_published: 2021-05-24T00:00:00Z
date_updated: 2024-09-10T12:04:26Z
day: '24'
ddc:
- '572'
department:
- _id: GaNo
- _id: JoDa
- _id: FlSc
- _id: MiSi
- _id: LifeSc
- _id: Bio
doi: 10.1038/s41467-021-23123-x
ec_funded: 1
external_id:
isi:
- '000658769900010'
file:
- access_level: open_access
checksum: 337e0f7959c35ec959984cacdcb472ba
content_type: application/pdf
creator: kschuh
date_created: 2021-05-28T12:39:43Z
date_updated: 2021-05-28T12:39:43Z
file_id: '9430'
file_name: 2021_NatureCommunications_Morandell.pdf
file_size: 9358599
relation: main_file
success: 1
file_date_updated: 2021-05-28T12:39:43Z
has_accepted_license: '1'
intvolume: ' 12'
isi: 1
issue: '1'
keyword:
- General Biochemistry
- Genetics and Molecular Biology
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
project:
- _id: 260C2330-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '754411'
name: ISTplus - Postdoctoral Fellowships
- _id: 25444568-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '715508'
name: Probing the Reversibility of Autism Spectrum Disorders by Employing in vivo
and in vitro Models
- _id: 2548AE96-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: W1232-B24
name: Molecular Drug Targets
- _id: 05A0D778-7A3F-11EA-A408-12923DDC885E
grant_number: F07807
name: Neural stem cells in autism and epilepsy
- _id: 265CB4D0-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: I03600
name: Optical control of synaptic function via adhesion molecules
publication: Nature Communications
publication_identifier:
eissn:
- 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
link:
- relation: press_release
url: https://ist.ac.at/en/news/defective-gene-slows-down-brain-cells/
record:
- id: '7800'
relation: earlier_version
status: public
- id: '12401'
relation: dissertation_contains
status: public
status: public
title: Cul3 regulates cytoskeleton protein homeostasis and cell migration during a
critical window of brain development
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 12
year: '2021'
...
---
_id: '9431'
abstract:
- lang: eng
text: Inositol hexakisphosphate (IP6) is an assembly cofactor for HIV-1. We report
here that IP6 is also used for assembly of Rous sarcoma virus (RSV), a retrovirus
from a different genus. IP6 is ~100-fold more potent at promoting RSV mature capsid
protein (CA) assembly than observed for HIV-1 and removal of IP6 in cells reduces
infectivity by 100-fold. Here, visualized by cryo-electron tomography and subtomogram
averaging, mature capsid-like particles show an IP6-like density in the CA hexamer,
coordinated by rings of six lysines and six arginines. Phosphate and IP6 have
opposing effects on CA in vitro assembly, inducing formation of T = 1 icosahedrons
and tubes, respectively, implying that phosphate promotes pentamer and IP6 hexamer
formation. Subtomogram averaging and classification optimized for analysis of
pleomorphic retrovirus particles reveal that the heterogeneity of mature RSV CA
polyhedrons results from an unexpected, intrinsic CA hexamer flexibility. In contrast,
the CA pentamer forms rigid units organizing the local architecture. These different
features of hexamers and pentamers determine the structural mechanism to form
CA polyhedrons of variable shape in mature RSV particles.
acknowledged_ssus:
- _id: ScienComp
- _id: LifeSc
- _id: EM-Fac
acknowledgement: This work was funded by the National Institute of Allergy and Infectious
Diseases under awards R01AI147890 to R.A.D., R01AI150454 to V.M.V, R35GM136258 in
support of J-P.R.F, and the Austrian Science Fund (FWF) grant P31445 to F.K.M.S.
Access to high-resolution cryo-ET data acquisition at EMBL Heidelberg was supported
by iNEXT (grant no. 653706), funded by the Horizon 2020 program of the European
Union (PID 4246). We thank Wim Hagen and Felix Weis at EMBL Heidelberg for support
in cryo-ET data acquisition. This work made use of the Cornell Center for Materials
Research Shared Facilities, which are supported through the NSF MRSEC program (DMR-179875).
This research was also supported by the Scientific Service Units (SSUs) of IST Austria
through resources provided by Scientific Computing (SciComp), the Life Science Facility
(LSF), and the Electron Microscopy Facility (EMF).
article_number: '3226'
article_processing_charge: No
article_type: original
author:
- first_name: Martin
full_name: Obr, Martin
id: 4741CA5A-F248-11E8-B48F-1D18A9856A87
last_name: Obr
- first_name: Clifton L.
full_name: Ricana, Clifton L.
last_name: Ricana
- first_name: Nadia
full_name: Nikulin, Nadia
last_name: Nikulin
- first_name: Jon-Philip R.
full_name: Feathers, Jon-Philip R.
last_name: Feathers
- first_name: Marco
full_name: Klanschnig, Marco
last_name: Klanschnig
- first_name: Andreas
full_name: Thader, Andreas
id: 3A18A7B8-F248-11E8-B48F-1D18A9856A87
last_name: Thader
- first_name: Marc C.
full_name: Johnson, Marc C.
last_name: Johnson
- first_name: Volker M.
full_name: Vogt, Volker M.
last_name: Vogt
- first_name: Florian KM
full_name: Schur, Florian KM
id: 48AD8942-F248-11E8-B48F-1D18A9856A87
last_name: Schur
orcid: 0000-0003-4790-8078
- first_name: Robert A.
full_name: Dick, Robert A.
last_name: Dick
citation:
ama: Obr M, Ricana CL, Nikulin N, et al. Structure of the mature Rous sarcoma virus
lattice reveals a role for IP6 in the formation of the capsid hexamer. Nature
Communications. 2021;12(1). doi:10.1038/s41467-021-23506-0
apa: Obr, M., Ricana, C. L., Nikulin, N., Feathers, J.-P. R., Klanschnig, M., Thader,
A., … Dick, R. A. (2021). Structure of the mature Rous sarcoma virus lattice reveals
a role for IP6 in the formation of the capsid hexamer. Nature Communications.
Nature Research. https://doi.org/10.1038/s41467-021-23506-0
chicago: Obr, Martin, Clifton L. Ricana, Nadia Nikulin, Jon-Philip R. Feathers,
Marco Klanschnig, Andreas Thader, Marc C. Johnson, Volker M. Vogt, Florian KM
Schur, and Robert A. Dick. “Structure of the Mature Rous Sarcoma Virus Lattice
Reveals a Role for IP6 in the Formation of the Capsid Hexamer.” Nature Communications.
Nature Research, 2021. https://doi.org/10.1038/s41467-021-23506-0.
ieee: M. Obr et al., “Structure of the mature Rous sarcoma virus lattice
reveals a role for IP6 in the formation of the capsid hexamer,” Nature Communications,
vol. 12, no. 1. Nature Research, 2021.
ista: Obr M, Ricana CL, Nikulin N, Feathers J-PR, Klanschnig M, Thader A, Johnson
MC, Vogt VM, Schur FK, Dick RA. 2021. Structure of the mature Rous sarcoma virus
lattice reveals a role for IP6 in the formation of the capsid hexamer. Nature
Communications. 12(1), 3226.
mla: Obr, Martin, et al. “Structure of the Mature Rous Sarcoma Virus Lattice Reveals
a Role for IP6 in the Formation of the Capsid Hexamer.” Nature Communications,
vol. 12, no. 1, 3226, Nature Research, 2021, doi:10.1038/s41467-021-23506-0.
short: M. Obr, C.L. Ricana, N. Nikulin, J.-P.R. Feathers, M. Klanschnig, A. Thader,
M.C. Johnson, V.M. Vogt, F.K. Schur, R.A. Dick, Nature Communications 12 (2021).
date_created: 2021-05-28T14:25:50Z
date_published: 2021-05-28T00:00:00Z
date_updated: 2023-08-08T13:53:53Z
day: '28'
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department:
- _id: FlSc
doi: 10.1038/s41467-021-23506-0
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title: Structure of the mature Rous sarcoma virus lattice reveals a role for IP6 in
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