---
_id: '6848'
abstract:
- lang: eng
text: Proton-translocating transhydrogenase (also known as nicotinamide nucleotide
transhydrogenase (NNT)) is found in the plasma membranes of bacteria and the inner
mitochondrial membranes of eukaryotes. NNT catalyses the transfer of a hydride
between NADH and NADP+, coupled to the translocation of one proton across the
membrane. Its main physiological function is the generation of NADPH, which is
a substrate in anabolic reactions and a regulator of oxidative status; however,
NNT may also fine-tune the Krebs cycle1,2. NNT deficiency causes familial glucocorticoid
deficiency in humans and metabolic abnormalities in mice, similar to those observed
in type II diabetes3,4. The catalytic mechanism of NNT has been proposed to involve
a rotation of around 180° of the entire NADP(H)-binding domain that alternately
participates in hydride transfer and proton-channel gating. However, owing to
the lack of high-resolution structures of intact NNT, the details of this process
remain unclear5,6. Here we present the cryo-electron microscopy structure of intact
mammalian NNT in different conformational states. We show how the NADP(H)-binding
domain opens the proton channel to the opposite sides of the membrane, and we
provide structures of these two states. We also describe the catalytically important
interfaces and linkers between the membrane and the soluble domains and their
roles in nucleotide exchange. These structures enable us to propose a revised
mechanism for a coupling process in NNT that is consistent with a large body of
previous biochemical work. Our results are relevant to the development of currently
unavailable NNT inhibitors, which may have therapeutic potential in ischaemia
reperfusion injury, metabolic syndrome and some cancers7,8,9.
acknowledged_ssus:
- _id: ScienComp
acknowledgement: " We thank R. Thompson, G. Effantin and V.-V. Hodirnau for their
assistance with collecting NADP+, NADPH and apo datasets, respectively. Data processing
was performed at the IST high-performance computing cluster.\r\nThis project has
received funding from the European Union’s Horizon 2020 research and innovation
programme under the Marie Skłodowska-Curie Grant Agreement no. 665385."
article_processing_charge: No
article_type: letter_note
author:
- first_name: Domen
full_name: Kampjut, Domen
id: 37233050-F248-11E8-B48F-1D18A9856A87
last_name: Kampjut
- first_name: Leonid A
full_name: Sazanov, Leonid A
id: 338D39FE-F248-11E8-B48F-1D18A9856A87
last_name: Sazanov
orcid: 0000-0002-0977-7989
citation:
ama: Kampjut D, Sazanov LA. Structure and mechanism of mitochondrial proton-translocating
transhydrogenase. Nature. 2019;573(7773):291–295. doi:10.1038/s41586-019-1519-2
apa: Kampjut, D., & Sazanov, L. A. (2019). Structure and mechanism of mitochondrial
proton-translocating transhydrogenase. Nature. Springer Nature. https://doi.org/10.1038/s41586-019-1519-2
chicago: Kampjut, Domen, and Leonid A Sazanov. “Structure and Mechanism of Mitochondrial
Proton-Translocating Transhydrogenase.” Nature. Springer Nature, 2019.
https://doi.org/10.1038/s41586-019-1519-2.
ieee: D. Kampjut and L. A. Sazanov, “Structure and mechanism of mitochondrial proton-translocating
transhydrogenase,” Nature, vol. 573, no. 7773. Springer Nature, pp. 291–295,
2019.
ista: Kampjut D, Sazanov LA. 2019. Structure and mechanism of mitochondrial proton-translocating
transhydrogenase. Nature. 573(7773), 291–295.
mla: Kampjut, Domen, and Leonid A. Sazanov. “Structure and Mechanism of Mitochondrial
Proton-Translocating Transhydrogenase.” Nature, vol. 573, no. 7773, Springer
Nature, 2019, pp. 291–295, doi:10.1038/s41586-019-1519-2.
short: D. Kampjut, L.A. Sazanov, Nature 573 (2019) 291–295.
date_created: 2019-09-04T06:21:41Z
date_published: 2019-09-12T00:00:00Z
date_updated: 2024-03-25T23:30:08Z
day: '12'
ddc:
- '572'
department:
- _id: LeSa
doi: 10.1038/s41586-019-1519-2
ec_funded: 1
external_id:
isi:
- '000485415400061'
pmid:
- '31462775'
file:
- access_level: open_access
checksum: 52728cda5210a3e9b74cc204e8aed3d5
content_type: application/pdf
creator: lsazanov
date_created: 2020-11-26T16:33:44Z
date_updated: 2020-11-26T16:33:44Z
file_id: '8821'
file_name: Manuscript_final_acc_withFigs_SI_opt_red.pdf
file_size: 3066206
relation: main_file
success: 1
file_date_updated: 2020-11-26T16:33:44Z
has_accepted_license: '1'
intvolume: ' 573'
isi: 1
issue: '7773'
language:
- iso: eng
month: '09'
oa: 1
oa_version: Submitted Version
page: 291–295
pmid: 1
project:
- _id: 2564DBCA-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '665385'
name: International IST Doctoral Program
publication: Nature
publication_identifier:
eissn:
- 1476-4687
issn:
- 0028-0836
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
link:
- description: News on IST Website
relation: press_release
url: https://ist.ac.at/en/news/high-end-microscopy-reveals-structure-and-function-of-crucial-metabolic-enzyme/
record:
- id: '8340'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Structure and mechanism of mitochondrial proton-translocating transhydrogenase
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 573
year: '2019'
...
---
_id: '6259'
abstract:
- lang: eng
text: The plant hormone auxin has crucial roles in almost all aspects of plant growth
and development. Concentrations of auxin vary across different tissues, mediating
distinct developmental outcomes and contributing to the functional diversity of
auxin. However, the mechanisms that underlie these activities are poorly understood.
Here we identify an auxin signalling mechanism, which acts in parallel to the
canonical auxin pathway based on the transport inhibitor response1 (TIR1) and
other auxin receptor F-box (AFB) family proteins (TIR1/AFB receptors)1,2, that
translates levels of cellular auxin to mediate differential growth during apical-hook
development. This signalling mechanism operates at the concave side of the apical
hook, and involves auxin-mediated C-terminal cleavage of transmembrane kinase
1 (TMK1). The cytosolic and nucleus-translocated C terminus of TMK1 specifically
interacts with and phosphorylates two non-canonical transcriptional repressors
of the auxin or indole-3-acetic acid (Aux/IAA) family (IAA32 and IAA34), thereby
regulating ARF transcription factors. In contrast to the degradation of Aux/IAA
transcriptional repressors in the canonical pathway, the newly identified mechanism
stabilizes the non-canonical IAA32 and IAA34 transcriptional repressors to regulate
gene expression and ultimately inhibit growth. The auxin–TMK1 signalling pathway
originates at the cell surface, is triggered by high levels of auxin and shares
a partially overlapping set of transcription factors with the TIR1/AFB signalling
pathway. This allows distinct interpretations of different concentrations of cellular
auxin, and thus enables this versatile signalling molecule to mediate complex
developmental outcomes.
article_processing_charge: No
article_type: original
author:
- first_name: Min
full_name: Cao, Min
last_name: Cao
- first_name: Rong
full_name: Chen, Rong
last_name: Chen
- first_name: Pan
full_name: Li, Pan
last_name: Li
- first_name: Yongqiang
full_name: Yu, Yongqiang
last_name: Yu
- first_name: Rui
full_name: Zheng, Rui
last_name: Zheng
- first_name: Danfeng
full_name: Ge, Danfeng
last_name: Ge
- first_name: Wei
full_name: Zheng, Wei
last_name: Zheng
- first_name: Xuhui
full_name: Wang, Xuhui
last_name: Wang
- first_name: Yangtao
full_name: Gu, Yangtao
last_name: Gu
- first_name: Zuzana
full_name: Gelová, Zuzana
id: 0AE74790-0E0B-11E9-ABC7-1ACFE5697425
last_name: Gelová
orcid: 0000-0003-4783-1752
- first_name: Jiří
full_name: Friml, Jiří
id: 4159519E-F248-11E8-B48F-1D18A9856A87
last_name: Friml
orcid: 0000-0002-8302-7596
- first_name: Heng
full_name: Zhang, Heng
last_name: Zhang
- first_name: Renyi
full_name: Liu, Renyi
last_name: Liu
- first_name: Jun
full_name: He, Jun
last_name: He
- first_name: Tongda
full_name: Xu, Tongda
last_name: Xu
citation:
ama: Cao M, Chen R, Li P, et al. TMK1-mediated auxin signalling regulates differential
growth of the apical hook. Nature. 2019;568:240-243. doi:10.1038/s41586-019-1069-7
apa: Cao, M., Chen, R., Li, P., Yu, Y., Zheng, R., Ge, D., … Xu, T. (2019). TMK1-mediated
auxin signalling regulates differential growth of the apical hook. Nature.
Springer Nature. https://doi.org/10.1038/s41586-019-1069-7
chicago: Cao, Min, Rong Chen, Pan Li, Yongqiang Yu, Rui Zheng, Danfeng Ge, Wei Zheng,
et al. “TMK1-Mediated Auxin Signalling Regulates Differential Growth of the Apical
Hook.” Nature. Springer Nature, 2019. https://doi.org/10.1038/s41586-019-1069-7.
ieee: M. Cao et al., “TMK1-mediated auxin signalling regulates differential
growth of the apical hook,” Nature, vol. 568. Springer Nature, pp. 240–243,
2019.
ista: Cao M, Chen R, Li P, Yu Y, Zheng R, Ge D, Zheng W, Wang X, Gu Y, Gelová Z,
Friml J, Zhang H, Liu R, He J, Xu T. 2019. TMK1-mediated auxin signalling regulates
differential growth of the apical hook. Nature. 568, 240–243.
mla: Cao, Min, et al. “TMK1-Mediated Auxin Signalling Regulates Differential Growth
of the Apical Hook.” Nature, vol. 568, Springer Nature, 2019, pp. 240–43,
doi:10.1038/s41586-019-1069-7.
short: M. Cao, R. Chen, P. Li, Y. Yu, R. Zheng, D. Ge, W. Zheng, X. Wang, Y. Gu,
Z. Gelová, J. Friml, H. Zhang, R. Liu, J. He, T. Xu, Nature 568 (2019) 240–243.
date_created: 2019-04-09T08:37:05Z
date_published: 2019-04-11T00:00:00Z
date_updated: 2023-09-05T14:58:41Z
day: '11'
ddc:
- '580'
department:
- _id: JiFr
doi: 10.1038/s41586-019-1069-7
ec_funded: 1
external_id:
isi:
- '000464412700050'
pmid:
- '30944466'
file:
- access_level: open_access
checksum: 6b84ab602a34382cf0340a37a1378c75
content_type: application/pdf
creator: dernst
date_created: 2020-11-13T07:37:41Z
date_updated: 2020-11-13T07:37:41Z
file_id: '8751'
file_name: 2019_Nature _Cao_accepted.pdf
file_size: 4321328
relation: main_file
success: 1
file_date_updated: 2020-11-13T07:37:41Z
has_accepted_license: '1'
intvolume: ' 568'
isi: 1
language:
- iso: eng
month: '04'
oa: 1
oa_version: Submitted Version
page: 240-243
pmid: 1
project:
- _id: 261099A6-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '742985'
name: Tracing Evolution of Auxin Transport and Polarity in Plants
publication: Nature
publication_identifier:
eissn:
- 1476-4687
issn:
- 0028-0836
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
link:
- description: News on IST Homepage
relation: press_release
url: https://ist.ac.at/en/news/newly-discovered-mechanism-of-plant-hormone-auxin-acts-the-opposite-way/
scopus_import: '1'
status: public
title: TMK1-mediated auxin signalling regulates differential growth of the apical
hook
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 568
year: '2019'
...
---
_id: '6117'
abstract:
- lang: eng
text: 'Interleukin-17 (IL-17) is a major pro-inflammatory cytokine: it mediates
responses to pathogens or tissue damage, and drives autoimmune diseases. Little
is known about its role in the nervous system. Here we show that IL-17 has neuromodulator-like
properties in Caenorhabditis elegans. IL-17 can act directly on neurons to alter
their response properties and contribution to behaviour. Using unbiased genetic
screens, we delineate an IL-17 signalling pathway and show that it acts in the
RMG hub interneurons. Disrupting IL-17 signalling reduces RMG responsiveness to
input from oxygen sensors, and renders sustained escape from 21% oxygen transient
and contingent on additional stimuli. Over-activating IL-17 receptors abnormally
heightens responses to 21% oxygen in RMG neurons and whole animals. IL-17 deficiency
can be bypassed by optogenetic stimulation of RMG. Inducing IL-17 expression in
adults can rescue mutant defects within 6 h. These findings reveal a non-immunological
role of IL-17 modulating circuit function and behaviour.'
author:
- first_name: Changchun
full_name: Chen, Changchun
last_name: Chen
- first_name: Eisuke
full_name: Itakura, Eisuke
last_name: Itakura
- first_name: Geoffrey M.
full_name: Nelson, Geoffrey M.
last_name: Nelson
- first_name: Ming
full_name: Sheng, Ming
last_name: Sheng
- first_name: Patrick
full_name: Laurent, Patrick
last_name: Laurent
- first_name: Lorenz A.
full_name: Fenk, Lorenz A.
last_name: Fenk
- first_name: Rebecca A.
full_name: Butcher, Rebecca A.
last_name: Butcher
- first_name: Ramanujan S.
full_name: Hegde, Ramanujan S.
last_name: Hegde
- first_name: Mario
full_name: de Bono, Mario
id: 4E3FF80E-F248-11E8-B48F-1D18A9856A87
last_name: de Bono
orcid: 0000-0001-8347-0443
citation:
ama: Chen C, Itakura E, Nelson GM, et al. IL-17 is a neuromodulator of Caenorhabditis
elegans sensory responses. Nature. 2017;542(7639):43-48. doi:10.1038/nature20818
apa: Chen, C., Itakura, E., Nelson, G. M., Sheng, M., Laurent, P., Fenk, L. A.,
… de Bono, M. (2017). IL-17 is a neuromodulator of Caenorhabditis elegans sensory
responses. Nature. Springer Nature. https://doi.org/10.1038/nature20818
chicago: Chen, Changchun, Eisuke Itakura, Geoffrey M. Nelson, Ming Sheng, Patrick
Laurent, Lorenz A. Fenk, Rebecca A. Butcher, Ramanujan S. Hegde, and Mario de
Bono. “IL-17 Is a Neuromodulator of Caenorhabditis Elegans Sensory Responses.”
Nature. Springer Nature, 2017. https://doi.org/10.1038/nature20818.
ieee: C. Chen et al., “IL-17 is a neuromodulator of Caenorhabditis elegans
sensory responses,” Nature, vol. 542, no. 7639. Springer Nature, pp. 43–48,
2017.
ista: Chen C, Itakura E, Nelson GM, Sheng M, Laurent P, Fenk LA, Butcher RA, Hegde
RS, de Bono M. 2017. IL-17 is a neuromodulator of Caenorhabditis elegans sensory
responses. Nature. 542(7639), 43–48.
mla: Chen, Changchun, et al. “IL-17 Is a Neuromodulator of Caenorhabditis Elegans
Sensory Responses.” Nature, vol. 542, no. 7639, Springer Nature, 2017,
pp. 43–48, doi:10.1038/nature20818.
short: C. Chen, E. Itakura, G.M. Nelson, M. Sheng, P. Laurent, L.A. Fenk, R.A. Butcher,
R.S. Hegde, M. de Bono, Nature 542 (2017) 43–48.
date_created: 2019-03-19T14:06:41Z
date_published: 2017-02-02T00:00:00Z
date_updated: 2021-01-12T08:06:12Z
day: '02'
doi: 10.1038/nature20818
extern: '1'
external_id:
pmid:
- ' 28099418'
intvolume: ' 542'
issue: '7639'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pubmed/28099418
month: '02'
oa: 1
oa_version: Submitted Version
page: 43-48
pmid: 1
publication: Nature
publication_identifier:
issn:
- 0028-0836
- 1476-4687
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
status: public
title: IL-17 is a neuromodulator of Caenorhabditis elegans sensory responses
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 542
year: '2017'
...
---
_id: '14290'
abstract:
- lang: eng
text: DNA nanotechnology, in particular DNA origami, enables the bottom-up self-assembly
of micrometre-scale, three-dimensional structures with nanometre-precise features1,2,3,4,5,6,7,8,9,10,11,12.
These structures are customizable in that they can be site-specifically functionalized13
or constructed to exhibit machine-like14,15 or logic-gating behaviour16. Their
use has been limited to applications that require only small amounts of material
(of the order of micrograms), owing to the limitations of current production methods.
But many proposed applications, for example as therapeutic agents or in complex
materials3,16,17,18,19,20,21,22, could be realized if more material could be used.
In DNA origami, a nanostructure is assembled from a very long single-stranded
scaffold molecule held in place by many short single-stranded staple oligonucleotides.
Only the bacteriophage-derived scaffold molecules are amenable to scalable and
efficient mass production23; the shorter staple strands are obtained through costly
solid-phase synthesis24 or enzymatic processes25. Here we show that single strands
of DNA of virtually arbitrary length and with virtually arbitrary sequences can
be produced in a scalable and cost-efficient manner by using bacteriophages to
generate single-stranded precursor DNA that contains target strand sequences interleaved
with self-excising ‘cassettes’, with each cassette comprising two Zn2+-dependent
DNA-cleaving DNA enzymes. We produce all of the necessary single strands of DNA
for several DNA origami using shaker-flask cultures, and demonstrate end-to-end
production of macroscopic amounts of a DNA origami nanorod in a litre-scale stirred-tank
bioreactor. Our method is compatible with existing DNA origami design frameworks
and retains the modularity and addressability of DNA origami objects that are
necessary for implementing custom modifications using functional groups. With
all of the production and purification steps amenable to scaling, we expect that
our method will expand the scope of DNA nanotechnology in many areas of science
and technology.
article_processing_charge: No
article_type: original
author:
- first_name: Florian M
full_name: Praetorius, Florian M
id: dfec9381-4341-11ee-8fd8-faa02bba7d62
last_name: Praetorius
- first_name: Benjamin
full_name: Kick, Benjamin
last_name: Kick
- first_name: Karl L.
full_name: Behler, Karl L.
last_name: Behler
- first_name: Maximilian N.
full_name: Honemann, Maximilian N.
last_name: Honemann
- first_name: Dirk
full_name: Weuster-Botz, Dirk
last_name: Weuster-Botz
- first_name: Hendrik
full_name: Dietz, Hendrik
last_name: Dietz
citation:
ama: Praetorius FM, Kick B, Behler KL, Honemann MN, Weuster-Botz D, Dietz H. Biotechnological
mass production of DNA origami. Nature. 2017;552(7683):84-87. doi:10.1038/nature24650
apa: Praetorius, F. M., Kick, B., Behler, K. L., Honemann, M. N., Weuster-Botz,
D., & Dietz, H. (2017). Biotechnological mass production of DNA origami. Nature.
Springer Nature. https://doi.org/10.1038/nature24650
chicago: Praetorius, Florian M, Benjamin Kick, Karl L. Behler, Maximilian N. Honemann,
Dirk Weuster-Botz, and Hendrik Dietz. “Biotechnological Mass Production of DNA
Origami.” Nature. Springer Nature, 2017. https://doi.org/10.1038/nature24650.
ieee: F. M. Praetorius, B. Kick, K. L. Behler, M. N. Honemann, D. Weuster-Botz,
and H. Dietz, “Biotechnological mass production of DNA origami,” Nature,
vol. 552, no. 7683. Springer Nature, pp. 84–87, 2017.
ista: Praetorius FM, Kick B, Behler KL, Honemann MN, Weuster-Botz D, Dietz H. 2017.
Biotechnological mass production of DNA origami. Nature. 552(7683), 84–87.
mla: Praetorius, Florian M., et al. “Biotechnological Mass Production of DNA Origami.”
Nature, vol. 552, no. 7683, Springer Nature, 2017, pp. 84–87, doi:10.1038/nature24650.
short: F.M. Praetorius, B. Kick, K.L. Behler, M.N. Honemann, D. Weuster-Botz, H.
Dietz, Nature 552 (2017) 84–87.
date_created: 2023-09-06T12:14:20Z
date_published: 2017-12-07T00:00:00Z
date_updated: 2023-11-07T12:24:49Z
day: '07'
doi: 10.1038/nature24650
extern: '1'
external_id:
pmid:
- '29219963'
intvolume: ' 552'
issue: '7683'
language:
- iso: eng
month: '12'
oa_version: None
page: 84-87
pmid: 1
publication: Nature
publication_identifier:
eissn:
- 1476-4687
issn:
- 0028-0836
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Biotechnological mass production of DNA origami
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 552
year: '2017'
...
---
_id: '9456'
abstract:
- lang: eng
text: The discovery of introns four decades ago was one of the most unexpected findings
in molecular biology. Introns are sequences interrupting genes that must be removed
as part of messenger RNA production. Genome sequencing projects have shown that
most eukaryotic genes contain at least one intron, and frequently many. Comparison
of these genomes reveals a history of long evolutionary periods during which few
introns were gained, punctuated by episodes of rapid, extensive gain. However,
although several detailed mechanisms for such episodic intron generation have
been proposed, none has been empirically supported on a genomic scale. Here we
show how short, non-autonomous DNA transposons independently generated hundreds
to thousands of introns in the prasinophyte Micromonas pusilla and the pelagophyte
Aureococcus anophagefferens. Each transposon carries one splice site. The other
splice site is co-opted from the gene sequence that is duplicated upon transposon
insertion, allowing perfect splicing out of the RNA. The distributions of sequences
that can be co-opted are biased with respect to codons, and phasing of transposon-generated
introns is similarly biased. These transposons insert between pre-existing nucleosomes,
so that multiple nearby insertions generate nucleosome-sized intervening segments.
Thus, transposon insertion and sequence co-option may explain the intron phase
biases and prevalence of nucleosome-sized exons observed in eukaryotes. Overall,
the two independent examples of proliferating elements illustrate a general DNA
transposon mechanism that can plausibly account for episodes of rapid, extensive
intron gain during eukaryotic evolution.
article_processing_charge: No
article_type: letter_note
author:
- first_name: Jason T.
full_name: Huff, Jason T.
last_name: Huff
- first_name: Daniel
full_name: Zilberman, Daniel
id: 6973db13-dd5f-11ea-814e-b3e5455e9ed1
last_name: Zilberman
orcid: 0000-0002-0123-8649
- first_name: Scott W.
full_name: Roy, Scott W.
last_name: Roy
citation:
ama: Huff JT, Zilberman D, Roy SW. Mechanism for DNA transposons to generate introns
on genomic scales. Nature. 2016;538(7626):533-536. doi:10.1038/nature20110
apa: Huff, J. T., Zilberman, D., & Roy, S. W. (2016). Mechanism for DNA transposons
to generate introns on genomic scales. Nature. Springer Nature . https://doi.org/10.1038/nature20110
chicago: Huff, Jason T., Daniel Zilberman, and Scott W. Roy. “Mechanism for DNA
Transposons to Generate Introns on Genomic Scales.” Nature. Springer Nature
, 2016. https://doi.org/10.1038/nature20110.
ieee: J. T. Huff, D. Zilberman, and S. W. Roy, “Mechanism for DNA transposons to
generate introns on genomic scales,” Nature, vol. 538, no. 7626. Springer
Nature , pp. 533–536, 2016.
ista: Huff JT, Zilberman D, Roy SW. 2016. Mechanism for DNA transposons to generate
introns on genomic scales. Nature. 538(7626), 533–536.
mla: Huff, Jason T., et al. “Mechanism for DNA Transposons to Generate Introns on
Genomic Scales.” Nature, vol. 538, no. 7626, Springer Nature , 2016, pp.
533–36, doi:10.1038/nature20110.
short: J.T. Huff, D. Zilberman, S.W. Roy, Nature 538 (2016) 533–536.
date_created: 2021-06-04T11:34:55Z
date_published: 2016-10-27T00:00:00Z
date_updated: 2021-12-14T07:55:30Z
day: '27'
department:
- _id: DaZi
doi: 10.1038/nature20110
extern: '1'
external_id:
pmid:
- '27760113'
intvolume: ' 538'
issue: '7626'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5684705/
month: '10'
oa: 1
oa_version: Submitted Version
page: 533-536
pmid: 1
publication: Nature
publication_identifier:
eissn:
- 1476-4687
issn:
- 0028-0836
publication_status: published
publisher: 'Springer Nature '
quality_controlled: '1'
scopus_import: '1'
status: public
title: Mechanism for DNA transposons to generate introns on genomic scales
type: journal_article
user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9
volume: 538
year: '2016'
...
---
_id: '9654'
abstract:
- lang: eng
text: RNA polymerase I (Pol I) is a highly processive enzyme that transcribes ribosomal
DNA (rDNA) and regulates growth of eukaryotic cells. Crystal structures of free
Pol I from the yeast Saccharomyces cerevisiae have revealed dimers of the enzyme
stabilized by a 'connector' element and an expanded cleft containing the active
centre in an inactive conformation. The central bridge helix was unfolded and
a Pol-I-specific 'expander' element occupied the DNA-template-binding site. The
structure of Pol I in its active transcribing conformation has yet to be determined,
whereas structures of Pol II and Pol III have been solved with bound DNA template
and RNA transcript. Here we report structures of active transcribing Pol I from
yeast solved by two different cryo-electron microscopy approaches. A single-particle
structure at 3.8 Å resolution reveals a contracted active centre cleft with bound
DNA and RNA, and a narrowed pore beneath the active site that no longer holds
the RNA-cleavage-stimulating domain of subunit A12.2. A structure at 29 Å resolution
that was determined from cryo-electron tomograms of Pol I enzymes transcribing
cellular rDNA confirms contraction of the cleft and reveals that incoming and
exiting rDNA enclose an angle of around 150°. The structures suggest a model for
the regulation of transcription elongation in which contracted and expanded polymerase
conformations are associated with active and inactive states, respectively.
article_processing_charge: No
article_type: letter_note
author:
- first_name: Simon
full_name: Neyer, Simon
last_name: Neyer
- first_name: Michael
full_name: Kunz, Michael
last_name: Kunz
- first_name: Christian
full_name: Geiss, Christian
last_name: Geiss
- first_name: Merle
full_name: Hantsche, Merle
last_name: Hantsche
- first_name: Victor-Valentin
full_name: Hodirnau, Victor-Valentin
id: 3661B498-F248-11E8-B48F-1D18A9856A87
last_name: Hodirnau
- first_name: Anja
full_name: Seybert, Anja
last_name: Seybert
- first_name: Christoph
full_name: Engel, Christoph
last_name: Engel
- first_name: Margot P.
full_name: Scheffer, Margot P.
last_name: Scheffer
- first_name: Patrick
full_name: Cramer, Patrick
last_name: Cramer
- first_name: Achilleas S.
full_name: Frangakis, Achilleas S.
last_name: Frangakis
citation:
ama: Neyer S, Kunz M, Geiss C, et al. Structure of RNA polymerase I transcribing
ribosomal DNA genes. Nature. 2016;540(7634):607-610. doi:10.1038/nature20561
apa: Neyer, S., Kunz, M., Geiss, C., Hantsche, M., Hodirnau, V.-V., Seybert, A.,
… Frangakis, A. S. (2016). Structure of RNA polymerase I transcribing ribosomal
DNA genes. Nature. Springer Nature. https://doi.org/10.1038/nature20561
chicago: Neyer, Simon, Michael Kunz, Christian Geiss, Merle Hantsche, Victor-Valentin
Hodirnau, Anja Seybert, Christoph Engel, Margot P. Scheffer, Patrick Cramer, and
Achilleas S. Frangakis. “Structure of RNA Polymerase I Transcribing Ribosomal
DNA Genes.” Nature. Springer Nature, 2016. https://doi.org/10.1038/nature20561.
ieee: S. Neyer et al., “Structure of RNA polymerase I transcribing ribosomal
DNA genes,” Nature, vol. 540, no. 7634. Springer Nature, pp. 607–610, 2016.
ista: Neyer S, Kunz M, Geiss C, Hantsche M, Hodirnau V-V, Seybert A, Engel C, Scheffer
MP, Cramer P, Frangakis AS. 2016. Structure of RNA polymerase I transcribing ribosomal
DNA genes. Nature. 540(7634), 607–610.
mla: Neyer, Simon, et al. “Structure of RNA Polymerase I Transcribing Ribosomal
DNA Genes.” Nature, vol. 540, no. 7634, Springer Nature, 2016, pp. 607–10,
doi:10.1038/nature20561.
short: S. Neyer, M. Kunz, C. Geiss, M. Hantsche, V.-V. Hodirnau, A. Seybert, C.
Engel, M.P. Scheffer, P. Cramer, A.S. Frangakis, Nature 540 (2016) 607–610.
date_created: 2021-07-14T09:04:24Z
date_published: 2016-12-22T00:00:00Z
date_updated: 2021-07-22T09:22:20Z
day: '22'
doi: 10.1038/nature20561
extern: '1'
external_id:
pmid:
- '27842382'
intvolume: ' 540'
issue: '7634'
language:
- iso: eng
month: '12'
oa_version: None
page: 607-610
pmid: 1
publication: Nature
publication_identifier:
eissn:
- 1476-4687
issn:
- 0028-0836
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Structure of RNA polymerase I transcribing ribosomal DNA genes
type: journal_article
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
volume: 540
year: '2016'
...
---
_id: '1862'
abstract:
- lang: eng
text: The prominent and evolutionarily ancient role of the plant hormone auxin is
the regulation of cell expansion. Cell expansion requires ordered arrangement
of the cytoskeleton but molecular mechanisms underlying its regulation by signalling
molecules including auxin are unknown. Here we show in the model plant Arabidopsis
thaliana that in elongating cells exogenous application of auxin or redistribution
of endogenous auxin induces very rapid microtubule re-orientation from transverse
to longitudinal, coherent with the inhibition of cell expansion. This fast auxin
effect requires auxin binding protein 1 (ABP1) and involves a contribution of
downstream signalling components such as ROP6 GTPase, ROP-interactive protein
RIC1 and the microtubule-severing protein katanin. These components are required
for rapid auxin-and ABP1-mediated re-orientation of microtubules to regulate cell
elongation in roots and dark-grown hypocotyls as well as asymmetric growth during
gravitropic responses.
acknowledgement: We thank R. Dixit for performing complementary experiments, D. W.
Ehrhardt and T. Hashimoto for providing the seeds of TUB6–RFP and EB1b–GFP respectively,
E. Zazimalova, J. Petrasek and M. Fendrych for discussing the manuscript and J.
Leung for text optimization. This work was supported by the European Research Council
(project ERC-2011-StG-20101109-PSDP, to J.F.), ANR blanc AuxiWall project (ANR-11-BSV5-0007,
to C.P.-R. and L.G.) and the Agency for Innovation by Science and Technology (IWT)
(to H.R.). This work benefited from the facilities and expertise of the Imagif Cell
Biology platform (http://www.imagif.cnrs.fr), which is supported by the Conseil
Général de l’Essonne.
article_processing_charge: No
article_type: original
author:
- first_name: Xu
full_name: Chen, Xu
id: 4E5ADCAA-F248-11E8-B48F-1D18A9856A87
last_name: Chen
- first_name: Laurie
full_name: Grandont, Laurie
last_name: Grandont
- first_name: Hongjiang
full_name: Li, Hongjiang
id: 33CA54A6-F248-11E8-B48F-1D18A9856A87
last_name: Li
orcid: 0000-0001-5039-9660
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Sébastien
full_name: Paque, Sébastien
last_name: Paque
- first_name: Anas
full_name: Abuzeineh, Anas
last_name: Abuzeineh
- first_name: Hana
full_name: Rakusova, Hana
id: 4CAAA450-78D2-11EA-8E57-B40A396E08BA
last_name: Rakusova
- first_name: Eva
full_name: Benková, Eva
id: 38F4F166-F248-11E8-B48F-1D18A9856A87
last_name: Benková
orcid: 0000-0002-8510-9739
- first_name: Catherine
full_name: Perrot Rechenmann, Catherine
last_name: Perrot Rechenmann
- first_name: Jirí
full_name: Friml, Jirí
id: 4159519E-F248-11E8-B48F-1D18A9856A87
last_name: Friml
orcid: 0000-0002-8302-7596
citation:
ama: Chen X, Grandont L, Li H, et al. Inhibition of cell expansion by rapid ABP1-mediated
auxin effect on microtubules. Nature. 2014;516(729):90-93. doi:10.1038/nature13889
apa: Chen, X., Grandont, L., Li, H., Hauschild, R., Paque, S., Abuzeineh, A., …
Friml, J. (2014). Inhibition of cell expansion by rapid ABP1-mediated auxin effect
on microtubules. Nature. Nature Publishing Group. https://doi.org/10.1038/nature13889
chicago: Chen, Xu, Laurie Grandont, Hongjiang Li, Robert Hauschild, Sébastien Paque,
Anas Abuzeineh, Hana Rakusova, Eva Benková, Catherine Perrot Rechenmann, and Jiří
Friml. “Inhibition of Cell Expansion by Rapid ABP1-Mediated Auxin Effect on Microtubules.”
Nature. Nature Publishing Group, 2014. https://doi.org/10.1038/nature13889.
ieee: X. Chen et al., “Inhibition of cell expansion by rapid ABP1-mediated
auxin effect on microtubules,” Nature, vol. 516, no. 729. Nature Publishing
Group, pp. 90–93, 2014.
ista: Chen X, Grandont L, Li H, Hauschild R, Paque S, Abuzeineh A, Rakusova H, Benková
E, Perrot Rechenmann C, Friml J. 2014. Inhibition of cell expansion by rapid ABP1-mediated
auxin effect on microtubules. Nature. 516(729), 90–93.
mla: Chen, Xu, et al. “Inhibition of Cell Expansion by Rapid ABP1-Mediated Auxin
Effect on Microtubules.” Nature, vol. 516, no. 729, Nature Publishing Group,
2014, pp. 90–93, doi:10.1038/nature13889.
short: X. Chen, L. Grandont, H. Li, R. Hauschild, S. Paque, A. Abuzeineh, H. Rakusova,
E. Benková, C. Perrot Rechenmann, J. Friml, Nature 516 (2014) 90–93.
date_created: 2018-12-11T11:54:25Z
date_published: 2014-12-04T00:00:00Z
date_updated: 2025-05-07T11:12:31Z
day: '04'
department:
- _id: JiFr
- _id: Bio
- _id: EvBe
doi: 10.1038/nature13889
ec_funded: 1
external_id:
pmid:
- '25409144'
intvolume: ' 516'
issue: '729'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4257754/
month: '12'
oa: 1
oa_version: Submitted Version
page: 90 - 93
pmid: 1
project:
- _id: 25716A02-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '282300'
name: Polarity and subcellular dynamics in plants
publication: Nature
publication_identifier:
eissn:
- 1476-4687
issn:
- 0028-0836
publication_status: published
publisher: Nature Publishing Group
publist_id: '5237'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Inhibition of cell expansion by rapid ABP1-mediated auxin effect on microtubules
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 516
year: '2014'
...
---
_id: '6144'
abstract:
- lang: eng
text: Behaviours evolve by iterations of natural selection, but we have few insights
into the molecular and neural mechanisms involved. Here we show that some Caenorhabditis
elegans wild strains switch between two foraging behaviours in response to subtle
changes in ambient oxygen. This finely tuned switch is conferred by a naturally
variable hexacoordinated globin, GLB-5. GLB-5 acts with the atypical soluble guanylate
cyclases1,2,3, which are a different type of oxygen binding protein, to tune the
dynamic range of oxygen-sensing neurons close to atmospheric (21%) concentrations.
Calcium imaging indicates that one group of these neurons is activated when oxygen
rises towards 21%, and is inhibited as oxygen drops below 21%. The soluble guanylate
cyclase GCY-35 is required for high oxygen to activate the neurons; GLB-5 provides
inhibitory input when oxygen decreases below 21%. Together, these oxygen binding
proteins tune neuronal and behavioural responses to a narrow oxygen concentration
range close to atmospheric levels. The effect of the glb-5 gene on oxygen sensing
and foraging is modified by the naturally variable neuropeptide receptor npr-1
(refs 4, 5), providing insights into how polygenic variation reshapes neural circuit
function.
author:
- first_name: Annelie
full_name: Persson, Annelie
last_name: Persson
- first_name: Einav
full_name: Gross, Einav
last_name: Gross
- first_name: Patrick
full_name: Laurent, Patrick
last_name: Laurent
- first_name: Karl Emanuel
full_name: Busch, Karl Emanuel
last_name: Busch
- first_name: Hugo
full_name: Bretes, Hugo
last_name: Bretes
- first_name: Mario
full_name: de Bono, Mario
id: 4E3FF80E-F248-11E8-B48F-1D18A9856A87
last_name: de Bono
orcid: 0000-0001-8347-0443
citation:
ama: Persson A, Gross E, Laurent P, Busch KE, Bretes H, de Bono M. Natural variation
in a neural globin tunes oxygen sensing in wild Caenorhabditis elegans. Nature.
2009;458(7241):1030-1033. doi:10.1038/nature07820
apa: Persson, A., Gross, E., Laurent, P., Busch, K. E., Bretes, H., & de Bono,
M. (2009). Natural variation in a neural globin tunes oxygen sensing in wild Caenorhabditis
elegans. Nature. Springer Nature. https://doi.org/10.1038/nature07820
chicago: Persson, Annelie, Einav Gross, Patrick Laurent, Karl Emanuel Busch, Hugo
Bretes, and Mario de Bono. “Natural Variation in a Neural Globin Tunes Oxygen
Sensing in Wild Caenorhabditis Elegans.” Nature. Springer Nature, 2009.
https://doi.org/10.1038/nature07820.
ieee: A. Persson, E. Gross, P. Laurent, K. E. Busch, H. Bretes, and M. de Bono,
“Natural variation in a neural globin tunes oxygen sensing in wild Caenorhabditis
elegans,” Nature, vol. 458, no. 7241. Springer Nature, pp. 1030–1033, 2009.
ista: Persson A, Gross E, Laurent P, Busch KE, Bretes H, de Bono M. 2009. Natural
variation in a neural globin tunes oxygen sensing in wild Caenorhabditis elegans.
Nature. 458(7241), 1030–1033.
mla: Persson, Annelie, et al. “Natural Variation in a Neural Globin Tunes Oxygen
Sensing in Wild Caenorhabditis Elegans.” Nature, vol. 458, no. 7241, Springer
Nature, 2009, pp. 1030–33, doi:10.1038/nature07820.
short: A. Persson, E. Gross, P. Laurent, K.E. Busch, H. Bretes, M. de Bono, Nature
458 (2009) 1030–1033.
date_created: 2019-03-21T07:48:44Z
date_published: 2009-04-23T00:00:00Z
date_updated: 2021-01-12T08:06:20Z
day: '23'
doi: 10.1038/nature07820
extern: '1'
external_id:
pmid:
- '19262507'
intvolume: ' 458'
issue: '7241'
language:
- iso: eng
month: '04'
oa_version: None
page: 1030-1033
pmid: 1
publication: Nature
publication_identifier:
issn:
- 0028-0836
- 1476-4687
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
status: public
title: Natural variation in a neural globin tunes oxygen sensing in wild Caenorhabditis
elegans
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 458
year: '2009'
...
---
_id: '13418'
abstract:
- lang: eng
text: In traditional photoconductors1,2,3, the impinging light generates mobile
charge carriers in the valence and/or conduction bands, causing the material’s
conductivity to increase4. Such positive photoconductance is observed in both
bulk and nanostructured5,6 photoconductors. Here we describe a class of nanoparticle-based
materials whose conductivity can either increase or decrease on irradiation with
visible light of wavelengths close to the particles’ surface plasmon resonance.
The remarkable feature of these plasmonic materials is that the sign of the conductivity
change and the nature of the electron transport between the nanoparticles depend
on the molecules comprising the self-assembled monolayers (SAMs)7,8 stabilizing
the nanoparticles. For SAMs made of electrically neutral (polar and non-polar)
molecules, conductivity increases on irradiation. If, however, the SAMs contain
electrically charged (either negatively or positively) groups, conductivity decreases.
The optical and electrical characteristics of these previously undescribed inverse
photoconductors can be engineered flexibly by adjusting the material properties
of the nanoparticles and of the coating SAMs. In particular, in films comprising
mixtures of different nanoparticles or nanoparticles coated with mixed SAMs, the
overall photoconductance is a weighted average of the changes induced by the individual
components. These and other observations can be rationalized in terms of light-induced
creation of mobile charge carriers whose transport through the charged SAMs is
inhibited by carrier trapping in transient polaron-like states9,10. The nanoparticle-based
photoconductors we describe could have uses in chemical sensors and/or in conjunction
with flexible substrates.
article_processing_charge: No
article_type: original
author:
- first_name: Hideyuki
full_name: Nakanishi, Hideyuki
last_name: Nakanishi
- first_name: Kyle J. M.
full_name: Bishop, Kyle J. M.
last_name: Bishop
- first_name: Bartlomiej
full_name: Kowalczyk, Bartlomiej
last_name: Kowalczyk
- first_name: Abraham
full_name: Nitzan, Abraham
last_name: Nitzan
- first_name: Emily A.
full_name: Weiss, Emily A.
last_name: Weiss
- first_name: Konstantin V.
full_name: Tretiakov, Konstantin V.
last_name: Tretiakov
- first_name: Mario M.
full_name: Apodaca, Mario M.
last_name: Apodaca
- first_name: Rafal
full_name: Klajn, Rafal
id: 8e84690e-1e48-11ed-a02b-a1e6fb8bb53b
last_name: Klajn
- first_name: J. Fraser
full_name: Stoddart, J. Fraser
last_name: Stoddart
- first_name: Bartosz A.
full_name: Grzybowski, Bartosz A.
last_name: Grzybowski
citation:
ama: Nakanishi H, Bishop KJM, Kowalczyk B, et al. Photoconductance and inverse photoconductance
in films of functionalized metal nanoparticles. Nature. 2009;460(7253):371-375.
doi:10.1038/nature08131
apa: Nakanishi, H., Bishop, K. J. M., Kowalczyk, B., Nitzan, A., Weiss, E. A., Tretiakov,
K. V., … Grzybowski, B. A. (2009). Photoconductance and inverse photoconductance
in films of functionalized metal nanoparticles. Nature. Springer Nature.
https://doi.org/10.1038/nature08131
chicago: Nakanishi, Hideyuki, Kyle J. M. Bishop, Bartlomiej Kowalczyk, Abraham Nitzan,
Emily A. Weiss, Konstantin V. Tretiakov, Mario M. Apodaca, Rafal Klajn, J. Fraser
Stoddart, and Bartosz A. Grzybowski. “Photoconductance and Inverse Photoconductance
in Films of Functionalized Metal Nanoparticles.” Nature. Springer Nature,
2009. https://doi.org/10.1038/nature08131.
ieee: H. Nakanishi et al., “Photoconductance and inverse photoconductance
in films of functionalized metal nanoparticles,” Nature, vol. 460, no.
7253. Springer Nature, pp. 371–375, 2009.
ista: Nakanishi H, Bishop KJM, Kowalczyk B, Nitzan A, Weiss EA, Tretiakov KV, Apodaca
MM, Klajn R, Stoddart JF, Grzybowski BA. 2009. Photoconductance and inverse photoconductance
in films of functionalized metal nanoparticles. Nature. 460(7253), 371–375.
mla: Nakanishi, Hideyuki, et al. “Photoconductance and Inverse Photoconductance
in Films of Functionalized Metal Nanoparticles.” Nature, vol. 460, no.
7253, Springer Nature, 2009, pp. 371–75, doi:10.1038/nature08131.
short: H. Nakanishi, K.J.M. Bishop, B. Kowalczyk, A. Nitzan, E.A. Weiss, K.V. Tretiakov,
M.M. Apodaca, R. Klajn, J.F. Stoddart, B.A. Grzybowski, Nature 460 (2009) 371–375.
date_created: 2023-08-01T10:29:50Z
date_published: 2009-07-16T00:00:00Z
date_updated: 2023-08-08T09:00:59Z
day: '16'
doi: 10.1038/nature08131
extern: '1'
external_id:
pmid:
- '19606145'
intvolume: ' 460'
issue: '7253'
keyword:
- Multidisciplinary
language:
- iso: eng
month: '07'
oa_version: None
page: 371-375
pmid: 1
publication: Nature
publication_identifier:
eissn:
- 1476-4687
issn:
- 0028-0836
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Photoconductance and inverse photoconductance in films of functionalized metal
nanoparticles
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 460
year: '2009'
...
---
_id: '9457'
abstract:
- lang: eng
text: Eukaryotic chromatin is separated into functional domains differentiated by
posttranslational histone modifications, histone variants, and DNA methylation1–6.
Methylation is associated with repression of transcriptional initiation in plants
and animals, and is frequently found in transposable elements. Proper methylation
patterns are critical for eukaryotic development4,5, and aberrant methylation-induced
silencing of tumor suppressor genes is a common feature of human cancer7. In contrast
to methylation, the histone variant H2A.Z is preferentially deposited by the Swr1
ATPase complex near 5′ ends of genes where it promotes transcriptional competence8–20.
How DNA methylation and H2A.Z influence transcription remains largely unknown.
Here we show that in the plant Arabidopsis thaliana, regions of DNA methylation
are quantitatively deficient in H2A.Z. Exclusion of H2A.Z is seen at sites of
DNA methylation in the bodies of actively transcribed genes and in methylated
transposons. Mutation of the MET1 DNA methyltransferase, which causes both losses
and gains of DNA methylation4,5, engenders opposite changes in H2A.Z deposition,
while mutation of the PIE1 subunit of the Swr1 complex that deposits H2A.Z17 leads
to genome-wide hypermethylation. Our findings indicate that DNA methylation can
influence chromatin structure and effect gene silencing by excluding H2A.Z, and
that H2A.Z protects genes from DNA methylation.
article_processing_charge: No
article_type: letter_note
author:
- first_name: Daniel
full_name: Zilberman, Daniel
id: 6973db13-dd5f-11ea-814e-b3e5455e9ed1
last_name: Zilberman
orcid: 0000-0002-0123-8649
- first_name: Devin
full_name: Coleman-Derr, Devin
last_name: Coleman-Derr
- first_name: Tracy
full_name: Ballinger, Tracy
last_name: Ballinger
- first_name: Steven
full_name: Henikoff, Steven
last_name: Henikoff
citation:
ama: Zilberman D, Coleman-Derr D, Ballinger T, Henikoff S. Histone H2A.Z and DNA
methylation are mutually antagonistic chromatin marks. Nature. 2008;456(7218):125-129.
doi:10.1038/nature07324
apa: Zilberman, D., Coleman-Derr, D., Ballinger, T., & Henikoff, S. (2008).
Histone H2A.Z and DNA methylation are mutually antagonistic chromatin marks. Nature.
Springer Nature. https://doi.org/10.1038/nature07324
chicago: Zilberman, Daniel, Devin Coleman-Derr, Tracy Ballinger, and Steven Henikoff.
“Histone H2A.Z and DNA Methylation Are Mutually Antagonistic Chromatin Marks.”
Nature. Springer Nature, 2008. https://doi.org/10.1038/nature07324.
ieee: D. Zilberman, D. Coleman-Derr, T. Ballinger, and S. Henikoff, “Histone H2A.Z
and DNA methylation are mutually antagonistic chromatin marks,” Nature,
vol. 456, no. 7218. Springer Nature, pp. 125–129, 2008.
ista: Zilberman D, Coleman-Derr D, Ballinger T, Henikoff S. 2008. Histone H2A.Z
and DNA methylation are mutually antagonistic chromatin marks. Nature. 456(7218),
125–129.
mla: Zilberman, Daniel, et al. “Histone H2A.Z and DNA Methylation Are Mutually Antagonistic
Chromatin Marks.” Nature, vol. 456, no. 7218, Springer Nature, 2008, pp.
125–29, doi:10.1038/nature07324.
short: D. Zilberman, D. Coleman-Derr, T. Ballinger, S. Henikoff, Nature 456 (2008)
125–129.
date_created: 2021-06-04T11:49:32Z
date_published: 2008-11-06T00:00:00Z
date_updated: 2021-12-14T08:54:36Z
day: '06'
department:
- _id: DaZi
doi: 10.1038/nature07324
extern: '1'
external_id:
pmid:
- '18815594'
intvolume: ' 456'
issue: '7218'
keyword:
- Multidisciplinary
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2877514/
month: '11'
oa: 1
oa_version: Submitted Version
page: 125-129
pmid: 1
publication: Nature
publication_identifier:
eissn:
- 1476-4687
issn:
- 0028-0836
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Histone H2A.Z and DNA methylation are mutually antagonistic chromatin marks
type: journal_article
user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9
volume: 456
year: '2008'
...
---
_id: '11121'
abstract:
- lang: eng
text: In metazoa, the nuclear envelope breaks down and reforms during each cell
cycle. Nuclear pore complexes (NPCs), which serve as channels for transport between
the nucleus and cytoplasm1, assemble into the reforming nuclear envelope in a
sequential process involving association of a subset of NPC proteins, nucleoporins,
with chromatin followed by the formation of a closed nuclear envelope fenestrated
by NPCs2,3,4,5,6,7. How chromatin recruitment of nucleoporins and NPC assembly
are regulated is unknown. Here we demonstrate that RanGTP production is required
to dissociate nucleoporins Nup107, Nup153 and Nup358 from Importin β, to target
them to chromatin and to induce association between separate NPC subcomplexes.
Additionally, either an excess of RanGTP or removal of Importin β induces formation
of NPC-containing membrane structures—annulate lamellae—both in vitro in the absence
of chromatin and in vivo. Annulate lamellae formation is strongly and specifically
inhibited by an excess of Importin β. The data demonstrate that RanGTP triggers
distinct steps of NPC assembly, and suggest a mechanism for the spatial restriction
of NPC assembly to the surface of chromatin.
article_processing_charge: No
article_type: original
author:
- first_name: Tobias C.
full_name: Walther, Tobias C.
last_name: Walther
- first_name: Peter
full_name: Askjaer, Peter
last_name: Askjaer
- first_name: Marc
full_name: Gentzel, Marc
last_name: Gentzel
- first_name: Anja
full_name: Habermann, Anja
last_name: Habermann
- first_name: Gareth
full_name: Griffiths, Gareth
last_name: Griffiths
- first_name: Matthias
full_name: Wilm, Matthias
last_name: Wilm
- first_name: Iain W.
full_name: Mattaj, Iain W.
last_name: Mattaj
- first_name: Martin W
full_name: HETZER, Martin W
id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
last_name: HETZER
orcid: 0000-0002-2111-992X
citation:
ama: Walther TC, Askjaer P, Gentzel M, et al. RanGTP mediates nuclear pore complex
assembly. Nature. 2003;424(6949):689-694. doi:10.1038/nature01898
apa: Walther, T. C., Askjaer, P., Gentzel, M., Habermann, A., Griffiths, G., Wilm,
M., … Hetzer, M. (2003). RanGTP mediates nuclear pore complex assembly. Nature.
Springer Nature. https://doi.org/10.1038/nature01898
chicago: Walther, Tobias C., Peter Askjaer, Marc Gentzel, Anja Habermann, Gareth
Griffiths, Matthias Wilm, Iain W. Mattaj, and Martin Hetzer. “RanGTP Mediates
Nuclear Pore Complex Assembly.” Nature. Springer Nature, 2003. https://doi.org/10.1038/nature01898.
ieee: T. C. Walther et al., “RanGTP mediates nuclear pore complex assembly,”
Nature, vol. 424, no. 6949. Springer Nature, pp. 689–694, 2003.
ista: Walther TC, Askjaer P, Gentzel M, Habermann A, Griffiths G, Wilm M, Mattaj
IW, Hetzer M. 2003. RanGTP mediates nuclear pore complex assembly. Nature. 424(6949),
689–694.
mla: Walther, Tobias C., et al. “RanGTP Mediates Nuclear Pore Complex Assembly.”
Nature, vol. 424, no. 6949, Springer Nature, 2003, pp. 689–94, doi:10.1038/nature01898.
short: T.C. Walther, P. Askjaer, M. Gentzel, A. Habermann, G. Griffiths, M. Wilm,
I.W. Mattaj, M. Hetzer, Nature 424 (2003) 689–694.
date_created: 2022-04-07T07:57:02Z
date_published: 2003-07-30T00:00:00Z
date_updated: 2022-07-18T08:57:40Z
day: '30'
doi: 10.1038/nature01898
extern: '1'
external_id:
pmid:
- '12894213'
intvolume: ' 424'
issue: '6949'
keyword:
- Multidisciplinary
language:
- iso: eng
month: '07'
oa_version: None
page: 689-694
pmid: 1
publication: Nature
publication_identifier:
eissn:
- 1476-4687
issn:
- 0028-0836
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: RanGTP mediates nuclear pore complex assembly
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 424
year: '2003'
...
---
_id: '2986'
abstract:
- lang: eng
text: Long-standing models propose that plant growth responses to light or gravity
are mediated by asymmetric distribution of the phytohormone auxin. Physiological
studies implicated a specific transport system that relocates auxin laterally,
thereby effecting differential growth; however, neither the molecular components
of this system nor the cellular mechanism of auxin redistribution on light or
gravity perception have been identified. Here, we show that auxin accumulates
asymmetrically during differential growth in an efflux-dependent manner. Mutations
in the Arabidopsis gene PIN3, a regulator of auxin efflux, alter differential
growth. PIN3 is expressed in gravity-sensing tissues, with PIN3 protein accumulating
predominantly at the lateral cell surface. PIN3 localizes to the plasma membrane
and to vesicles that cycle in an actin-dependent manner. In the root columella,
PIN3 is positioned symmetrically at the plasma membrane but rapidly relocalizes
laterally on gravity stimulation. Our data indicate that PIN3 is a component of
the lateral auxin transport system regulating tropic growth. In addition, actin-dependent
relocalization of PIN3 in response to gravity provides a mechanism for redirecting
auxin flux to trigger asymmetric growth.
acknowledgement: We thank G. Jürgens for enabling J.F. to accomplish part of this
work in his laboratory; P. Tänzler and M. Sauer for technical assistance; H. Vahlenkamp
for technical assistance in immunocytochemistry; M. Estelle for providing material
and suggestions; T. Altman for BAC filter sets; the ADIS (Automated DNA Isolation
and Sequencing) service group for DNA sequencing; ZIGIA (Center for Functional Genomics
in Arabidopsis) for the En lines; and N. Geldner, T. Hamann, G. Jürgens, K. Schrick
and C. Schwechheimer for comments and critical reading of the manuscript. This work
was supported by a fellowship of the DAAD (J.F.), the DFG (Schwerpunktprogramm Phytohormone),
the Fonds der chemischen Industrie, the European Communities Biotechnology Programs,
the INCO-Copernicus Program and the European Space Agency MAP-Biotechnology Programme
article_processing_charge: No
article_type: original
author:
- first_name: Jirí
full_name: Friml, Jirí
id: 4159519E-F248-11E8-B48F-1D18A9856A87
last_name: Friml
orcid: 0000-0002-8302-7596
- first_name: Justyna
full_name: Wiśniewska, Justyna
last_name: Wiśniewska
- first_name: Eva
full_name: Benková, Eva
id: 38F4F166-F248-11E8-B48F-1D18A9856A87
last_name: Benková
orcid: 0000-0002-8510-9739
- first_name: Kurt
full_name: Mendgen, Kurt
last_name: Mendgen
- first_name: Klaus
full_name: Palme, Klaus
last_name: Palme
citation:
ama: Friml J, Wiśniewska J, Benková E, Mendgen K, Palme K. Lateral relocation of
auxin efflux regulator PIN3 mediates tropism in Arabidopsis. Nature. 2002;415(6873):806-809.
doi:10.1038/415806a
apa: Friml, J., Wiśniewska, J., Benková, E., Mendgen, K., & Palme, K. (2002).
Lateral relocation of auxin efflux regulator PIN3 mediates tropism in Arabidopsis.
Nature. Nature Publishing Group. https://doi.org/10.1038/415806a
chicago: Friml, Jiří, Justyna Wiśniewska, Eva Benková, Kurt Mendgen, and Klaus Palme.
“Lateral Relocation of Auxin Efflux Regulator PIN3 Mediates Tropism in Arabidopsis.”
Nature. Nature Publishing Group, 2002. https://doi.org/10.1038/415806a.
ieee: J. Friml, J. Wiśniewska, E. Benková, K. Mendgen, and K. Palme, “Lateral relocation
of auxin efflux regulator PIN3 mediates tropism in Arabidopsis,” Nature,
vol. 415, no. 6873. Nature Publishing Group, pp. 806–809, 2002.
ista: Friml J, Wiśniewska J, Benková E, Mendgen K, Palme K. 2002. Lateral relocation
of auxin efflux regulator PIN3 mediates tropism in Arabidopsis. Nature. 415(6873),
806–809.
mla: Friml, Jiří, et al. “Lateral Relocation of Auxin Efflux Regulator PIN3 Mediates
Tropism in Arabidopsis.” Nature, vol. 415, no. 6873, Nature Publishing
Group, 2002, pp. 806–09, doi:10.1038/415806a.
short: J. Friml, J. Wiśniewska, E. Benková, K. Mendgen, K. Palme, Nature 415 (2002)
806–809.
date_created: 2018-12-11T12:00:42Z
date_published: 2002-02-14T00:00:00Z
date_updated: 2023-07-18T07:30:27Z
day: '14'
doi: 10.1038/415806a
extern: '1'
external_id:
pmid:
- '11845211 '
intvolume: ' 415'
issue: '6873'
language:
- iso: eng
month: '02'
oa_version: None
page: 806 - 809
pmid: 1
publication: Nature
publication_identifier:
issn:
- 0028-0836
publication_status: published
publisher: Nature Publishing Group
publist_id: '3715'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Lateral relocation of auxin efflux regulator PIN3 mediates tropism in Arabidopsis
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 415
year: '2002'
...
---
_id: '6158'
abstract:
- lang: eng
text: Wild isolates of Caenorhabditis elegans can feed either alone or in groups1,2.
This natural variation in behaviour is associated with a single residue difference
in NPR-1, a predicted G-protein-coupled neuropeptide receptor related to Neuropeptide
Y receptors2. Here we show that the NPR-1 isoform associated with solitary feeding
acts in neurons exposed to the body fluid to inhibit social feeding. Furthermore,
suppressing the activity of these neurons, called AQR, PQR and URX, using an activated
K+ channel, inhibits social feeding. NPR-1 activity in AQR, PQR and URX neurons
seems to suppress social feeding by antagonizing signalling through a cyclic GMP-gated
ion channel encoded by tax-2 and tax-4. We show that mutations in tax-2 or tax-4
disrupt social feeding, and that tax-4 is required in several neurons for social
feeding, including one or more of AQR, PQR and URX. The AQR, PQR and URX neurons
are unusual in C. elegans because they are directly exposed to the pseudocoelomic
body fluid3. Our data suggest a model in which these neurons integrate antagonistic
signals to control the choice between social and solitary feeding behaviour.
author:
- first_name: Juliet C.
full_name: Coates, Juliet C.
last_name: Coates
- first_name: Mario
full_name: de Bono, Mario
id: 4E3FF80E-F248-11E8-B48F-1D18A9856A87
last_name: de Bono
orcid: 0000-0001-8347-0443
citation:
ama: Coates JC, de Bono M. Antagonistic pathways in neurons exposed to body fluid
regulate social feeding in Caenorhabditis elegans. Nature. 2002;419(6910):925-929.
doi:10.1038/nature01170
apa: Coates, J. C., & de Bono, M. (2002). Antagonistic pathways in neurons exposed
to body fluid regulate social feeding in Caenorhabditis elegans. Nature.
Springer Nature. https://doi.org/10.1038/nature01170
chicago: Coates, Juliet C., and Mario de Bono. “Antagonistic Pathways in Neurons
Exposed to Body Fluid Regulate Social Feeding in Caenorhabditis Elegans.” Nature.
Springer Nature, 2002. https://doi.org/10.1038/nature01170.
ieee: J. C. Coates and M. de Bono, “Antagonistic pathways in neurons exposed to
body fluid regulate social feeding in Caenorhabditis elegans,” Nature,
vol. 419, no. 6910. Springer Nature, pp. 925–929, 2002.
ista: Coates JC, de Bono M. 2002. Antagonistic pathways in neurons exposed to body
fluid regulate social feeding in Caenorhabditis elegans. Nature. 419(6910), 925–929.
mla: Coates, Juliet C., and Mario de Bono. “Antagonistic Pathways in Neurons Exposed
to Body Fluid Regulate Social Feeding in Caenorhabditis Elegans.” Nature,
vol. 419, no. 6910, Springer Nature, 2002, pp. 925–29, doi:10.1038/nature01170.
short: J.C. Coates, M. de Bono, Nature 419 (2002) 925–929.
date_created: 2019-03-21T10:09:20Z
date_published: 2002-10-31T00:00:00Z
date_updated: 2021-01-12T08:06:26Z
day: '31'
doi: 10.1038/nature01170
extern: '1'
external_id:
pmid:
- '12410311'
intvolume: ' 419'
issue: '6910'
language:
- iso: eng
month: '10'
oa_version: None
page: 925-929
pmid: 1
publication: Nature
publication_identifier:
issn:
- 0028-0836
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
status: public
title: Antagonistic pathways in neurons exposed to body fluid regulate social feeding
in Caenorhabditis elegans
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 419
year: '2002'
...
---
_id: '6159'
abstract:
- lang: eng
text: 'Natural Caenorhabditis elegans isolates exhibit either social or solitary
feeding on bacteria. We show here that social feeding is induced by nociceptive
neurons that detect adverse or stressful conditions. Ablation of the nociceptive
neurons ASH and ADL transforms social animals into solitary feeders. Social feeding
is probably due to the sensation of noxious chemicals by ASH and ADL neurons;
it requires the genes ocr-2 and osm-9, which encode TRP-related transduction channels,
and odr-4 and odr-8, which are required to localize sensory chemoreceptors to
cilia. Other sensory neurons may suppress social feeding, as social feeding in
ocr-2 and odr-4 mutants is restored by mutations in osm-3, a gene required for
the development of 26 ciliated sensory neurons. Our data suggest a model for regulation
of social feeding by opposing sensory inputs: aversive inputs to nociceptive neurons
promote social feeding, whereas antagonistic inputs from neurons that express
osm-3 inhibit aggregation.'
author:
- first_name: Mario
full_name: de Bono, Mario
id: 4E3FF80E-F248-11E8-B48F-1D18A9856A87
last_name: de Bono
orcid: 0000-0001-8347-0443
- first_name: David M.
full_name: Tobin, David M.
last_name: Tobin
- first_name: M. Wayne
full_name: Davis, M. Wayne
last_name: Davis
- first_name: Leon
full_name: Avery, Leon
last_name: Avery
- first_name: Cornelia I.
full_name: Bargmann, Cornelia I.
last_name: Bargmann
citation:
ama: de Bono M, Tobin DM, Davis MW, Avery L, Bargmann CI. Social feeding in Caenorhabditis
elegans is induced by neurons that detect aversive stimuli. Nature. 2002;419(6910):899-903.
doi:10.1038/nature01169
apa: de Bono, M., Tobin, D. M., Davis, M. W., Avery, L., & Bargmann, C. I. (2002).
Social feeding in Caenorhabditis elegans is induced by neurons that detect aversive
stimuli. Nature. Springer Nature. https://doi.org/10.1038/nature01169
chicago: Bono, Mario de, David M. Tobin, M. Wayne Davis, Leon Avery, and Cornelia
I. Bargmann. “Social Feeding in Caenorhabditis Elegans Is Induced by Neurons That
Detect Aversive Stimuli.” Nature. Springer Nature, 2002. https://doi.org/10.1038/nature01169.
ieee: M. de Bono, D. M. Tobin, M. W. Davis, L. Avery, and C. I. Bargmann, “Social
feeding in Caenorhabditis elegans is induced by neurons that detect aversive stimuli,”
Nature, vol. 419, no. 6910. Springer Nature, pp. 899–903, 2002.
ista: de Bono M, Tobin DM, Davis MW, Avery L, Bargmann CI. 2002. Social feeding
in Caenorhabditis elegans is induced by neurons that detect aversive stimuli.
Nature. 419(6910), 899–903.
mla: de Bono, Mario, et al. “Social Feeding in Caenorhabditis Elegans Is Induced
by Neurons That Detect Aversive Stimuli.” Nature, vol. 419, no. 6910, Springer
Nature, 2002, pp. 899–903, doi:10.1038/nature01169.
short: M. de Bono, D.M. Tobin, M.W. Davis, L. Avery, C.I. Bargmann, Nature 419 (2002)
899–903.
date_created: 2019-03-21T10:27:04Z
date_published: 2002-10-31T00:00:00Z
date_updated: 2021-01-12T08:06:27Z
day: '31'
doi: 10.1038/nature01169
extern: '1'
external_id:
pmid:
- '12410303'
intvolume: ' 419'
issue: '6910'
language:
- iso: eng
month: '10'
oa_version: None
page: 899-903
pmid: 1
publication: Nature
publication_identifier:
issn:
- 0028-0836
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
status: public
title: Social feeding in Caenorhabditis elegans is induced by neurons that detect
aversive stimuli
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 419
year: '2002'
...
---
_id: '3925'
abstract:
- lang: eng
text: Males of the tropical ant Cardiocondyla obscurior are either wingless and
aggressive or winged and docile, and both compete for access to virgin queens
in the nest1, 2. Although the fighter males (ergatoids) attack and kill other
ergatoids, they tolerate and even attempt to mate with their winged rivals. Here
we show that the winged males avoid the aggression of wingless males by mimicking
the chemical bouquet of virgin queens, but that their mating success is not reduced
as a result. This example of female mimicry by vigorous males is surprising, as
in other species it is typically used as a protective strategy by weaker males,
and may explain the coexistence and equal mating success of two male morphs.
article_processing_charge: No
article_type: original
author:
- first_name: Sylvia
full_name: Cremer, Sylvia
id: 2F64EC8C-F248-11E8-B48F-1D18A9856A87
last_name: Cremer
orcid: 0000-0002-2193-3868
- first_name: Matthew
full_name: Sledge, Matthew
last_name: Sledge
- first_name: Jürgen
full_name: Heinze, Jürgen
last_name: Heinze
citation:
ama: 'Cremer S, Sledge M, Heinze J. Chemical mimicry: Male ants disguised by the
queen’s bouquet. Nature. 2002;419:897-897. doi:10.1038/419897a'
apa: 'Cremer, S., Sledge, M., & Heinze, J. (2002). Chemical mimicry: Male ants
disguised by the queen’s bouquet. Nature. Nature Publishing Group. https://doi.org/10.1038/419897a'
chicago: 'Cremer, Sylvia, Matthew Sledge, and Jürgen Heinze. “Chemical Mimicry:
Male Ants Disguised by the Queen’s Bouquet.” Nature. Nature Publishing
Group, 2002. https://doi.org/10.1038/419897a.'
ieee: 'S. Cremer, M. Sledge, and J. Heinze, “Chemical mimicry: Male ants disguised
by the queen’s bouquet,” Nature, vol. 419. Nature Publishing Group, pp.
897–897, 2002.'
ista: 'Cremer S, Sledge M, Heinze J. 2002. Chemical mimicry: Male ants disguised
by the queen’s bouquet. Nature. 419, 897–897.'
mla: 'Cremer, Sylvia, et al. “Chemical Mimicry: Male Ants Disguised by the Queen’s
Bouquet.” Nature, vol. 419, Nature Publishing Group, 2002, pp. 897–897,
doi:10.1038/419897a.'
short: S. Cremer, M. Sledge, J. Heinze, Nature 419 (2002) 897–897.
date_created: 2018-12-11T12:05:55Z
date_published: 2002-10-31T00:00:00Z
date_updated: 2023-06-13T11:47:19Z
day: '31'
doi: 10.1038/419897a
extern: '1'
external_id:
pmid:
- '12410300'
intvolume: ' 419'
language:
- iso: eng
month: '10'
oa_version: None
page: 897 - 897
pmid: 1
publication: Nature
publication_identifier:
issn:
- 0028-0836
publication_status: published
publisher: Nature Publishing Group
publist_id: '2230'
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Chemical mimicry: Male ants disguised by the queen''s bouquet'
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 419
year: '2002'
...
---
_id: '2983'
abstract:
- lang: eng
text: Polar transport of the phytohormone auxin mediates various processes in plant
growth and development, such as apical dominance, tropisms, vascular patterning
and axis formation. This view is based largely on the effects of polar auxin transport
inhibitors. These compounds disrupt auxin efflux from the cell but their mode
of action is unknown. It is thought that polar auxin flux is caused by the asymmetric
distribution of efflux carriers acting at the plasma membrane. The polar localization
of efflux carrier candidate PIN1 supports this model. Here we show that the seemingly
static localization of PIN1 results from rapid actin-dependent cycling between
the plasma membrane and endosomal compartments. Auxin transport inhibitors block
PIN1 cycling and inhibit trafficking of membrane proteins that are unrelated to
auxin transport. Our data suggest that PIN1 cycling is of central importance for
auxin transport and that auxin transport inhibitors affect efflux by generally
interfering with membrane-trafficking processes. In support of our conclusion,
the vesicle-trafficking inhibitor brefeldin A mimics physiological effects of
auxin transport inhibitors.
article_processing_charge: No
article_type: letter_note
author:
- first_name: Niko
full_name: Geldner, Niko
last_name: Geldner
- first_name: Jirí
full_name: Friml, Jirí
id: 4159519E-F248-11E8-B48F-1D18A9856A87
last_name: Friml
orcid: 0000-0002-8302-7596
- first_name: York
full_name: Stierhof, York
last_name: Stierhof
- first_name: Gerd
full_name: Jürgens, Gerd
last_name: Jürgens
- first_name: Klaus
full_name: Palme, Klaus
last_name: Palme
citation:
ama: Geldner N, Friml J, Stierhof Y, Jürgens G, Palme K. Auxin transport inhibitors
block PIN1 cycling and vesicle trafficking. Nature. 2001;413(6854):425-428.
doi:10.1038/35096571
apa: Geldner, N., Friml, J., Stierhof, Y., Jürgens, G., & Palme, K. (2001).
Auxin transport inhibitors block PIN1 cycling and vesicle trafficking. Nature.
Nature Publishing Group. https://doi.org/10.1038/35096571
chicago: Geldner, Niko, Jiří Friml, York Stierhof, Gerd Jürgens, and Klaus Palme.
“Auxin Transport Inhibitors Block PIN1 Cycling and Vesicle Trafficking.” Nature.
Nature Publishing Group, 2001. https://doi.org/10.1038/35096571.
ieee: N. Geldner, J. Friml, Y. Stierhof, G. Jürgens, and K. Palme, “Auxin transport
inhibitors block PIN1 cycling and vesicle trafficking,” Nature, vol. 413,
no. 6854. Nature Publishing Group, pp. 425–428, 2001.
ista: Geldner N, Friml J, Stierhof Y, Jürgens G, Palme K. 2001. Auxin transport
inhibitors block PIN1 cycling and vesicle trafficking. Nature. 413(6854), 425–428.
mla: Geldner, Niko, et al. “Auxin Transport Inhibitors Block PIN1 Cycling and Vesicle
Trafficking.” Nature, vol. 413, no. 6854, Nature Publishing Group, 2001,
pp. 425–28, doi:10.1038/35096571.
short: N. Geldner, J. Friml, Y. Stierhof, G. Jürgens, K. Palme, Nature 413 (2001)
425–428.
date_created: 2018-12-11T12:00:41Z
date_published: 2001-09-27T00:00:00Z
date_updated: 2023-05-16T11:51:44Z
day: '27'
doi: 10.1038/35096571
extern: '1'
external_id:
pmid:
- '11574889'
intvolume: ' 413'
issue: '6854'
language:
- iso: eng
month: '09'
oa_version: None
page: 425 - 428
pmid: 1
publication: Nature
publication_identifier:
issn:
- 0028-0836
publication_status: published
publisher: Nature Publishing Group
publist_id: '3719'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Auxin transport inhibitors block PIN1 cycling and vesicle trafficking
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 413
year: '2001'
...
---
_id: '4197'
abstract:
- lang: eng
text: Vertebrate gastrulation involves the specification and coordinated movement
of large populations of cells that give rise to the ectodermal, mesodermal and
endodermal germ layers. Although many of the genes involved in the specification
of cell identity during this process have been identified, little is known of
the genes that coordinate cell movement. Here we show that the zebrafish silberblick
(slb) locus(1) encodes Wnt11 and that Slb/Wnt11 activity is required for cells
to undergo correct convergent extension movements during gastrulation. In the
absence of Slb/Wnt11 function, abnormal extension of axial tissue results in cyclopia
and other midline defects in the head(2). The requirement for Slb/Wnt11 is cell
non-autonomous, and our results indicate that the correct extension of axial tissue
is at least partly dependent on medio-lateral cell intercalation in paraxial tissue.
We also show that the slb phenotype is rescued by a truncated form of Dishevelled
that does not signal through the canonical Wnt pathway(3), suggesting that, as
in flies(4), Wnt signalling might mediate morphogenetic events through a divergent
signal transduction cascade. Our results provide genetic and experimental evidence
that Wnt activity in lateral tissues has a crucial role in driving the convergent
extension movements underlying vertebrate gastrulation.
article_processing_charge: No
article_type: original
author:
- 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
- first_name: Masazumi
full_name: Tada, Masazumi
last_name: Tada
- first_name: Gerd
full_name: Rauch, Gerd
last_name: Rauch
- first_name: Leonor
full_name: Saúde, Leonor
last_name: Saúde
- first_name: Miguel
full_name: Concha, Miguel
last_name: Concha
- first_name: Robert
full_name: Geisler, Robert
last_name: Geisler
- first_name: Derek
full_name: Stemple, Derek
last_name: Stemple
- first_name: James
full_name: Smith, James
last_name: Smith
- first_name: Stephen
full_name: Wilson, Stephen
last_name: Wilson
citation:
ama: Heisenberg C-PJ, Tada M, Rauch G, et al. Silberblick/Wnt11 mediates convergent
extension movements during zebrafish gastrulation. Nature. 2000;405(6782):76-81.
doi:10.1038/35011068
apa: Heisenberg, C.-P. J., Tada, M., Rauch, G., Saúde, L., Concha, M., Geisler,
R., … Wilson, S. (2000). Silberblick/Wnt11 mediates convergent extension movements
during zebrafish gastrulation. Nature. Nature Publishing Group. https://doi.org/10.1038/35011068
chicago: Heisenberg, Carl-Philipp J, Masazumi Tada, Gerd Rauch, Leonor Saúde, Miguel
Concha, Robert Geisler, Derek Stemple, James Smith, and Stephen Wilson. “Silberblick/Wnt11
Mediates Convergent Extension Movements during Zebrafish Gastrulation.” Nature.
Nature Publishing Group, 2000. https://doi.org/10.1038/35011068.
ieee: C.-P. J. Heisenberg et al., “Silberblick/Wnt11 mediates convergent
extension movements during zebrafish gastrulation,” Nature, vol. 405, no.
6782. Nature Publishing Group, pp. 76–81, 2000.
ista: Heisenberg C-PJ, Tada M, Rauch G, Saúde L, Concha M, Geisler R, Stemple D,
Smith J, Wilson S. 2000. Silberblick/Wnt11 mediates convergent extension movements
during zebrafish gastrulation. Nature. 405(6782), 76–81.
mla: Heisenberg, Carl-Philipp J., et al. “Silberblick/Wnt11 Mediates Convergent
Extension Movements during Zebrafish Gastrulation.” Nature, vol. 405, no.
6782, Nature Publishing Group, 2000, pp. 76–81, doi:10.1038/35011068.
short: C.-P.J. Heisenberg, M. Tada, G. Rauch, L. Saúde, M. Concha, R. Geisler, D.
Stemple, J. Smith, S. Wilson, Nature 405 (2000) 76–81.
date_created: 2018-12-11T12:07:32Z
date_published: 2000-05-04T00:00:00Z
date_updated: 2023-04-19T14:40:45Z
day: '04'
doi: 10.1038/35011068
extern: '1'
external_id:
pmid:
- '10811221 '
intvolume: ' 405'
issue: '6782'
language:
- iso: eng
month: '05'
oa_version: None
page: 76 - 81
pmid: 1
publication: Nature
publication_identifier:
issn:
- 0028-0836
publication_status: published
publisher: Nature Publishing Group
publist_id: '1921'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Silberblick/Wnt11 mediates convergent extension movements during zebrafish
gastrulation
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 405
year: '2000'
...
---
_id: '4268'
article_processing_charge: No
author:
- first_name: Linda
full_name: Partridge, Linda
last_name: Partridge
- first_name: Nicholas H
full_name: Barton, Nicholas H
id: 4880FE40-F248-11E8-B48F-1D18A9856A87
last_name: Barton
orcid: 0000-0002-8548-5240
citation:
ama: Partridge L, Barton NH. Evolving evolvability. Nature. 2000;407(6803):457-458.
doi:10.1038/35035173
apa: Partridge, L., & Barton, N. H. (2000). Evolving evolvability. Nature.
Nature Publishing Group. https://doi.org/10.1038/35035173
chicago: Partridge, Linda, and Nicholas H Barton. “Evolving Evolvability.” Nature.
Nature Publishing Group, 2000. https://doi.org/10.1038/35035173.
ieee: L. Partridge and N. H. Barton, “Evolving evolvability,” Nature, vol.
407, no. 6803. Nature Publishing Group, pp. 457–458, 2000.
ista: Partridge L, Barton NH. 2000. Evolving evolvability. Nature. 407(6803), 457–458.
mla: Partridge, Linda, and Nicholas H. Barton. “Evolving Evolvability.” Nature,
vol. 407, no. 6803, Nature Publishing Group, 2000, pp. 457–58, doi:10.1038/35035173.
short: L. Partridge, N.H. Barton, Nature 407 (2000) 457–458.
date_created: 2018-12-11T12:07:57Z
date_published: 2000-09-01T00:00:00Z
date_updated: 2023-04-19T14:37:19Z
day: '01'
doi: 10.1038/35035173
extern: '1'
intvolume: ' 407'
issue: '6803'
language:
- iso: eng
month: '09'
oa_version: None
page: 457 - 458
publication: Nature
publication_identifier:
issn:
- 0028-0836
publication_status: published
publisher: Nature Publishing Group
publist_id: '1823'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Evolving evolvability
type: review
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 407
year: '2000'
...
---
_id: '883'
abstract:
- lang: eng
text: Sympatric speciation, the origin of two or more species from a single local
population, has almost certainly been involved in formation of several species
flocks, and may be fairly common in nature. The most straightforward scenario
for sympatric speciation requires disruptive selection favouring two substantially
different phenotypes, and consists of the evolution of reproductive isolation
between them followed by the elimination of all intermediate phenotypes. Here
we use the hypergeometric phenotypic model to show that sympatric speciation is
possible even when fitness and mate choice depend on different quantitative traits,
so that speciation must involve formation of covariance between these traits.
The increase in the number of variable loci affecting fitness facilitates sympatric
speciation, whereas the increase in the number of variable loci affecting mate
choice has the opposite effect. These predictions may enable more cases of sympatric
speciation to be identified.
acknowledgement: This study was supported by a grant from the NSF.
article_processing_charge: No
article_type: original
author:
- first_name: Alexey
full_name: Kondrashov, Alexey
last_name: Kondrashov
- first_name: Fyodor
full_name: Kondrashov, Fyodor
id: 44FDEF62-F248-11E8-B48F-1D18A9856A87
last_name: Kondrashov
orcid: 0000-0001-8243-4694
citation:
ama: Kondrashov A, Kondrashov F. Interactions among quantitative traits in the course
of sympatric speciation. Nature. 1999;400(6742):351-354. doi:10.1038/22514
apa: Kondrashov, A., & Kondrashov, F. (1999). Interactions among quantitative
traits in the course of sympatric speciation. Nature. Nature Publishing
Group. https://doi.org/10.1038/22514
chicago: Kondrashov, Alexey, and Fyodor Kondrashov. “Interactions among Quantitative
Traits in the Course of Sympatric Speciation.” Nature. Nature Publishing
Group, 1999. https://doi.org/10.1038/22514.
ieee: A. Kondrashov and F. Kondrashov, “Interactions among quantitative traits in
the course of sympatric speciation,” Nature, vol. 400, no. 6742. Nature
Publishing Group, pp. 351–354, 1999.
ista: Kondrashov A, Kondrashov F. 1999. Interactions among quantitative traits in
the course of sympatric speciation. Nature. 400(6742), 351–354.
mla: Kondrashov, Alexey, and Fyodor Kondrashov. “Interactions among Quantitative
Traits in the Course of Sympatric Speciation.” Nature, vol. 400, no. 6742,
Nature Publishing Group, 1999, pp. 351–54, doi:10.1038/22514.
short: A. Kondrashov, F. Kondrashov, Nature 400 (1999) 351–354.
date_created: 2018-12-11T11:49:00Z
date_published: 1999-07-01T00:00:00Z
date_updated: 2023-04-13T10:33:44Z
day: '01'
doi: 10.1038/22514
extern: '1'
external_id:
pmid:
- '10432111'
intvolume: ' 400'
issue: '6742'
language:
- iso: eng
month: '07'
oa_version: None
page: 351 - 354
pmid: 1
publication: Nature
publication_identifier:
issn:
- 0028-0836
publication_status: published
publisher: Nature Publishing Group
publist_id: '6761'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Interactions among quantitative traits in the course of sympatric speciation
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 400
year: '1999'
...
---
_id: '2588'
abstract:
- lang: eng
text: "B-type receptors for the neurotransmitter GABA (γ-aminobutyric acid) inhibit
neuronal activity through G-protein-coupled second-messenger systems, which regulate
the release of neurotransmitters and the activity of ion channels and adenylyl
cyclase. Physiological and biochemical studies show that there are differences
in drug efficiencies at different GABA(B) receptors, so it is expected that GABA(B)-receptor
(GABA(B)R) subtypes exist. Two GABA(B)-receptor splice variants have been cloned
(GABA(B)R1a and GABA(B)R1b), but native GABA(B) receptors and recombinant receptors
showed unexplained differences in agonist-binding potencies. Moreover, the activation
of presumed effector ion channels in heterologous cells expressing the recombinant
receptors proved difficult. Here we describe a new GABA(B) receptor subtype, GABA(B)R2,
which does not bind available GABA(B) antagonists with measurable potency. GABA(B)R1a,
GABA(B)R1b and GABA(B)R2 alone do not activate Kir3-type potassium channels efficiently,
but co- expression of these receptors yields a robust coupling to activation of
Kir3 channels. We provide evidence for the assembly of heteromeric GABA(B) receptors
in vivo and show that GABA(B)R2 and GABA(B)R1a/b proteins immunoprecipitate and
localize together at dendritic spines. The heteromeric receptor complexes exhibit
a significant increase in agonist- and partial- agonist-binding potencies as compared
with individual receptors and probably represent the predominant native GABA(B)
receptor. Heteromeric assembly among G-protein-coupled receptors has not, to our
knowledge, been described before.\r\n"
acknowledgement: We thank D. Ristig, A. Begrich, I. Meigel and S. Leonhard for technical
assistance.
article_processing_charge: No
article_type: original
author:
- first_name: Klemens
full_name: Kaupmann, Klemens
last_name: Kaupmann
- first_name: Barbara
full_name: Malitschek, Barbara
last_name: Malitschek
- first_name: Valérie
full_name: Schuler, Valérie
last_name: Schuler
- first_name: Jacob
full_name: Heid, Jacob
last_name: Heid
- first_name: Wolfgang
full_name: Froestl, Wolfgang
last_name: Froestl
- first_name: Pascal
full_name: Beck, Pascal
last_name: Beck
- first_name: Johannes
full_name: Mosbacher, Johannes
last_name: Mosbacher
- first_name: Serge
full_name: Bischoff, Serge
last_name: Bischoff
- first_name: Ákos
full_name: Kulik, Ákos
last_name: Kulik
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Andreas
full_name: Karschin, Andreas
last_name: Karschin
- first_name: Bernhard
full_name: Bettler, Bernhard
last_name: Bettler
citation:
ama: Kaupmann K, Malitschek B, Schuler V, et al. GABA(B)-receptor subtypes assemble
into functional heteromeric complexes. Nature. 1998;396(6712):683-687.
doi:10.1038/25360
apa: Kaupmann, K., Malitschek, B., Schuler, V., Heid, J., Froestl, W., Beck, P.,
… Bettler, B. (1998). GABA(B)-receptor subtypes assemble into functional heteromeric
complexes. Nature. Nature Publishing Group. https://doi.org/10.1038/25360
chicago: Kaupmann, Klemens, Barbara Malitschek, Valérie Schuler, Jacob Heid, Wolfgang
Froestl, Pascal Beck, Johannes Mosbacher, et al. “ GABA(B)-Receptor Subtypes Assemble
into Functional Heteromeric Complexes.” Nature. Nature Publishing Group,
1998. https://doi.org/10.1038/25360.
ieee: K. Kaupmann et al., “ GABA(B)-receptor subtypes assemble into functional
heteromeric complexes,” Nature, vol. 396, no. 6712. Nature Publishing Group,
pp. 683–687, 1998.
ista: Kaupmann K, Malitschek B, Schuler V, Heid J, Froestl W, Beck P, Mosbacher
J, Bischoff S, Kulik Á, Shigemoto R, Karschin A, Bettler B. 1998. GABA(B)-receptor
subtypes assemble into functional heteromeric complexes. Nature. 396(6712), 683–687.
mla: Kaupmann, Klemens, et al. “ GABA(B)-Receptor Subtypes Assemble into Functional
Heteromeric Complexes.” Nature, vol. 396, no. 6712, Nature Publishing Group,
1998, pp. 683–87, doi:10.1038/25360.
short: K. Kaupmann, B. Malitschek, V. Schuler, J. Heid, W. Froestl, P. Beck, J.
Mosbacher, S. Bischoff, Á. Kulik, R. Shigemoto, A. Karschin, B. Bettler, Nature
396 (1998) 683–687.
date_created: 2018-12-11T11:58:32Z
date_published: 1998-12-17T00:00:00Z
date_updated: 2022-08-31T12:43:05Z
day: '17'
doi: 10.1038/25360
extern: '1'
external_id:
pmid:
- '9872317'
intvolume: ' 396'
issue: '6712'
language:
- iso: eng
month: '12'
oa_version: None
page: 683 - 687
pmid: 1
publication: Nature
publication_identifier:
issn:
- 0028-0836
publication_status: published
publisher: Nature Publishing Group
publist_id: '4309'
quality_controlled: '1'
scopus_import: '1'
status: public
title: ' GABA(B)-receptor subtypes assemble into functional heteromeric complexes'
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 396
year: '1998'
...