---
_id: '15048'
abstract:
- lang: eng
text: Embryogenesis results from the coordinated activities of different signaling
pathways controlling cell fate specification and morphogenesis. In vertebrate
gastrulation, both Nodal and BMP signaling play key roles in germ layer specification
and morphogenesis, yet their interplay to coordinate embryo patterning with morphogenesis
is still insufficiently understood. Here, we took a reductionist approach using
zebrafish embryonic explants to study the coordination of Nodal and BMP signaling
for embryo patterning and morphogenesis. We show that Nodal signaling triggers
explant elongation by inducing mesendodermal progenitors but also suppressing
BMP signaling activity at the site of mesendoderm induction. Consistent with this,
ectopic BMP signaling in the mesendoderm blocks cell alignment and oriented mesendoderm
intercalations, key processes during explant elongation. Translating these ex
vivo observations to the intact embryo showed that, similar to explants, Nodal
signaling suppresses the effect of BMP signaling on cell intercalations in the
dorsal domain, thus allowing robust embryonic axis elongation. These findings
suggest a dual function of Nodal signaling in embryonic axis elongation by both
inducing mesendoderm and suppressing BMP effects in the dorsal portion of the
mesendoderm.
acknowledged_ssus:
- _id: Bio
- _id: LifeSc
acknowledgement: "We thank Patrick Müller for sharing the chordintt250 mutant zebrafish
line as well as the plasmid for chrd-GFP, Katherine Rogers for sharing the bmp2b
plasmid and Andrea Pauli for sharing the draculin plasmid. Diana Pinheiro generated
the MZlefty1,2;Tg(sebox::EGFP) line. We are grateful to Patrick Müller, Diana Pinheiro
and Katherine Rogers and members of the Heisenberg lab for discussions, technical
advice and feedback on the manuscript. We also thank Anna Kicheva and Edouard Hannezo
for discussions. We thank the Imaging and Optics Facility as well as the Life Science
facility at IST Austria for support with microscopy and fish maintenance.\r\nThis
work was supported by a European Research Council Advanced Grant\r\n(MECSPEC 742573
to C.-P.H.). A.S. is a recipient of a DOC Fellowship of the Austrian\r\nAcademy
of Sciences at IST Austria. Open Access funding provided by Institute of\r\nScience
and Technology Austria. "
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: Kornelija
full_name: Pranjic-Ferscha, Kornelija
id: 4362B3C2-F248-11E8-B48F-1D18A9856A87
last_name: Pranjic-Ferscha
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- 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, Pranjic-Ferscha K, Hauschild R, Heisenberg C-PJ. Robust axis elongation
by Nodal-dependent restriction of BMP signaling. Development. 2024;151(4):1-18.
doi:10.1242/dev.202316
apa: Schauer, A., Pranjic-Ferscha, K., Hauschild, R., & Heisenberg, C.-P. J.
(2024). Robust axis elongation by Nodal-dependent restriction of BMP signaling.
Development. The Company of Biologists. https://doi.org/10.1242/dev.202316
chicago: Schauer, Alexandra, Kornelija Pranjic-Ferscha, Robert Hauschild, and Carl-Philipp
J Heisenberg. “Robust Axis Elongation by Nodal-Dependent Restriction of BMP Signaling.”
Development. The Company of Biologists, 2024. https://doi.org/10.1242/dev.202316.
ieee: A. Schauer, K. Pranjic-Ferscha, R. Hauschild, and C.-P. J. Heisenberg, “Robust
axis elongation by Nodal-dependent restriction of BMP signaling,” Development,
vol. 151, no. 4. The Company of Biologists, pp. 1–18, 2024.
ista: Schauer A, Pranjic-Ferscha K, Hauschild R, Heisenberg C-PJ. 2024. Robust axis
elongation by Nodal-dependent restriction of BMP signaling. Development. 151(4),
1–18.
mla: Schauer, Alexandra, et al. “Robust Axis Elongation by Nodal-Dependent Restriction
of BMP Signaling.” Development, vol. 151, no. 4, The Company of Biologists,
2024, pp. 1–18, doi:10.1242/dev.202316.
short: A. Schauer, K. Pranjic-Ferscha, R. Hauschild, C.-P.J. Heisenberg, Development
151 (2024) 1–18.
date_created: 2024-03-03T23:00:50Z
date_published: 2024-02-01T00:00:00Z
date_updated: 2024-03-04T07:28:25Z
day: '01'
ddc:
- '570'
department:
- _id: CaHe
- _id: Bio
doi: 10.1242/dev.202316
ec_funded: 1
file:
- access_level: open_access
checksum: 6961ea10012bf0d266681f9628bb8f13
content_type: application/pdf
creator: dernst
date_created: 2024-03-04T07:24:43Z
date_updated: 2024-03-04T07:24:43Z
file_id: '15050'
file_name: 2024_Development_Schauer.pdf
file_size: 14839986
relation: main_file
success: 1
file_date_updated: 2024-03-04T07:24:43Z
has_accepted_license: '1'
intvolume: ' 151'
issue: '4'
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
page: 1-18
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: Development
publication_identifier:
eissn:
- 1477-9129
issn:
- 0950-1991
publication_status: published
publisher: The Company of Biologists
quality_controlled: '1'
related_material:
record:
- id: '14926'
relation: research_data
status: public
scopus_import: '1'
status: public
title: Robust axis elongation by Nodal-dependent restriction of BMP signaling
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: 151
year: '2024'
...
---
_id: '14774'
abstract:
- lang: eng
text: Morphogen gradients impart positional information to cells in a homogenous
tissue field. Fgf8a, a highly conserved growth factor, has been proposed to act
as a morphogen during zebrafish gastrulation. However, technical limitations have
so far prevented direct visualization of the endogenous Fgf8a gradient and confirmation
of its morphogenic activity. Here, we monitor Fgf8a propagation in the developing
neural plate using a CRISPR/Cas9-mediated EGFP knock-in at the endogenous fgf8a
locus. By combining sensitive imaging with single-molecule fluorescence correlation
spectroscopy, we demonstrate that Fgf8a, which is produced at the embryonic margin,
propagates by diffusion through the extracellular space and forms a graded distribution
towards the animal pole. Overlaying the Fgf8a gradient curve with expression profiles
of its downstream targets determines the precise input-output relationship of
Fgf8a-mediated patterning. Manipulation of the extracellular Fgf8a levels alters
the signaling outcome, thus establishing Fgf8a as a bona fide morphogen during
zebrafish gastrulation. Furthermore, by hindering Fgf8a diffusion, we demonstrate
that extracellular diffusion of the protein from the source is crucial for it
to achieve its morphogenic potential.
acknowledgement: "We thank members of the Brand lab, as well as Justina Stark (Ivo
Sbalzarini group, Max Planck Institute of Molecular Cell Biology and Genetics, Dresden,
Germany) for project-related discussions; Darren Gilmour (University of Zurich),
Karuna Sampath (University of Warwick) and Gokul Kesavan (Vowels Lifesciences Private
Limited, Bangalore) for comments on the manuscript; personnel of the CMCB technology
platform, TU Dresden for imaging and image analysis-related support; and Maurizio
Abbate (Technical support, Arivis) for help with image analysis. We are also grateful
to Stapornwongkul and Briscoe for commenting on a preprint version of our work (Stapornwongkul
and Briscoe, 2022).\r\nThis work was supported by the Deutsche Forschungsgemeinschaft
(BR 1746/6-2, BR 1746/11-1 and BR 1746/3 to M.B.), by a Cluster of Excellence ‘Physics
of Life’ seed grant and by institutional funds from Technische Universitat Dresden
(to M.B.). Open Access funding provided by Technische Universitat Dresden. Deposited
in PMC for immediate release."
article_number: dev201559
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Rohit K
full_name: Harish, Rohit K
id: 1bae78aa-ee0e-11ec-9b76-bc42990f409d
last_name: Harish
- first_name: Mansi
full_name: Gupta, Mansi
last_name: Gupta
- first_name: Daniela
full_name: Zöller, Daniela
last_name: Zöller
- first_name: Hella
full_name: Hartmann, Hella
last_name: Hartmann
- first_name: Ali
full_name: Gheisari, Ali
last_name: Gheisari
- first_name: Anja
full_name: Machate, Anja
last_name: Machate
- first_name: Stefan
full_name: Hans, Stefan
last_name: Hans
- first_name: Michael
full_name: Brand, Michael
last_name: Brand
citation:
ama: Harish RK, Gupta M, Zöller D, et al. Real-time monitoring of an endogenous
Fgf8a gradient attests to its role as a morphogen during zebrafish gastrulation.
Development. 2023;150(19). doi:10.1242/dev.201559
apa: Harish, R. K., Gupta, M., Zöller, D., Hartmann, H., Gheisari, A., Machate,
A., … Brand, M. (2023). Real-time monitoring of an endogenous Fgf8a gradient attests
to its role as a morphogen during zebrafish gastrulation. Development.
The Company of Biologists. https://doi.org/10.1242/dev.201559
chicago: Harish, Rohit K, Mansi Gupta, Daniela Zöller, Hella Hartmann, Ali Gheisari,
Anja Machate, Stefan Hans, and Michael Brand. “Real-Time Monitoring of an Endogenous
Fgf8a Gradient Attests to Its Role as a Morphogen during Zebrafish Gastrulation.”
Development. The Company of Biologists, 2023. https://doi.org/10.1242/dev.201559.
ieee: R. K. Harish et al., “Real-time monitoring of an endogenous Fgf8a gradient
attests to its role as a morphogen during zebrafish gastrulation,” Development,
vol. 150, no. 19. The Company of Biologists, 2023.
ista: Harish RK, Gupta M, Zöller D, Hartmann H, Gheisari A, Machate A, Hans S, Brand
M. 2023. Real-time monitoring of an endogenous Fgf8a gradient attests to its role
as a morphogen during zebrafish gastrulation. Development. 150(19), dev201559.
mla: Harish, Rohit K., et al. “Real-Time Monitoring of an Endogenous Fgf8a Gradient
Attests to Its Role as a Morphogen during Zebrafish Gastrulation.” Development,
vol. 150, no. 19, dev201559, The Company of Biologists, 2023, doi:10.1242/dev.201559.
short: R.K. Harish, M. Gupta, D. Zöller, H. Hartmann, A. Gheisari, A. Machate, S.
Hans, M. Brand, Development 150 (2023).
date_created: 2024-01-10T09:18:54Z
date_published: 2023-10-01T00:00:00Z
date_updated: 2024-01-10T12:45:25Z
day: '01'
ddc:
- '570'
department:
- _id: AnKi
doi: 10.1242/dev.201559
external_id:
isi:
- '001097449100002'
pmid:
- '37665167'
file:
- access_level: open_access
checksum: 2d6f52dc33260a9b2352b8f28374ba5f
content_type: application/pdf
creator: dernst
date_created: 2024-01-10T12:41:13Z
date_updated: 2024-01-10T12:41:13Z
file_id: '14790'
file_name: 2023_Development_Harish.pdf
file_size: 12836306
relation: main_file
success: 1
file_date_updated: 2024-01-10T12:41:13Z
has_accepted_license: '1'
intvolume: ' 150'
isi: 1
issue: '19'
keyword:
- Developmental Biology
- Molecular Biology
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
pmid: 1
publication: Development
publication_identifier:
eissn:
- 1477-9129
issn:
- 0950-1991
publication_status: published
publisher: The Company of Biologists
quality_controlled: '1'
status: public
title: Real-time monitoring of an endogenous Fgf8a gradient attests to its role as
a morphogen during zebrafish gastrulation
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: 150
year: '2023'
...
---
_id: '12231'
abstract:
- lang: eng
text: Ventral tail bending, which is transient but pronounced, is found in many
chordate embryos and constitutes an interesting model of how tissue interactions
control embryo shape. Here, we identify one key upstream regulator of ventral
tail bending in embryos of the ascidian Ciona. We show that during the early tailbud
stages, ventral epidermal cells exhibit a boat-shaped morphology (boat cell) with
a narrow apical surface where phosphorylated myosin light chain (pMLC) accumulates.
We further show that interfering with the function of the BMP ligand Admp led
to pMLC localizing to the basal instead of the apical side of ventral epidermal
cells and a reduced number of boat cells. Finally, we show that cutting ventral
epidermal midline cells at their apex using an ultraviolet laser relaxed ventral
tail bending. Based on these results, we propose a previously unreported function
for Admp in localizing pMLC to the apical side of ventral epidermal cells, which
causes the tail to bend ventrally by resisting antero-posterior notochord extension
at the ventral side of the tail.
acknowledgement: "iona intestinalis adults were provided by Dr Yutaka Satou (Kyoto
University) and Dr Manabu Yoshida (the University of Tokyo) with support from the
National Bio-Resource Project of AMED, Japan. We thank Dr Hidehiko Hashimoto and
Dr Yuji Mizotani for technical information about 1P-myosin antibody staining. We
thank Dr Kaoru Imai and Dr Yutaka Satou for valuable discussion about Admp and for
the DNA construct of Bmp2/4 under the Dlx.b upstream sequence. We thank Ms Maki
Kogure for constructing the FUSION360 of the intercalating epidermal cell.\r\nThis
work was supported by funding from the Japan Society for the Promotion of Science
(JP16H01451, JP21H00440). Open Access funding provided by Keio University: Keio
Gijuku Daigaku."
article_number: dev200215
article_processing_charge: No
article_type: original
author:
- first_name: Yuki S.
full_name: Kogure, Yuki S.
last_name: Kogure
- first_name: Hiromochi
full_name: Muraoka, Hiromochi
last_name: Muraoka
- first_name: Wataru C.
full_name: Koizumi, Wataru C.
last_name: Koizumi
- first_name: Raphaël
full_name: Gelin-alessi, Raphaël
last_name: Gelin-alessi
- first_name: Benoit G
full_name: Godard, Benoit G
id: 3263621A-F248-11E8-B48F-1D18A9856A87
last_name: Godard
- first_name: Kotaro
full_name: Oka, Kotaro
last_name: Oka
- 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: Kohji
full_name: Hotta, Kohji
last_name: Hotta
citation:
ama: Kogure YS, Muraoka H, Koizumi WC, et al. Admp regulates tail bending by controlling
ventral epidermal cell polarity via phosphorylated myosin localization in Ciona.
Development. 2022;149(21). doi:10.1242/dev.200215
apa: Kogure, Y. S., Muraoka, H., Koizumi, W. C., Gelin-alessi, R., Godard, B. G.,
Oka, K., … Hotta, K. (2022). Admp regulates tail bending by controlling ventral
epidermal cell polarity via phosphorylated myosin localization in Ciona. Development.
The Company of Biologists. https://doi.org/10.1242/dev.200215
chicago: Kogure, Yuki S., Hiromochi Muraoka, Wataru C. Koizumi, Raphaël Gelin-alessi,
Benoit G Godard, Kotaro Oka, Carl-Philipp J Heisenberg, and Kohji Hotta. “Admp
Regulates Tail Bending by Controlling Ventral Epidermal Cell Polarity via Phosphorylated
Myosin Localization in Ciona.” Development. The Company of Biologists,
2022. https://doi.org/10.1242/dev.200215.
ieee: Y. S. Kogure et al., “Admp regulates tail bending by controlling ventral
epidermal cell polarity via phosphorylated myosin localization in Ciona,” Development,
vol. 149, no. 21. The Company of Biologists, 2022.
ista: Kogure YS, Muraoka H, Koizumi WC, Gelin-alessi R, Godard BG, Oka K, Heisenberg
C-PJ, Hotta K. 2022. Admp regulates tail bending by controlling ventral epidermal
cell polarity via phosphorylated myosin localization in Ciona. Development. 149(21),
dev200215.
mla: Kogure, Yuki S., et al. “Admp Regulates Tail Bending by Controlling Ventral
Epidermal Cell Polarity via Phosphorylated Myosin Localization in Ciona.” Development,
vol. 149, no. 21, dev200215, The Company of Biologists, 2022, doi:10.1242/dev.200215.
short: Y.S. Kogure, H. Muraoka, W.C. Koizumi, R. Gelin-alessi, B.G. Godard, K. Oka,
C.-P.J. Heisenberg, K. Hotta, Development 149 (2022).
date_created: 2023-01-16T09:50:12Z
date_published: 2022-11-01T00:00:00Z
date_updated: 2023-08-04T09:33:24Z
day: '01'
ddc:
- '570'
department:
- _id: CaHe
doi: 10.1242/dev.200215
external_id:
isi:
- '000903991700002'
pmid:
- '36227591'
file:
- access_level: open_access
checksum: 871b9c58eb79b9e60752de25a46938d6
content_type: application/pdf
creator: dernst
date_created: 2023-01-27T10:36:50Z
date_updated: 2023-01-27T10:36:50Z
file_id: '12423'
file_name: 2022_Development_Kogure.pdf
file_size: 9160451
relation: main_file
success: 1
file_date_updated: 2023-01-27T10:36:50Z
has_accepted_license: '1'
intvolume: ' 149'
isi: 1
issue: '21'
keyword:
- Developmental Biology
- Molecular Biology
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
pmid: 1
publication: Development
publication_identifier:
eissn:
- 1477-9129
issn:
- 0950-1991
publication_status: published
publisher: The Company of Biologists
quality_controlled: '1'
scopus_import: '1'
status: public
title: Admp regulates tail bending by controlling ventral epidermal cell polarity
via phosphorylated myosin localization in Ciona
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: 149
year: '2022'
...
---
_id: '12245'
abstract:
- lang: eng
text: MicroRNAs (miRs) have an important role in tuning dynamic gene expression.
However, the mechanism by which they are quantitatively controlled is unknown.
We show that the amount of mature miR-9, a key regulator of neuronal development,
increases during zebrafish neurogenesis in a sharp stepwise manner. We characterize
the spatiotemporal profile of seven distinct microRNA primary transcripts (pri-mir)-9s
that produce the same mature miR-9 and show that they are sequentially expressed
during hindbrain neurogenesis. Expression of late-onset pri-mir-9-1 is added on
to, rather than replacing, the expression of early onset pri-mir-9-4 and -9-5
in single cells. CRISPR/Cas9 mutation of the late-onset pri-mir-9-1 prevents the
developmental increase of mature miR-9, reduces late neuronal differentiation
and fails to downregulate Her6 at late stages. Mathematical modelling shows that
an adaptive network containing Her6 is insensitive to linear increases in miR-9
but responds to stepwise increases of miR-9. We suggest that a sharp stepwise
increase of mature miR-9 is created by sequential and additive temporal activation
of distinct loci. This may be a strategy to overcome adaptation and facilitate
a transition of Her6 to a new dynamic regime or steady state.
acknowledgement: "We are grateful to Dr Tom Pettini for the advice on smiFISH technique
and Dr Laure Bally-Cuif for sharing plasmids. The authors also thank the Biological
Services Facility, Bioimaging and Systems Microscopy Facilities of the University
of Manchester for technical support.\r\nThis work was supported by a Wellcome Trust
Senior Research Fellowship (090868/Z/09/Z) and a Wellcome Trust Investigator Award
(224394/Z/21/Z) to N.P. and a Medical Research Council Career Development Award
to C.S.M. (MR/V032534/1). J.B. was supported by a Wellcome Trust Four-Year PhD Studentship
in Basic Science (219992/Z/19/Z). Open Access funding provided by The University
of Manchester. Deposited in PMC for immediate release."
article_number: dev200474
article_processing_charge: No
article_type: original
author:
- first_name: Ximena
full_name: Soto, Ximena
last_name: Soto
- first_name: Joshua
full_name: Burton, Joshua
last_name: Burton
- first_name: Cerys S.
full_name: Manning, Cerys S.
last_name: Manning
- first_name: Thomas
full_name: Minchington, Thomas
id: 7d1648cb-19e9-11eb-8e7a-f8c037fb3e3f
last_name: Minchington
- first_name: Robert
full_name: Lea, Robert
last_name: Lea
- first_name: Jessica
full_name: Lee, Jessica
last_name: Lee
- first_name: Jochen
full_name: Kursawe, Jochen
last_name: Kursawe
- first_name: Magnus
full_name: Rattray, Magnus
last_name: Rattray
- first_name: Nancy
full_name: Papalopulu, Nancy
last_name: Papalopulu
citation:
ama: Soto X, Burton J, Manning CS, et al. Sequential and additive expression of
miR-9 precursors control timing of neurogenesis. Development. 2022;149(19).
doi:10.1242/dev.200474
apa: Soto, X., Burton, J., Manning, C. S., Minchington, T., Lea, R., Lee, J., …
Papalopulu, N. (2022). Sequential and additive expression of miR-9 precursors
control timing of neurogenesis. Development. The Company of Biologists.
https://doi.org/10.1242/dev.200474
chicago: Soto, Ximena, Joshua Burton, Cerys S. Manning, Thomas Minchington, Robert
Lea, Jessica Lee, Jochen Kursawe, Magnus Rattray, and Nancy Papalopulu. “Sequential
and Additive Expression of MiR-9 Precursors Control Timing of Neurogenesis.” Development.
The Company of Biologists, 2022. https://doi.org/10.1242/dev.200474.
ieee: X. Soto et al., “Sequential and additive expression of miR-9 precursors
control timing of neurogenesis,” Development, vol. 149, no. 19. The Company
of Biologists, 2022.
ista: Soto X, Burton J, Manning CS, Minchington T, Lea R, Lee J, Kursawe J, Rattray
M, Papalopulu N. 2022. Sequential and additive expression of miR-9 precursors
control timing of neurogenesis. Development. 149(19), dev200474.
mla: Soto, Ximena, et al. “Sequential and Additive Expression of MiR-9 Precursors
Control Timing of Neurogenesis.” Development, vol. 149, no. 19, dev200474,
The Company of Biologists, 2022, doi:10.1242/dev.200474.
short: X. Soto, J. Burton, C.S. Manning, T. Minchington, R. Lea, J. Lee, J. Kursawe,
M. Rattray, N. Papalopulu, Development 149 (2022).
date_created: 2023-01-16T09:53:17Z
date_published: 2022-10-01T00:00:00Z
date_updated: 2023-08-04T09:41:08Z
day: '01'
ddc:
- '570'
department:
- _id: AnKi
doi: 10.1242/dev.200474
external_id:
isi:
- '000918161000003'
pmid:
- '36189829'
file:
- access_level: open_access
checksum: d7c29b74e9e4032308228cc704a30e88
content_type: application/pdf
creator: dernst
date_created: 2023-01-30T08:35:44Z
date_updated: 2023-01-30T08:35:44Z
file_id: '12438'
file_name: 2022_Development_Soto.pdf
file_size: 9348839
relation: main_file
success: 1
file_date_updated: 2023-01-30T08:35:44Z
has_accepted_license: '1'
intvolume: ' 149'
isi: 1
issue: '19'
keyword:
- Developmental Biology
- Molecular Biology
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
pmid: 1
publication: Development
publication_identifier:
eissn:
- 1477-9129
issn:
- 0950-1991
publication_status: published
publisher: The Company of Biologists
quality_controlled: '1'
related_material:
link:
- relation: software
url: ' https://github.com/burtonjosh/StepwiseMir9'
scopus_import: '1'
status: public
title: Sequential and additive expression of miR-9 precursors control timing of neurogenesis
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: 149
year: '2022'
...
---
_id: '7165'
abstract:
- lang: eng
text: Cell division, movement and differentiation contribute to pattern formation
in developing tissues. This is the case in the vertebrate neural tube, in which
neurons differentiate in a characteristic pattern from a highly dynamic proliferating
pseudostratified epithelium. To investigate how progenitor proliferation and differentiation
affect cell arrangement and growth of the neural tube, we used experimental measurements
to develop a mechanical model of the apical surface of the neuroepithelium that
incorporates the effect of interkinetic nuclear movement and spatially varying
rates of neuronal differentiation. Simulations predict that tissue growth and
the shape of lineage-related clones of cells differ with the rate of differentiation.
Growth is isotropic in regions of high differentiation, but dorsoventrally biased
in regions of low differentiation. This is consistent with experimental observations.
The absence of directional signalling in the simulations indicates that global
mechanical constraints are sufficient to explain the observed differences in anisotropy.
This provides insight into how the tissue growth rate affects cell dynamics and
growth anisotropy and opens up possibilities to study the coupling between mechanics,
pattern formation and growth in the neural tube.
article_number: dev176297
article_processing_charge: No
article_type: original
author:
- first_name: Pilar
full_name: Guerrero, Pilar
last_name: Guerrero
- first_name: Ruben
full_name: Perez-Carrasco, Ruben
last_name: Perez-Carrasco
- first_name: Marcin P
full_name: Zagórski, Marcin P
id: 343DA0DC-F248-11E8-B48F-1D18A9856A87
last_name: Zagórski
orcid: 0000-0001-7896-7762
- first_name: David
full_name: Page, David
last_name: Page
- first_name: Anna
full_name: Kicheva, Anna
id: 3959A2A0-F248-11E8-B48F-1D18A9856A87
last_name: Kicheva
orcid: 0000-0003-4509-4998
- first_name: James
full_name: Briscoe, James
last_name: Briscoe
- first_name: Karen M.
full_name: Page, Karen M.
last_name: Page
citation:
ama: Guerrero P, Perez-Carrasco R, Zagórski MP, et al. Neuronal differentiation
influences progenitor arrangement in the vertebrate neuroepithelium. Development.
2019;146(23). doi:10.1242/dev.176297
apa: Guerrero, P., Perez-Carrasco, R., Zagórski, M. P., Page, D., Kicheva, A., Briscoe,
J., & Page, K. M. (2019). Neuronal differentiation influences progenitor arrangement
in the vertebrate neuroepithelium. Development. The Company of Biologists.
https://doi.org/10.1242/dev.176297
chicago: Guerrero, Pilar, Ruben Perez-Carrasco, Marcin P Zagórski, David Page, Anna
Kicheva, James Briscoe, and Karen M. Page. “Neuronal Differentiation Influences
Progenitor Arrangement in the Vertebrate Neuroepithelium.” Development.
The Company of Biologists, 2019. https://doi.org/10.1242/dev.176297.
ieee: P. Guerrero et al., “Neuronal differentiation influences progenitor
arrangement in the vertebrate neuroepithelium,” Development, vol. 146,
no. 23. The Company of Biologists, 2019.
ista: Guerrero P, Perez-Carrasco R, Zagórski MP, Page D, Kicheva A, Briscoe J, Page
KM. 2019. Neuronal differentiation influences progenitor arrangement in the vertebrate
neuroepithelium. Development. 146(23), dev176297.
mla: Guerrero, Pilar, et al. “Neuronal Differentiation Influences Progenitor Arrangement
in the Vertebrate Neuroepithelium.” Development, vol. 146, no. 23, dev176297,
The Company of Biologists, 2019, doi:10.1242/dev.176297.
short: P. Guerrero, R. Perez-Carrasco, M.P. Zagórski, D. Page, A. Kicheva, J. Briscoe,
K.M. Page, Development 146 (2019).
date_created: 2019-12-10T14:39:50Z
date_published: 2019-12-04T00:00:00Z
date_updated: 2023-09-06T11:26:36Z
day: '04'
ddc:
- '570'
department:
- _id: AnKi
doi: 10.1242/dev.176297
ec_funded: 1
external_id:
isi:
- '000507575700004'
pmid:
- '31784457'
file:
- access_level: open_access
checksum: b6533c37dc8fbd803ffeca216e0a8b8a
content_type: application/pdf
creator: dernst
date_created: 2019-12-13T07:34:06Z
date_updated: 2020-07-14T12:47:50Z
file_id: '7177'
file_name: 2019_Development_Guerrero.pdf
file_size: 7797881
relation: main_file
file_date_updated: 2020-07-14T12:47:50Z
has_accepted_license: '1'
intvolume: ' 146'
isi: 1
issue: '23'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: B6FC0238-B512-11E9-945C-1524E6697425
call_identifier: H2020
grant_number: '680037'
name: Coordination of Patterning And Growth In the Spinal Cord
publication: Development
publication_identifier:
eissn:
- 1477-9129
issn:
- 0950-1991
publication_status: published
publisher: The Company of Biologists
quality_controlled: '1'
scopus_import: '1'
status: public
title: Neuronal differentiation influences progenitor arrangement in the vertebrate
neuroepithelium
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: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 146
year: '2019'
...
---
_id: '7404'
abstract:
- lang: eng
text: The formation of neuronal dendrite branches is fundamental for the wiring
and function of the nervous system. Indeed, dendrite branching enhances the coverage
of the neuron's receptive field and modulates the initial processing of incoming
stimuli. Complex dendrite patterns are achieved in vivo through a dynamic process
of de novo branch formation, branch extension and retraction. The first step towards
branch formation is the generation of a dynamic filopodium-like branchlet. The
mechanisms underlying the initiation of dendrite branchlets are therefore crucial
to the shaping of dendrites. Through in vivo time-lapse imaging of the subcellular
localization of actin during the process of branching of Drosophila larva sensory
neurons, combined with genetic analysis and electron tomography, we have identified
the Actin-related protein (Arp) 2/3 complex as the major actin nucleator involved
in the initiation of dendrite branchlet formation, under the control of the activator
WAVE and of the small GTPase Rac1. Transient recruitment of an Arp2/3 component
marks the site of branchlet initiation in vivo. These data position the activation
of Arp2/3 as an early hub for the initiation of branchlet formation.
article_number: dev171397
article_processing_charge: No
article_type: original
author:
- first_name: Tomke
full_name: Stürner, Tomke
last_name: Stürner
- first_name: Anastasia
full_name: Tatarnikova, Anastasia
last_name: Tatarnikova
- first_name: Jan
full_name: Müller, Jan
id: AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D
last_name: Müller
- first_name: Barbara
full_name: Schaffran, Barbara
last_name: Schaffran
- first_name: Hermann
full_name: Cuntz, Hermann
last_name: Cuntz
- first_name: Yun
full_name: Zhang, Yun
last_name: Zhang
- first_name: Maria
full_name: Nemethova, Maria
id: 34E27F1C-F248-11E8-B48F-1D18A9856A87
last_name: Nemethova
- first_name: Sven
full_name: Bogdan, Sven
last_name: Bogdan
- first_name: Vic
full_name: Small, Vic
last_name: Small
- first_name: Gaia
full_name: Tavosanis, Gaia
last_name: Tavosanis
citation:
ama: Stürner T, Tatarnikova A, Müller J, et al. Transient localization of the Arp2/3
complex initiates neuronal dendrite branching in vivo. Development. 2019;146(7).
doi:10.1242/dev.171397
apa: Stürner, T., Tatarnikova, A., Müller, J., Schaffran, B., Cuntz, H., Zhang,
Y., … Tavosanis, G. (2019). Transient localization of the Arp2/3 complex initiates
neuronal dendrite branching in vivo. Development. The Company of Biologists.
https://doi.org/10.1242/dev.171397
chicago: Stürner, Tomke, Anastasia Tatarnikova, Jan Müller, Barbara Schaffran, Hermann
Cuntz, Yun Zhang, Maria Nemethova, Sven Bogdan, Vic Small, and Gaia Tavosanis.
“Transient Localization of the Arp2/3 Complex Initiates Neuronal Dendrite Branching
in Vivo.” Development. The Company of Biologists, 2019. https://doi.org/10.1242/dev.171397.
ieee: T. Stürner et al., “Transient localization of the Arp2/3 complex initiates
neuronal dendrite branching in vivo,” Development, vol. 146, no. 7. The
Company of Biologists, 2019.
ista: Stürner T, Tatarnikova A, Müller J, Schaffran B, Cuntz H, Zhang Y, Nemethova
M, Bogdan S, Small V, Tavosanis G. 2019. Transient localization of the Arp2/3
complex initiates neuronal dendrite branching in vivo. Development. 146(7), dev171397.
mla: Stürner, Tomke, et al. “Transient Localization of the Arp2/3 Complex Initiates
Neuronal Dendrite Branching in Vivo.” Development, vol. 146, no. 7, dev171397,
The Company of Biologists, 2019, doi:10.1242/dev.171397.
short: T. Stürner, A. Tatarnikova, J. Müller, B. Schaffran, H. Cuntz, Y. Zhang,
M. Nemethova, S. Bogdan, V. Small, G. Tavosanis, Development 146 (2019).
date_created: 2020-01-29T16:27:10Z
date_published: 2019-04-04T00:00:00Z
date_updated: 2023-09-07T14:47:00Z
day: '04'
department:
- _id: MiSi
doi: 10.1242/dev.171397
external_id:
isi:
- '000464583200006'
pmid:
- '30910826'
intvolume: ' 146'
isi: 1
issue: '7'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1242/dev.171397
month: '04'
oa: 1
oa_version: Published Version
pmid: 1
publication: Development
publication_identifier:
eissn:
- 1477-9129
issn:
- 0950-1991
publication_status: published
publisher: The Company of Biologists
quality_controlled: '1'
scopus_import: '1'
status: public
title: Transient localization of the Arp2/3 complex initiates neuronal dendrite branching
in vivo
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 146
year: '2019'
...
---
_id: '12199'
abstract:
- lang: eng
text: The four microsporangia of the flowering plant anther develop from archesporial
cells in the L2 of the primordium. Within each microsporangium, developing microsporocytes
are surrounded by concentric monolayers of tapetal, middle layer and endothecial
cells. How this intricate array of tissues, each containing relatively few cells,
is established in an organ possessing no formal meristems is poorly understood.
We describe here the pivotal role of the LRR receptor kinase EXCESS MICROSPOROCYTES
1 (EMS1) in forming the monolayer of tapetal nurse cells in Arabidopsis. Unusually
for plants, tapetal cells are specified very early in development, and are subsequently
stimulated to proliferate by a receptor-like kinase (RLK) complex that includes
EMS1. Mutations in members of this EMS1 signalling complex and its putative ligand
result in male-sterile plants in which tapetal initials fail to proliferate. Surprisingly,
these cells continue to develop, isolated at the locular periphery. Mutant and
wild-type microsporangia expand at similar rates and the ‘tapetal’ space at the
periphery of mutant locules becomes occupied by microsporocytes. However, induction
of late expression of EMS1 in the few tapetal initials in ems1 plants results
in their proliferation to generate a functional tapetum, and this proliferation
suppresses microsporocyte number. Our experiments also show that integrity of
the tapetal monolayer is crucial for the maintenance of the polarity of divisions
within it. This unexpected autonomy of the tapetal ‘lineage’ is discussed in the
context of tissue development in complex plant organs, where constancy in size,
shape and cell number is crucial.
acknowledgement: 'We thank the following for providing mutant lines and reagents:
Hong Ma, De Ye, Sacco De Vries, and Rod Scott for providing the pA9::Barnase lines
and information on A9 expression patterns. Carla Galinha and Paolo Piazza gave valuable
help with in situ hybridisation and qRT-PCR, respectively, and we acknowledge Qing
Zhang, Helen Prescott and Matthew Dicks for providing excellent technical assistance.
We are indebted to Miltos Tsiantis and Angela Hay for helpful discussion, and the
research was funded by Oxford University through a Clarendon Scholarship to X.F.,
with additional financial support from Magdalen College (Oxford).'
article_processing_charge: No
article_type: original
author:
- first_name: Xiaoqi
full_name: Feng, Xiaoqi
id: e0164712-22ee-11ed-b12a-d80fcdf35958
last_name: Feng
orcid: 0000-0002-4008-1234
- first_name: Hugh G.
full_name: Dickinson, Hugh G.
last_name: Dickinson
citation:
ama: Feng X, Dickinson HG. Tapetal cell fate, lineage and proliferation in the Arabidopsis
anther. Development. 2010;137(14):2409-2416. doi:10.1242/dev.049320
apa: Feng, X., & Dickinson, H. G. (2010). Tapetal cell fate, lineage and proliferation
in the Arabidopsis anther. Development. The Company of Biologists. https://doi.org/10.1242/dev.049320
chicago: Feng, Xiaoqi, and Hugh G. Dickinson. “Tapetal Cell Fate, Lineage and Proliferation
in the Arabidopsis Anther.” Development. The Company of Biologists, 2010.
https://doi.org/10.1242/dev.049320.
ieee: X. Feng and H. G. Dickinson, “Tapetal cell fate, lineage and proliferation
in the Arabidopsis anther,” Development, vol. 137, no. 14. The Company
of Biologists, pp. 2409–2416, 2010.
ista: Feng X, Dickinson HG. 2010. Tapetal cell fate, lineage and proliferation in
the Arabidopsis anther. Development. 137(14), 2409–2416.
mla: Feng, Xiaoqi, and Hugh G. Dickinson. “Tapetal Cell Fate, Lineage and Proliferation
in the Arabidopsis Anther.” Development, vol. 137, no. 14, The Company
of Biologists, 2010, pp. 2409–16, doi:10.1242/dev.049320.
short: X. Feng, H.G. Dickinson, Development 137 (2010) 2409–2416.
date_created: 2023-01-16T09:21:54Z
date_published: 2010-07-15T00:00:00Z
date_updated: 2023-05-08T10:57:11Z
day: '15'
department:
- _id: XiFe
doi: 10.1242/dev.049320
extern: '1'
external_id:
pmid:
- '20570940'
intvolume: ' 137'
issue: '14'
keyword:
- Developmental Biology
- Molecular Biology
- Anther Tapetum
- Arabidopsis
- Cell Fate Establishment
- EMS1
- Reproductive Cell Lineage
language:
- iso: eng
month: '07'
oa_version: None
page: 2409-2416
pmid: 1
publication: Development
publication_identifier:
issn:
- 1477-9129
- 0950-1991
publication_status: published
publisher: The Company of Biologists
quality_controlled: '1'
scopus_import: '1'
status: public
title: Tapetal cell fate, lineage and proliferation in the Arabidopsis anther
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 137
year: '2010'
...
---
_id: '9524'
abstract:
- lang: eng
text: Cytosine methylation is the most common covalent modification of DNA in eukaryotes.
DNA methylation has an important role in many aspects of biology, including development
and disease. Methylation can be detected using bisulfite conversion, methylation-sensitive
restriction enzymes, methyl-binding proteins and anti-methylcytosine antibodies.
Combining these techniques with DNA microarrays and high-throughput sequencing
has made the mapping of DNA methylation feasible on a genome-wide scale. Here
we discuss recent developments and future directions for identifying and mapping
methylation, in an effort to help colleagues to identify the approaches that best
serve their research interests.
article_processing_charge: No
article_type: review
author:
- first_name: Daniel
full_name: Zilberman, Daniel
id: 6973db13-dd5f-11ea-814e-b3e5455e9ed1
last_name: Zilberman
orcid: 0000-0002-0123-8649
- first_name: Steven
full_name: Henikoff, Steven
last_name: Henikoff
citation:
ama: Zilberman D, Henikoff S. Genome-wide analysis of DNA methylation patterns.
Development. 2007;134(22):3959-3965. doi:10.1242/dev.001131
apa: Zilberman, D., & Henikoff, S. (2007). Genome-wide analysis of DNA methylation
patterns. Development. The Company of Biologists. https://doi.org/10.1242/dev.001131
chicago: Zilberman, Daniel, and Steven Henikoff. “Genome-Wide Analysis of DNA Methylation
Patterns.” Development. The Company of Biologists, 2007. https://doi.org/10.1242/dev.001131.
ieee: D. Zilberman and S. Henikoff, “Genome-wide analysis of DNA methylation patterns,”
Development, vol. 134, no. 22. The Company of Biologists, pp. 3959–3965,
2007.
ista: Zilberman D, Henikoff S. 2007. Genome-wide analysis of DNA methylation patterns.
Development. 134(22), 3959–3965.
mla: Zilberman, Daniel, and Steven Henikoff. “Genome-Wide Analysis of DNA Methylation
Patterns.” Development, vol. 134, no. 22, The Company of Biologists, 2007,
pp. 3959–65, doi:10.1242/dev.001131.
short: D. Zilberman, S. Henikoff, Development 134 (2007) 3959–3965.
date_created: 2021-06-08T06:29:50Z
date_published: 2007-11-15T00:00:00Z
date_updated: 2021-12-14T08:57:58Z
day: '15'
department:
- _id: DaZi
doi: 10.1242/dev.001131
extern: '1'
external_id:
pmid:
- '17928417'
intvolume: ' 134'
issue: '22'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1242/dev.001131
month: '11'
oa: 1
oa_version: Published Version
page: 3959-3965
pmid: 1
publication: Development
publication_identifier:
eissn:
- 1477-9129
issn:
- 0950-1991
publication_status: published
publisher: The Company of Biologists
quality_controlled: '1'
scopus_import: '1'
status: public
title: Genome-wide analysis of DNA methylation patterns
type: journal_article
user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9
volume: 134
year: '2007'
...
---
_id: '4209'
abstract:
- lang: eng
text: We have identified widerborst (wdb), a B' regulatory subunit of PP2A, as a
conserved component of planar cell polarization mechanisms in both Drosophila
and in zebrafish. In Drosophila, wdb acts at two steps during planar polarization
of wing epithelial cells. It is required to organize tissue polarity proteins
into proximal and distal cortical domains, thus determining wing hair orientation.
It is also needed to generate the polarized membrane outgrowth that becomes the
wing hair. Widerborst activates the catalytic subunit of PP2A and localizes to
the distal side of a planar microtubule web that lies at the level of apical cell
junctions. This suggests that polarized PP2A activation along the planar microtubule
web is important for planar polarization. In zebrafish, two wdb homologs are required
for convergent extension during gastrulation, supporting the conjecture that Drosophila
planar cell polarization and vertebrate gastrulation movements are regulated by
similar mechanisms.
acknowledgement: We gratefully acknowledge Bianca Habermann for assistance with bioinformatics,
Jens Rietdorf and Arshad Desai for help with deconvolution, and Tadashi Uemura and
Rick Fehon for providing antibodies. Arshad Desai, Christian Dahmann, Tony Hyman
and Elly Tanaka provided helpful comments on the manuscript. Part of this work was
performed at the EMBL in Heidelberg.
article_processing_charge: No
article_type: original
author:
- first_name: Michael
full_name: Hannus, Michael
last_name: Hannus
- first_name: Fabian
full_name: Feiguin, Fabian
last_name: Feiguin
- 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: Suzanne
full_name: Eaton, Suzanne
last_name: Eaton
citation:
ama: Hannus M, Feiguin F, Heisenberg C-PJ, Eaton S. Planar cell polarization requires
Widerborst, a B′ regulatory subunit of protein phosphatase 2A. Development.
2002;129(14):3493-3503. doi:10.1242/dev.129.14.3493
apa: Hannus, M., Feiguin, F., Heisenberg, C.-P. J., & Eaton, S. (2002). Planar
cell polarization requires Widerborst, a B′ regulatory subunit of protein phosphatase
2A. Development. Company of Biologists. https://doi.org/10.1242/dev.129.14.3493
chicago: Hannus, Michael, Fabian Feiguin, Carl-Philipp J Heisenberg, and Suzanne
Eaton. “Planar Cell Polarization Requires Widerborst, a B′ Regulatory Subunit
of Protein Phosphatase 2A.” Development. Company of Biologists, 2002. https://doi.org/10.1242/dev.129.14.3493.
ieee: M. Hannus, F. Feiguin, C.-P. J. Heisenberg, and S. Eaton, “Planar cell polarization
requires Widerborst, a B′ regulatory subunit of protein phosphatase 2A,” Development,
vol. 129, no. 14. Company of Biologists, pp. 3493–3503, 2002.
ista: Hannus M, Feiguin F, Heisenberg C-PJ, Eaton S. 2002. Planar cell polarization
requires Widerborst, a B′ regulatory subunit of protein phosphatase 2A. Development.
129(14), 3493–3503.
mla: Hannus, Michael, et al. “Planar Cell Polarization Requires Widerborst, a B′
Regulatory Subunit of Protein Phosphatase 2A.” Development, vol. 129, no.
14, Company of Biologists, 2002, pp. 3493–503, doi:10.1242/dev.129.14.3493.
short: M. Hannus, F. Feiguin, C.-P.J. Heisenberg, S. Eaton, Development 129 (2002)
3493–3503.
date_created: 2018-12-11T12:07:36Z
date_published: 2002-07-15T00:00:00Z
date_updated: 2023-06-06T14:07:49Z
day: '15'
doi: 10.1242/dev.129.14.3493
extern: '1'
external_id:
pmid:
- '12091318'
intvolume: ' 129'
issue: '14'
language:
- iso: eng
month: '07'
oa_version: None
page: 3493 - 3503
pmid: 1
publication: Development
publication_identifier:
issn:
- 0950-1991
publication_status: published
publisher: Company of Biologists
publist_id: '1909'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Planar cell polarization requires Widerborst, a B′ regulatory subunit of protein
phosphatase 2A
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 129
year: '2002'
...
---
_id: '4204'
abstract:
- lang: eng
text: During the development of the zebrafish nervous system both noi, a zebrafish
pax2 homolog, and ace, a zebrafish fgf8 homolog, are required for development
of the midbrain and cerebellum. Here we describe a dominant mutation, aussicht
(aus), in which the expression of noi and ace is upregulated, In aus mutant embryos,
ace is upregulated at many sites in the embryo, while Itoi expression is only
upregulated in regions of the forebrain and midbrain which also express ace. Subsequent
to the alterations in noi and ace expression, aus mutants exhibit defects in the
differentiation of the forebrain, midbrain and eyes. Within the forebrain, the
formation of the anterior and postoptic commissures is delayed and the expression
of markers within the pretectal area is reduced. Within the midbrain, En and wnt1
expression is expanded. In heterozygous aus embryos, there is ectopic outgrowth
of neural retina in the temporal half of the eyes, whereas in putative homozygous
aus embryos, the ventral retina is reduced and the pigmented retinal epithelium
is expanded towards the midline, The observation that ans mutant embryos exhibit
widespread upregulation of ace raised the possibility that aus might represent
an allele of the ace gene itself. However, by crossing carriers for both aus and
ace, we were able to generate homozygous ace mutant embryos that also exhibited
the aus phenotype, This indicated that aus is not tightly linked to ace and is
unlikely to be a mutation directly affecting the ace locus. However, increased
Ace activity may underly many aspects of the aus phenotype and we show that the
upregulation of noi in the forebrain of aus mutants is partially dependent upon
functional Ace activity. Conversely, increased ace expression in the forebrain
of arcs mutants is not dependent upon functional Noi activity. We conclude that
aus represents a mutation involving a locus normally required for the regulation
of ace expression during embryogenesis.
acknowledgement: "We thank Corinne Houart, Michael Brand and the late Nigel Holder
for comments and advice on this study, many colleagues for providing probes used
in this analysis, other members of our laboratories for suggestions throughout the
course of the work and Michael Brand, Jörg Rauch and Pascal Haffter for providing
data prior to publication. We also would like to thank Christiane Nüsslein-Volhard
in whose laboratory the mutant described in this study was initially isolated.\r\nThis
study was supported by grants from The Wellcome Trust and\r\nBBSRC. C. P. H. was
supported by Fellowships from EMBO and the\r\nEC, and S. W. W. is a Wellcome Trust
Senior Research Fellow.\r\n"
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: Caroline
full_name: Brennan, Caroline
last_name: Brennan
- first_name: Stephen
full_name: Wilson, Stephen
last_name: Wilson
citation:
ama: Heisenberg C-PJ, Brennan C, Wilson S. Zebrafish aussicht mutant embryos exhibit
widespread overexpression of ace (fgf8) and coincident defects in CNS development.
Development. 1999;126(10):2129-2140. doi:10.1242/dev.126.10.2129
apa: Heisenberg, C.-P. J., Brennan, C., & Wilson, S. (1999). Zebrafish aussicht
mutant embryos exhibit widespread overexpression of ace (fgf8) and coincident
defects in CNS development. Development. Company of Biologists. https://doi.org/10.1242/dev.126.10.2129
chicago: Heisenberg, Carl-Philipp J, Caroline Brennan, and Stephen Wilson. “Zebrafish
Aussicht Mutant Embryos Exhibit Widespread Overexpression of Ace (Fgf8) and Coincident
Defects in CNS Development.” Development. Company of Biologists, 1999.
https://doi.org/10.1242/dev.126.10.2129.
ieee: C.-P. J. Heisenberg, C. Brennan, and S. Wilson, “Zebrafish aussicht mutant
embryos exhibit widespread overexpression of ace (fgf8) and coincident defects
in CNS development,” Development, vol. 126, no. 10. Company of Biologists,
pp. 2129–2140, 1999.
ista: Heisenberg C-PJ, Brennan C, Wilson S. 1999. Zebrafish aussicht mutant embryos
exhibit widespread overexpression of ace (fgf8) and coincident defects in CNS
development. Development. 126(10), 2129–2140.
mla: Heisenberg, Carl-Philipp J., et al. “Zebrafish Aussicht Mutant Embryos Exhibit
Widespread Overexpression of Ace (Fgf8) and Coincident Defects in CNS Development.”
Development, vol. 126, no. 10, Company of Biologists, 1999, pp. 2129–40,
doi:10.1242/dev.126.10.2129.
short: C.-P.J. Heisenberg, C. Brennan, S. Wilson, Development 126 (1999) 2129–2140.
date_created: 2018-12-11T12:07:34Z
date_published: 1999-05-15T00:00:00Z
date_updated: 2022-09-06T08:38:01Z
day: '15'
doi: 10.1242/dev.126.10.2129
extern: '1'
external_id:
pmid:
- '10207138'
intvolume: ' 126'
issue: '10'
language:
- iso: eng
month: '05'
oa_version: None
page: 2129 - 2140
pmid: 1
publication: Development
publication_identifier:
issn:
- 0950-1991
publication_status: published
publisher: Company of Biologists
publist_id: '1914'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Zebrafish aussicht mutant embryos exhibit widespread overexpression of ace
(fgf8) and coincident defects in CNS development
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 126
year: '1999'
...
---
_id: '4142'
abstract:
- lang: eng
text: 'Mutations giving rise to anatomical defects in the inner ear have been isolated
in a large scale screen for mutations causing visible abnormalities in the zebrafish
embryo (Haffter, P., Granato, M., Brand, M. et al. (1996) Development 123, 1-36).
58 mutants have been classified as having a primary ear phenotype; these fall
into several phenotypic classes, affecting presence or size of the otoliths, size
and shape of the otic vesicle and formation of the semicircular canals, and define
at least 20 complementation groups. Mutations in seven genes cause loss of one
or both otoliths, but do not appear to affect development of other structures
within the ear. Mutations in seven genes affect morphology and patterning of the
inner ear epithelium, including formation of the semicircular canals and, in some,
development of sensory patches (maculae and cristae). Within this class, dog-eared
mutants show abnormal development of semicircular canals and lack cristae within
the ear, while in van gogh, semicircular canals fail to form altogether, resulting
in a tiny otic vesicle containing a single sensory patch. Both these mutants show
defects in the expression of homeobox genes within the otic vesicle. In a further
class of mutants, ear size is affected while patterning appears to be relatively
normal; mutations in three genes cause expansion of the otic vesicle, while in
little ears and microtic, the ear is abnormally small, but still contains all
five sensory patches, as in the wild type. Many of the ear and otolith mutants
show an expected behavioural phenotype: embryos fail to balance correctly, and
may swim on their sides, upside down, or in circles. Several mutants with similar
balance defects have also been isolated that have no obvious structural ear defect,
but that may include mutants with vestibular dysfunction of the inner ear (Granato,
M., van Eeden, F. J. M., Schach, U. et al. (1996) Development, 123, 399-413,).
Mutations in 19 genes causing primary defects in other structures also show an
ear defect. In particular, ear phenotypes are often found in conjunction with
defects of neural crest derivatives (pigment cells and/or cartilaginous elements
of the jaw). At least one mutant, dog-eared, shows defects in both the ear and
another placodally derived sensory system, the lateral line, while hypersensitive
mutants have additional trunk lateral line organs.'
acknowledgement: T. T. W. thanks all members of the Tübingen fish and fly groups for
their hospitality and generosity during her visits to the laboratory. We thank Julian
Lewis, in whose laboratory much of this work was carried out, for many helpful discussions
and suggestions, Catherine Haddon for advice on wild-type ear development and techniques,
and Stephen Massey for fish husbandry in Oxford. We are grateful to Julian Lewis,
Catherine Haddon, Nick Monk and Patrick Blader for comments on the manuscript, and
to Trevor Jowett, Tom Schilling,Eric Weinberg and Monte Westerfield for providing
cDNAs. We also thank Jarema Malicki and Wolfgang Driever for making some of the
Boston otolith mutants available before publication. T. T. W. thanks the EMBO (ASTF
7668; ASTF 7918), the Imperial Cancer Research Fund and the Wellcome Trust (03643/Z/92)
for support.
article_processing_charge: No
article_type: original
author:
- first_name: Tanya
full_name: Whitfield, Tanya
last_name: Whitfield
- first_name: Michael
full_name: Granato, Michael
last_name: Granato
- first_name: Fredericus
full_name: Van Eeden, Fredericus
last_name: Van Eeden
- first_name: Ursula
full_name: Schach, Ursula
last_name: Schach
- first_name: Michael
full_name: Brand, Michael
last_name: Brand
- first_name: Makoto
full_name: Furutani Seiki, Makoto
last_name: Furutani Seiki
- first_name: Pascal
full_name: Haffter, Pascal
last_name: Haffter
- first_name: Matthias
full_name: Hammerschmidt, Matthias
last_name: Hammerschmidt
- 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: Yunjin
full_name: Jiang, Yunjin
last_name: Jiang
- first_name: Donald
full_name: Kane, Donald
last_name: Kane
- first_name: Robert
full_name: Kelsh, Robert
last_name: Kelsh
- first_name: Mary
full_name: Mullins, Mary
last_name: Mullins
- first_name: Jörg
full_name: Odenthal, Jörg
last_name: Odenthal
- first_name: Christiane
full_name: Nüsslein Volhard, Christiane
last_name: Nüsslein Volhard
citation:
ama: Whitfield T, Granato M, Van Eeden F, et al. Mutations affecting development
of the zebrafish inner ear and lateral line. Development. 1996;123:241-254.
doi:10.1242/dev.123.1.241
apa: Whitfield, T., Granato, M., Van Eeden, F., Schach, U., Brand, M., Furutani
Seiki, M., … Nüsslein Volhard, C. (1996). Mutations affecting development of the
zebrafish inner ear and lateral line. Development. Company of Biologists.
https://doi.org/10.1242/dev.123.1.241
chicago: Whitfield, Tanya, Michael Granato, Fredericus Van Eeden, Ursula Schach,
Michael Brand, Makoto Furutani Seiki, Pascal Haffter, et al. “Mutations Affecting
Development of the Zebrafish Inner Ear and Lateral Line.” Development.
Company of Biologists, 1996. https://doi.org/10.1242/dev.123.1.241.
ieee: T. Whitfield et al., “Mutations affecting development of the zebrafish
inner ear and lateral line,” Development, vol. 123. Company of Biologists,
pp. 241–254, 1996.
ista: Whitfield T, Granato M, Van Eeden F, Schach U, Brand M, Furutani Seiki M,
Haffter P, Hammerschmidt M, Heisenberg C-PJ, Jiang Y, Kane D, Kelsh R, Mullins
M, Odenthal J, Nüsslein Volhard C. 1996. Mutations affecting development of the
zebrafish inner ear and lateral line. Development. 123, 241–254.
mla: Whitfield, Tanya, et al. “Mutations Affecting Development of the Zebrafish
Inner Ear and Lateral Line.” Development, vol. 123, Company of Biologists,
1996, pp. 241–54, doi:10.1242/dev.123.1.241.
short: T. Whitfield, M. Granato, F. Van Eeden, U. Schach, M. Brand, M. Furutani
Seiki, P. Haffter, M. Hammerschmidt, C.-P.J. Heisenberg, Y. Jiang, D. Kane, R.
Kelsh, M. Mullins, J. Odenthal, C. Nüsslein Volhard, Development 123 (1996) 241–254.
date_created: 2018-12-11T12:07:11Z
date_published: 1996-12-01T00:00:00Z
date_updated: 2022-08-08T08:45:59Z
day: '01'
doi: 10.1242/dev.123.1.241
extern: '1'
external_id:
pmid:
- '9007244'
intvolume: ' 123'
language:
- iso: eng
month: '12'
oa_version: None
page: 241 - 254
pmid: 1
publication: Development
publication_identifier:
issn:
- 0950-1991
publication_status: published
publisher: Company of Biologists
publist_id: '1979'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Mutations affecting development of the zebrafish inner ear and lateral line
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 123
year: '1996'
...
---
_id: '4151'
abstract:
- lang: eng
text: 'Jaws and branchial arches together are a basic, segmented feature of the
vertebrate head, Seven arches develop in the zebrafish embryo (Danio rerio), derived
largely from neural crest cells that form the cartilaginous skeleton, In this
and the following paper we describe the phenotypes of 109 arch mutants, focusing
here on three classes that affect the posterior pharyngeal arches, including the
hyoid and five gill-bearing arches, In lockjaw, the hyoid arch is strongly reduced
and subsets of branchial arches do not develop, Mutants of a large second class,
designated the flathead group, lack several adjacent branchial arches and their
associated cartilages. Five alleles at the flathead locus all lead to larvae that
lack arches 4-6, Among 34 other flathead group members complementation tests are
incomplete, but at least six unique phenotypes can be distinguished, These all
delete continuous stretches of adjacent branchial arches and unpaired cartilages
in the ventral midline, Many show cell death in the midbrain, from which some
neural crest precursors of the arches originate, lockjaw and a few mutants in
the flathead group, including pistachio, affect both jaw cartilage and pigmentation,
reflecting essential functions of these genes in at least two neural crest lineages,
Mutants of a third class, including boxer, dackel and pincher, affect pectoral
fins and axonal trajectories in the brain, as well as the arches. Their skeletal
phenotypes suggest that they disrupt cartilage morphogenesis in all arches, Our
results suggest that there are sets of genes that: (1) specify neural crest cells
in groups of adjacent head segments, and (2) function in common genetic pathways
in a variety of tissues including the brain, pectoral fins and pigment cells as
well as pharyngeal arches.'
acknowledgement: We thank Drs Charles Kimmel, Philip Ingham, Paula Mabee and members
of the Ingham lab for critical comments on the manuscript.
article_processing_charge: No
article_type: original
author:
- first_name: Thomas
full_name: Schilling, Thomas
last_name: Schilling
- first_name: Tatjana
full_name: Piotrowski, Tatjana
last_name: Piotrowski
- first_name: Heiner
full_name: Grandel, Heiner
last_name: Grandel
- first_name: Michael
full_name: Brand, Michael
last_name: Brand
- 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: Yunjin
full_name: Jiang, Yunjin
last_name: Jiang
- first_name: Dirk
full_name: Beuchle, Dirk
last_name: Beuchle
- first_name: Matthias
full_name: Hammerschmidt, Matthias
last_name: Hammerschmidt
- first_name: Donald
full_name: Kane, Donald
last_name: Kane
- first_name: Mary
full_name: Mullins, Mary
last_name: Mullins
- first_name: Fredericus
full_name: Van Eeden, Fredericus
last_name: Van Eeden
- first_name: Robert
full_name: Kelsh, Robert
last_name: Kelsh
- first_name: Makoto
full_name: Furutani Seiki, Makoto
last_name: Furutani Seiki
- first_name: Michael
full_name: Granato, Michael
last_name: Granato
- first_name: Pascal
full_name: Haffter, Pascal
last_name: Haffter
- first_name: Jörg
full_name: Odenthal, Jörg
last_name: Odenthal
- first_name: Rachel
full_name: Warga, Rachel
last_name: Warga
- first_name: Torsten
full_name: Trowe, Torsten
last_name: Trowe
- first_name: Christiane
full_name: Nüsslein Volhard, Christiane
last_name: Nüsslein Volhard
citation:
ama: 'Schilling T, Piotrowski T, Grandel H, et al. Jaw and branchial arch mutants
in zebrafish I: Branchial arches. Development. 1996;123(1):329-344. doi:10.1242/dev.123.1.329'
apa: 'Schilling, T., Piotrowski, T., Grandel, H., Brand, M., Heisenberg, C.-P. J.,
Jiang, Y., … Nüsslein Volhard, C. (1996). Jaw and branchial arch mutants in zebrafish
I: Branchial arches. Development. Company of Biologists. https://doi.org/10.1242/dev.123.1.329'
chicago: 'Schilling, Thomas, Tatjana Piotrowski, Heiner Grandel, Michael Brand,
Carl-Philipp J Heisenberg, Yunjin Jiang, Dirk Beuchle, et al. “Jaw and Branchial
Arch Mutants in Zebrafish I: Branchial Arches.” Development. Company of
Biologists, 1996. https://doi.org/10.1242/dev.123.1.329.'
ieee: 'T. Schilling et al., “Jaw and branchial arch mutants in zebrafish
I: Branchial arches,” Development, vol. 123, no. 1. Company of Biologists,
pp. 329–344, 1996.'
ista: 'Schilling T, Piotrowski T, Grandel H, Brand M, Heisenberg C-PJ, Jiang Y,
Beuchle D, Hammerschmidt M, Kane D, Mullins M, Van Eeden F, Kelsh R, Furutani
Seiki M, Granato M, Haffter P, Odenthal J, Warga R, Trowe T, Nüsslein Volhard
C. 1996. Jaw and branchial arch mutants in zebrafish I: Branchial arches. Development.
123(1), 329–344.'
mla: 'Schilling, Thomas, et al. “Jaw and Branchial Arch Mutants in Zebrafish I:
Branchial Arches.” Development, vol. 123, no. 1, Company of Biologists,
1996, pp. 329–44, doi:10.1242/dev.123.1.329.'
short: T. Schilling, T. Piotrowski, H. Grandel, M. Brand, C.-P.J. Heisenberg, Y.
Jiang, D. Beuchle, M. Hammerschmidt, D. Kane, M. Mullins, F. Van Eeden, R. Kelsh,
M. Furutani Seiki, M. Granato, P. Haffter, J. Odenthal, R. Warga, T. Trowe, C.
Nüsslein Volhard, Development 123 (1996) 329–344.
date_created: 2018-12-11T12:07:15Z
date_published: 1996-12-01T00:00:00Z
date_updated: 2022-08-08T08:41:00Z
day: '01'
doi: 10.1242/dev.123.1.329
extern: '1'
external_id:
pmid:
- '9007253'
intvolume: ' 123'
issue: '1'
language:
- iso: eng
month: '12'
oa_version: None
page: 329 - 344
pmid: 1
publication: Development
publication_identifier:
issn:
- 0950-1991
publication_status: published
publisher: Company of Biologists
publist_id: '1968'
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Jaw and branchial arch mutants in zebrafish I: Branchial arches'
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 123
year: '1996'
...
---
_id: '4154'
abstract:
- lang: eng
text: As part of a large scale chemical mutagenesis screen of the zebrafish (Danio
rerio) genome, we have identified 33 mutants with defects in hematopoiesis, Complementation
analysis placed 32 of these mutants into 17 complementation groups, The allelism
of the remaining 1 blood mutant is currently unresolved, We have categorized these
blood mutants into four phenotypic classes based on analyses of whole embryos
and isolated blood cells, as well as by in situ hybridization using the hematopoietic
transcription factors GATA-1 and GATA-2, Embryos mutant for the gene moonshine
have few if any proerythroblasts visible on the day circulation begins and normal
erythroid cell differentiation is blocked as determined by staining for hemoglobin
and GATA-1 expression, Mutations in five genes, chablis, frascati, merlot, retsina,
thunderbird and two possibly unique mutations cause a progressive decrease in
the number of blood cells during the first 5 days of development, Mutations in
another seven genes, chardonnay, chianti, grenache, sauternes, weibherbst and
zinfandel, and two additional mutations result in hypochromic blood cells which
also decrease in number as development proceeds, Several of these mutants have
immature cells in the circulation, indicating a block in normal erythroid development.
The mutation in zinfandel is dominant, and 2-day old heterozygous carriers fail
to express detectable levels of hemoglobin and have decreasing numbers of circulating
cells during the first 5 days of development, Mutations in two genes, freixenet
and yquem, result in the animals that are photosensitive with autofluorescent
blood, similar to that found in the human congenital porphyrias, The collection
of mutants presented here represent several steps required for normal erythropoiesis,
The analysis of these mutants provides a powerful approach towards defining the
molecular mechanisms involved in vertebrate hematopoietic development.
acknowledgement: 'We thank Leonard Zon for his generous support of D. G. R. and A.
B., for critical review of this manuscript and for many helpful discussions. We
also thank Lauren Barone and Stephen Pratt for technical assistance. D. G. R. is
a postdoctoral fellow of the Howard Hughes Medical Institute. '
article_processing_charge: No
article_type: original
author:
- first_name: David
full_name: Ransom, David
last_name: Ransom
- first_name: Pascal
full_name: Haffter, Pascal
last_name: Haffter
- first_name: Jörg
full_name: Odenthal, Jörg
last_name: Odenthal
- first_name: Alison
full_name: Brownlie, Alison
last_name: Brownlie
- first_name: Elisabeth
full_name: Vogelsang, Elisabeth
last_name: Vogelsang
- first_name: Robert
full_name: Kelsh, Robert
last_name: Kelsh
- first_name: Michael
full_name: Brand, Michael
last_name: Brand
- first_name: Fredericus
full_name: Van Eeden, Fredericus
last_name: Van Eeden
- first_name: Makoto
full_name: Furutani Seiki, Makoto
last_name: Furutani Seiki
- first_name: Michael
full_name: Granato, Michael
last_name: Granato
- first_name: Matthias
full_name: Hammerschmidt, Matthias
last_name: Hammerschmidt
- 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: Yunjin
full_name: Jiang, Yunjin
last_name: Jiang
- first_name: Donald
full_name: Kane, Donald
last_name: Kane
- first_name: Mary
full_name: Mullins, Mary
last_name: Mullins
- first_name: Christiane
full_name: Nüsslein Volhard, Christiane
last_name: Nüsslein Volhard
citation:
ama: Ransom D, Haffter P, Odenthal J, et al. Characterization of zebrafish mutants
with defects in embryonic hematopoiesis. Development. 1996;123(1):311-319.
doi:10.1242/dev.123.1.311
apa: Ransom, D., Haffter, P., Odenthal, J., Brownlie, A., Vogelsang, E., Kelsh,
R., … Nüsslein Volhard, C. (1996). Characterization of zebrafish mutants with
defects in embryonic hematopoiesis. Development. Company of Biologists.
https://doi.org/10.1242/dev.123.1.311
chicago: Ransom, David, Pascal Haffter, Jörg Odenthal, Alison Brownlie, Elisabeth
Vogelsang, Robert Kelsh, Michael Brand, et al. “Characterization of Zebrafish
Mutants with Defects in Embryonic Hematopoiesis.” Development. Company
of Biologists, 1996. https://doi.org/10.1242/dev.123.1.311.
ieee: D. Ransom et al., “Characterization of zebrafish mutants with defects
in embryonic hematopoiesis,” Development, vol. 123, no. 1. Company of Biologists,
pp. 311–319, 1996.
ista: Ransom D, Haffter P, Odenthal J, Brownlie A, Vogelsang E, Kelsh R, Brand M,
Van Eeden F, Furutani Seiki M, Granato M, Hammerschmidt M, Heisenberg C-PJ, Jiang
Y, Kane D, Mullins M, Nüsslein Volhard C. 1996. Characterization of zebrafish
mutants with defects in embryonic hematopoiesis. Development. 123(1), 311–319.
mla: Ransom, David, et al. “Characterization of Zebrafish Mutants with Defects in
Embryonic Hematopoiesis.” Development, vol. 123, no. 1, Company of Biologists,
1996, pp. 311–19, doi:10.1242/dev.123.1.311.
short: D. Ransom, P. Haffter, J. Odenthal, A. Brownlie, E. Vogelsang, R. Kelsh,
M. Brand, F. Van Eeden, M. Furutani Seiki, M. Granato, M. Hammerschmidt, C.-P.J.
Heisenberg, Y. Jiang, D. Kane, M. Mullins, C. Nüsslein Volhard, Development 123
(1996) 311–319.
date_created: 2018-12-11T12:07:16Z
date_published: 1996-12-01T00:00:00Z
date_updated: 2022-08-08T08:23:35Z
day: '01'
doi: 10.1242/dev.123.1.311
extern: '1'
external_id:
pmid:
- '9007251'
intvolume: ' 123'
issue: '1'
language:
- iso: eng
month: '12'
oa_version: None
page: 311 - 319
pmid: 1
publication: Development
publication_identifier:
issn:
- 0950-1991
publication_status: published
publisher: Company of Biologists
publist_id: '1966'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Characterization of zebrafish mutants with defects in embryonic hematopoiesis
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 123
year: '1996'
...
---
_id: '4156'
abstract:
- lang: eng
text: 'In a large scale screen for mutants that affect the early development of
the zebrafish, 109 mutants were found that cause defects in the formation of the
jaw and the more posterior pharyngeal arches, Here we present the phenotypic description
and results of the complementation analysis of mutants belonging to two major
classes: (1) mutants with defects in the mandibular and hyoid arches and (2) mutants
with defects in cartilage differentiation and growth in all arches, Mutations
in four of the genes identified during the screen show specific defects in the
first two arches and leave the more posterior pharyngeal arches largely unaffected
(schmerle, sucker, hoover and sturgeon). In these mutants ventral components of
the mandibular and hyoid arches are reduced (Meckel''s cartilage and ceratohyal
cartilage) whereas dorsal structures (palato-quadrate and hyosymplectic cartilages)
are of normal size or enlarged, Thus, mutations in single genes cause defects
in the formation of first and second arch structures but also differentially affect
development of the dorsal and ventral structures within one arch. In 27 mutants
that define at least 8 genes, the differentiation of cartilage and growth is affected.
In hammerhead mutants particularly the mesodermally derived cartilages are reduced,
whereas jellyfish mutant larvae are characterized by a severe reduction of all
cartilaginous elements, leaving only two pieces in the position of the ceratohyal
cartilages. In all other mutant larvae all skeletal elements are present, but
consist of smaller and disorganized chondrocytes. These mutants also exhibit shortened
heads and reduced pectoral fins. In homozygous knorrig embryos, tumor-like outgrowths
of chondrocytes occur along the edges of all cartilaginous elements. The mutants
presented here may be valuable tools for elucidating the genetic mechanisms that
underlie the development of the mandibular and the hyoid arches, as well as the
process of cartilage differentiation.'
acknowledgement: We would like to thank Siegfried Roth, Stefan Schulte-Merker and
Tanya Whitfield for critically reading the manuscript.
article_processing_charge: No
article_type: original
author:
- first_name: Tatjana
full_name: Piotrowski, Tatjana
last_name: Piotrowski
- first_name: Thomas
full_name: Schilling, Thomas
last_name: Schilling
- first_name: Michael
full_name: Brand, Michael
last_name: Brand
- first_name: Yunjin
full_name: Jiang, Yunjin
last_name: Jiang
- 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: Dirk
full_name: Beuchle, Dirk
last_name: Beuchle
- first_name: Heiner
full_name: Grandel, Heiner
last_name: Grandel
- first_name: Fredericus
full_name: Van Eeden, Fredericus
last_name: Van Eeden
- first_name: Makoto
full_name: Furutani Seiki, Makoto
last_name: Furutani Seiki
- first_name: Michael
full_name: Granato, Michael
last_name: Granato
- first_name: Pascal
full_name: Haffter, Pascal
last_name: Haffter
- first_name: Matthias
full_name: Hammerschmidt, Matthias
last_name: Hammerschmidt
- first_name: Donald
full_name: Kane, Donald
last_name: Kane
- first_name: Robert
full_name: Kelsh, Robert
last_name: Kelsh
- first_name: Mary
full_name: Mullins, Mary
last_name: Mullins
- first_name: Jörg
full_name: Odenthal, Jörg
last_name: Odenthal
- first_name: Rachel
full_name: Warga, Rachel
last_name: Warga
- first_name: Christiane
full_name: Nüsslein Volhard, Christiane
last_name: Nüsslein Volhard
citation:
ama: 'Piotrowski T, Schilling T, Brand M, et al. Jaw and branchial arch mutants
in zebrafish II: Anterior arches and cartilage differentiation. Development.
1996;123(1):345-356. doi:10.1242/dev.123.1.345'
apa: 'Piotrowski, T., Schilling, T., Brand, M., Jiang, Y., Heisenberg, C.-P. J.,
Beuchle, D., … Nüsslein Volhard, C. (1996). Jaw and branchial arch mutants in
zebrafish II: Anterior arches and cartilage differentiation. Development.
Company of Biologists. https://doi.org/10.1242/dev.123.1.345'
chicago: 'Piotrowski, Tatjana, Thomas Schilling, Michael Brand, Yunjin Jiang, Carl-Philipp
J Heisenberg, Dirk Beuchle, Heiner Grandel, et al. “Jaw and Branchial Arch Mutants
in Zebrafish II: Anterior Arches and Cartilage Differentiation.” Development.
Company of Biologists, 1996. https://doi.org/10.1242/dev.123.1.345.'
ieee: 'T. Piotrowski et al., “Jaw and branchial arch mutants in zebrafish
II: Anterior arches and cartilage differentiation,” Development, vol. 123,
no. 1. Company of Biologists, pp. 345–356, 1996.'
ista: 'Piotrowski T, Schilling T, Brand M, Jiang Y, Heisenberg C-PJ, Beuchle D,
Grandel H, Van Eeden F, Furutani Seiki M, Granato M, Haffter P, Hammerschmidt
M, Kane D, Kelsh R, Mullins M, Odenthal J, Warga R, Nüsslein Volhard C. 1996.
Jaw and branchial arch mutants in zebrafish II: Anterior arches and cartilage
differentiation. Development. 123(1), 345–356.'
mla: 'Piotrowski, Tatjana, et al. “Jaw and Branchial Arch Mutants in Zebrafish II:
Anterior Arches and Cartilage Differentiation.” Development, vol. 123,
no. 1, Company of Biologists, 1996, pp. 345–56, doi:10.1242/dev.123.1.345.'
short: T. Piotrowski, T. Schilling, M. Brand, Y. Jiang, C.-P.J. Heisenberg, D. Beuchle,
H. Grandel, F. Van Eeden, M. Furutani Seiki, M. Granato, P. Haffter, M. Hammerschmidt,
D. Kane, R. Kelsh, M. Mullins, J. Odenthal, R. Warga, C. Nüsslein Volhard, Development
123 (1996) 345–356.
date_created: 2018-12-11T12:07:17Z
date_published: 1996-12-01T00:00:00Z
date_updated: 2022-08-08T08:13:07Z
day: '01'
doi: 10.1242/dev.123.1.345
extern: '1'
external_id:
pmid:
- '9007254 '
intvolume: ' 123'
issue: '1'
language:
- iso: eng
month: '12'
oa_version: None
page: 345 - 356
pmid: 1
publication: Development
publication_identifier:
issn:
- 0950-1991
publication_status: published
publisher: Company of Biologists
publist_id: '1963'
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Jaw and branchial arch mutants in zebrafish II: Anterior arches and cartilage
differentiation'
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 123
year: '1996'
...
---
_id: '4164'
abstract:
- lang: eng
text: In a large-scale screen for mutants with defects in embryonic development
we identified 17 genes (65 mutants) specifically required for the development
of xanthophores, We provide evidence that these genes are required for three different
aspects of xanthophore development, (1) Pigment cell formation and migration (pfeffer
and salt); (2) pigment synthesis (edison, yobo, yocca and brie) and (3) pigment
translocation (esrom, tilsit and tofu). The number of xanthophore cells that appear
in the body is reduced in embryos with mutations in the two genes, salt and pfeffer.
In heterozygous and homozygous salt and pfeffer adults, the melanophore stripes
are interrupted, indicating that xanthophore cells have an important function
in adult melanophore pattern formation, Most other genes affect only larval pigmentation,
In embryos mutant for edison, yobo, yocca and brie, differences in pteridine synthesis
can be observed under UV light and by thin-layer chromatography. Homozygous mutant
females of yobo show a recessive maternal effect, Embryonic development is slowed
down and embryos display head and tail truncations, Xanthophores in larvae mutant
in the three genes esrom, tilsit and tofu appear less spread out, In addition,
these mutants display a defect in retinotectal axon pathfinding, These mutations
may affect xanthophore pigment distribution within the cells or xanthophore cell
shape, Mutations in seven genes affecting xanthophore pigmentation remain unclassified.
acknowledgement: We thank Silke Rudolph for technical assistance, Joel Wilson and
Cornelia Fricke for their help in the fish work and the thin layer chromatography,
and Darren Gilmour for help with the manuscript.
article_processing_charge: No
article_type: original
author:
- first_name: Jörg
full_name: Odenthal, Jörg
last_name: Odenthal
- first_name: Karin
full_name: Rossnagel, Karin
last_name: Rossnagel
- first_name: Pascal
full_name: Haffter, Pascal
last_name: Haffter
- first_name: Robert
full_name: Kelsh, Robert
last_name: Kelsh
- first_name: Elisabeth
full_name: Vogelsang, Elisabeth
last_name: Vogelsang
- first_name: Michael
full_name: Brand, Michael
last_name: Brand
- first_name: Fredericus
full_name: Van Eeden, Fredericus
last_name: Van Eeden
- first_name: Makoto
full_name: Furutani Seiki, Makoto
last_name: Furutani Seiki
- first_name: Michael
full_name: Granato, Michael
last_name: Granato
- first_name: Matthias
full_name: Hammerschmidt, Matthias
last_name: Hammerschmidt
- 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: Yunjin
full_name: Jiang, Yunjin
last_name: Jiang
- first_name: Donald
full_name: Kane, Donald
last_name: Kane
- first_name: Mary
full_name: Mullins, Mary
last_name: Mullins
- first_name: Christiane
full_name: Nüsslein Volhard, Christiane
last_name: Nüsslein Volhard
citation:
ama: Odenthal J, Rossnagel K, Haffter P, et al. Mutations affecting xanthophore
pigmentation in the zebrafish, Danio rerio. Development. 1996;123(1):391-398.
doi:10.1242/dev.123.1.391
apa: Odenthal, J., Rossnagel, K., Haffter, P., Kelsh, R., Vogelsang, E., Brand,
M., … Nüsslein Volhard, C. (1996). Mutations affecting xanthophore pigmentation
in the zebrafish, Danio rerio. Development. Company of Biologists. https://doi.org/10.1242/dev.123.1.391
chicago: Odenthal, Jörg, Karin Rossnagel, Pascal Haffter, Robert Kelsh, Elisabeth
Vogelsang, Michael Brand, Fredericus Van Eeden, et al. “Mutations Affecting Xanthophore
Pigmentation in the Zebrafish, Danio Rerio.” Development. Company of Biologists,
1996. https://doi.org/10.1242/dev.123.1.391.
ieee: J. Odenthal et al., “Mutations affecting xanthophore pigmentation in
the zebrafish, Danio rerio,” Development, vol. 123, no. 1. Company of Biologists,
pp. 391–398, 1996.
ista: Odenthal J, Rossnagel K, Haffter P, Kelsh R, Vogelsang E, Brand M, Van Eeden
F, Furutani Seiki M, Granato M, Hammerschmidt M, Heisenberg C-PJ, Jiang Y, Kane
D, Mullins M, Nüsslein Volhard C. 1996. Mutations affecting xanthophore pigmentation
in the zebrafish, Danio rerio. Development. 123(1), 391–398.
mla: Odenthal, Jörg, et al. “Mutations Affecting Xanthophore Pigmentation in the
Zebrafish, Danio Rerio.” Development, vol. 123, no. 1, Company of Biologists,
1996, pp. 391–98, doi:10.1242/dev.123.1.391.
short: J. Odenthal, K. Rossnagel, P. Haffter, R. Kelsh, E. Vogelsang, M. Brand,
F. Van Eeden, M. Furutani Seiki, M. Granato, M. Hammerschmidt, C.-P.J. Heisenberg,
Y. Jiang, D. Kane, M. Mullins, C. Nüsslein Volhard, Development 123 (1996) 391–398.
date_created: 2018-12-11T12:07:20Z
date_published: 1996-12-01T00:00:00Z
date_updated: 2022-08-08T08:08:51Z
day: '01'
doi: 10.1242/dev.123.1.391
extern: '1'
external_id:
pmid:
- '9007257 '
intvolume: ' 123'
issue: '1'
language:
- iso: eng
month: '12'
oa_version: None
page: 391 - 398
pmid: 1
publication: Development
publication_identifier:
issn:
- 0950-1991
publication_status: published
publisher: Company of Biologists
publist_id: '1955'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Mutations affecting xanthophore pigmentation in the zebrafish, Danio rerio
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 123
year: '1996'
...
---
_id: '4166'
abstract:
- lang: eng
text: In a large scale screen for mutants with defects in the embryonic development
of the zebrafish we identified mutations in four genes, floating head (flh), memo
(mom), no tail (ntl), and dec, that are required for early notochord formation.
Mutations in flh and ntl have been described previously, while mom and doe are
newly identified genes. Mutant mom embryos lack a notochord in the trunk, and
trunk somites from the right and left side of the embryo fuse underneath the neural
tube. In this respect morn appears similar to flh. In contrast, notochord precursor
cells are present in both ntl and doc embryos. In order to gain a greater understanding
of the phenotypes, we have analysed the expression of several axial mesoderm markers
in mutant embryos of all four genes. In flh and mom, Ntl expression is normal
in the germ ring and tailbud, while the expression of Nd and other notochord markers
in the axial mesodermal region is disrupted. Nd expression is normal in doc embryos
until early semitic stages, when there is a reduction in expression which is first
seen in anterior regions of the embryo. This suggests a function for doc in the
maintenance of ntl expression. Other notochord markers such as twist, sonic hedgehog
and axial are not expressed in the axial mesoderm of ntl embryos, their expression
parallels the expression of ntl in the axial mesoderm of mutant doc,flh and mom
embryos, indicating that ntl is required for the expression of these markers.
The role of doc in the expression of the notochord markers appears indirect via
ntl. Floor plate formation is disrupted in most regions in flh and mom mutant
embryos but is present in mutant ntl and doc embryos. In mutant embryos with strong
ntl alleles the band of cells expressing floor plate markers is broadened. A similar
broadening is also observed in the axial mesoderm underlying the floor plate of
ntl embryos, suggesting a direct involvement of the notochord precursor cells
in floor plate induction. Mutations in al of these four genes result in embryos
lacking a horizontal myoseptum and muscle pioneer cells, both of which are thought
to be induced by the notochord. These somite defects can be traced back to an
impairment of the specification of the adaxial cells during early stages of development.
Transplantation of wild-type cells into mutant doc embryos reveals that wild-type
notochord cells are sufficient to induce horizontal myoseptum formation in the
flanking mutant tissue. Thus dec, like flh and ntl, acts cell autonomously in
the notochord. In addition to the four mutants with defects in early notochord
formation, we have isolated 84 mutants, defining at least 15 genes, with defects
in later stages of notochord development. These are listed in an appendix to this
study.
acknowledgement: We thank Bob Riggleman for providing the twist probe prior to publication,
William Talbot, Anne Melby, Marnie Halpern and Chuck Kimmel for communicating results
prior to publication, Bill Trevarrow for the flhn1 allele, Stefan Schulte-Merker
for providing the ntl antibody, and N. H. Patel for providing the Eng antibody (4D9).
We thank Klaus Trummler, Frank Uhlmann and Mathias Metz for assistance in the analysis
of the ntl alleles, Silke Rudolph for technical assistance, Heike Schauerte for
helping with the in situ hybridization, and Joel Wilson and Cornelia Fricke for
their help with the fish work, and finally Tanya Whitfield, Francisco Pelegri, Darren
Gilmour and Stefan Schulte-Merker for discussion and help with the manuscript.
article_processing_charge: No
article_type: original
author:
- first_name: Jörg
full_name: Odenthal, Jörg
last_name: Odenthal
- first_name: Pascal
full_name: Haffter, Pascal
last_name: Haffter
- first_name: Elisabeth
full_name: Vogelsang, Elisabeth
last_name: Vogelsang
- first_name: Michael
full_name: Brand, Michael
last_name: Brand
- first_name: Fredericus
full_name: Van Eeden, Fredericus
last_name: Van Eeden
- first_name: Makoto
full_name: Furutani Seiki, Makoto
last_name: Furutani Seiki
- first_name: Michael
full_name: Granato, Michael
last_name: Granato
- first_name: Matthias
full_name: Hammerschmidt, Matthias
last_name: Hammerschmidt
- 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: Yunjin
full_name: Jiang, Yunjin
last_name: Jiang
- first_name: Donald
full_name: Kane, Donald
last_name: Kane
- first_name: Robert
full_name: Kelsh, Robert
last_name: Kelsh
- first_name: Mary
full_name: Mullins, Mary
last_name: Mullins
- first_name: Rachel
full_name: Warga, Rachel
last_name: Warga
- first_name: Miguel
full_name: Allende, Miguel
last_name: Allende
- first_name: Eric
full_name: Weinberg, Eric
last_name: Weinberg
- first_name: Christiane
full_name: Nüsslein Volhard, Christiane
last_name: Nüsslein Volhard
citation:
ama: Odenthal J, Haffter P, Vogelsang E, et al. Mutations affecting the formation
of the notochord in the zebrafish, Danio rerio. Development. 1996;123(1):103-115.
doi:10.1242/dev.123.1.103
apa: Odenthal, J., Haffter, P., Vogelsang, E., Brand, M., Van Eeden, F., Furutani
Seiki, M., … Nüsslein Volhard, C. (1996). Mutations affecting the formation of
the notochord in the zebrafish, Danio rerio. Development. Company of Biologists.
https://doi.org/10.1242/dev.123.1.103
chicago: Odenthal, Jörg, Pascal Haffter, Elisabeth Vogelsang, Michael Brand, Fredericus
Van Eeden, Makoto Furutani Seiki, Michael Granato, et al. “Mutations Affecting
the Formation of the Notochord in the Zebrafish, Danio Rerio.” Development.
Company of Biologists, 1996. https://doi.org/10.1242/dev.123.1.103.
ieee: J. Odenthal et al., “Mutations affecting the formation of the notochord
in the zebrafish, Danio rerio,” Development, vol. 123, no. 1. Company of
Biologists, pp. 103–115, 1996.
ista: Odenthal J, Haffter P, Vogelsang E, Brand M, Van Eeden F, Furutani Seiki M,
Granato M, Hammerschmidt M, Heisenberg C-PJ, Jiang Y, Kane D, Kelsh R, Mullins
M, Warga R, Allende M, Weinberg E, Nüsslein Volhard C. 1996. Mutations affecting
the formation of the notochord in the zebrafish, Danio rerio. Development. 123(1),
103–115.
mla: Odenthal, Jörg, et al. “Mutations Affecting the Formation of the Notochord
in the Zebrafish, Danio Rerio.” Development, vol. 123, no. 1, Company of
Biologists, 1996, pp. 103–15, doi:10.1242/dev.123.1.103.
short: J. Odenthal, P. Haffter, E. Vogelsang, M. Brand, F. Van Eeden, M. Furutani
Seiki, M. Granato, M. Hammerschmidt, C.-P.J. Heisenberg, Y. Jiang, D. Kane, R.
Kelsh, M. Mullins, R. Warga, M. Allende, E. Weinberg, C. Nüsslein Volhard, Development
123 (1996) 103–115.
date_created: 2018-12-11T12:07:21Z
date_published: 1996-12-01T00:00:00Z
date_updated: 2022-08-08T08:06:12Z
day: '01'
doi: 10.1242/dev.123.1.103
extern: '1'
external_id:
pmid:
- '9007233'
intvolume: ' 123'
issue: '1'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://journals.biologists.com/dev/article/123/1/103/39325/Mutations-affecting-the-formation-of-the-notochord
month: '12'
oa: 1
oa_version: Published Version
page: 103 - 115
pmid: 1
publication: Development
publication_identifier:
issn:
- 0950-1991
publication_status: published
publisher: Company of Biologists
publist_id: '1954'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Mutations affecting the formation of the notochord in the zebrafish, Danio
rerio
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 123
year: '1996'
...
---
_id: '4170'
abstract:
- lang: eng
text: We identified 6 genes that are essential for specifying ventral regions of
the early zebrafish embryo, Mutations in these genes cause an expansion of structures
normally derived from dorsal-lateral regions of the blastula at the expense of
ventrally derived structures, A series of phenotypes of varied strengths is observed
with different alleles of these mutants, The weakest phenotype is a reduction
in the ventral tail fin, observed as a dominant phenotype of swirl, piggytail,
and somitabun and a recessive phenotype of min fin, lost-a-fin and some piggytail
alleles, With increasing phenotypic strength, the blood and pronephric anlagen
are also reduced or absent, while the paraxial mesoderm and anterior neuroectoderm
is progressively expanded, In the strong phenotypes, displayed by homozygous embryos
of snailhouse, swirl and somitabun, the somites circle around the embryo and the
midbrain region is expanded laterally, Several mutations in this group of genes
are semidominant as well as recessive indicating a strong dosage sensitivity of
the processes involved, Mutations in the piggytail gene display an unusual dominance
that depends on both a maternal and zygotic heterozygous genotype, while somitabun
is a fully penetrant dominant maternal-effect mutation, The similar and overlapping
phenotypes of mutants of the 6 genes identified suggest that they function in
a common pathway, which begins in oogenesis, but also depends on factors provided
after the onset of zygotic transcription, presumably during blastula stages, This
pathway provides ventral positional information, counteracting the dorsalizing
instructions of the organizer, which is localized in the dorsal shield.
acknowledgement: 'We would like to thank: Eric Weinberg, and David Ransom and Leonard
Zon for providing the myoD and gata1 cDNA clone, respectively, prior to publication;
David Ransom for pointing out the histological blood staining method; J. S. Joly
for the eve1 cDNA clone; Mary Ellen Lane, Siegfried Roth, Stefan Schulte-Merker,
Herbert Steinbeiser for helpful comments on the manuscript; and very special thanks
to Karin Finger-Miller for technical support, as well as to Hans-Martin Maischein,
Amanda Wilson, Jörg Zeller, and Cosima Fabian. This work was supported by an NIH
postdoctoral fellowship to M. C. M.'
article_processing_charge: No
article_type: original
author:
- first_name: Mary
full_name: Mullins, Mary
last_name: Mullins
- first_name: Matthias
full_name: Hammerschmidt, Matthias
last_name: Hammerschmidt
- first_name: Donald
full_name: Kane, Donald
last_name: Kane
- first_name: Jörg
full_name: Odenthal, Jörg
last_name: Odenthal
- first_name: Michael
full_name: Brand, Michael
last_name: Brand
- first_name: Fredericus
full_name: Van Eeden, Fredericus
last_name: Van Eeden
- first_name: Makoto
full_name: Furutani Seiki, Makoto
last_name: Furutani Seiki
- first_name: Michael
full_name: Granato, Michael
last_name: Granato
- first_name: Pascal
full_name: Haffter, Pascal
last_name: Haffter
- 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: Yunjin
full_name: Jiang, Yunjin
last_name: Jiang
- first_name: Robert
full_name: Kelsh, Robert
last_name: Kelsh
- first_name: Christiane
full_name: Nüsslein Volhard, Christiane
last_name: Nüsslein Volhard
citation:
ama: 'Mullins M, Hammerschmidt M, Kane D, et al. Genes establishing dorsoventral
pattern formation in the zebrafish embryo: The ventral specifying genes. Development.
1996;123(1):81-93. doi:10.1242/dev.123.1.81'
apa: 'Mullins, M., Hammerschmidt, M., Kane, D., Odenthal, J., Brand, M., Van Eeden,
F., … Nüsslein Volhard, C. (1996). Genes establishing dorsoventral pattern formation
in the zebrafish embryo: The ventral specifying genes. Development. Company
of Biologists. https://doi.org/10.1242/dev.123.1.81'
chicago: 'Mullins, Mary, Matthias Hammerschmidt, Donald Kane, Jörg Odenthal, Michael
Brand, Fredericus Van Eeden, Makoto Furutani Seiki, et al. “Genes Establishing
Dorsoventral Pattern Formation in the Zebrafish Embryo: The Ventral Specifying
Genes.” Development. Company of Biologists, 1996. https://doi.org/10.1242/dev.123.1.81.'
ieee: 'M. Mullins et al., “Genes establishing dorsoventral pattern formation
in the zebrafish embryo: The ventral specifying genes,” Development, vol.
123, no. 1. Company of Biologists, pp. 81–93, 1996.'
ista: 'Mullins M, Hammerschmidt M, Kane D, Odenthal J, Brand M, Van Eeden F, Furutani
Seiki M, Granato M, Haffter P, Heisenberg C-PJ, Jiang Y, Kelsh R, Nüsslein Volhard
C. 1996. Genes establishing dorsoventral pattern formation in the zebrafish embryo:
The ventral specifying genes. Development. 123(1), 81–93.'
mla: 'Mullins, Mary, et al. “Genes Establishing Dorsoventral Pattern Formation in
the Zebrafish Embryo: The Ventral Specifying Genes.” Development, vol.
123, no. 1, Company of Biologists, 1996, pp. 81–93, doi:10.1242/dev.123.1.81.'
short: M. Mullins, M. Hammerschmidt, D. Kane, J. Odenthal, M. Brand, F. Van Eeden,
M. Furutani Seiki, M. Granato, P. Haffter, C.-P.J. Heisenberg, Y. Jiang, R. Kelsh,
C. Nüsslein Volhard, Development 123 (1996) 81–93.
date_created: 2018-12-11T12:07:22Z
date_published: 1996-12-01T00:00:00Z
date_updated: 2022-08-05T12:01:06Z
day: '01'
doi: 10.1242/dev.123.1.81
extern: '1'
external_id:
pmid:
- '9007231'
intvolume: ' 123'
issue: '1'
language:
- iso: eng
month: '12'
oa_version: None
page: 81 - 93
pmid: 1
publication: Development
publication_identifier:
issn:
- 0950-1991
publication_status: published
publisher: Company of Biologists
publist_id: '1951'
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Genes establishing dorsoventral pattern formation in the zebrafish embryo:
The ventral specifying genes'
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 123
year: '1996'
...
---
_id: '4186'
abstract:
- lang: eng
text: 'Neural crest development involves cell-fate specification, proliferation,
patterned cell migration, survival and differentiation, Zebrafish neural crest
derivatives include three distinct chromatophores, which are well-suited to genetic
analysis of their development, As part of a large-scale mutagenesis screen for
embryonic/early larval mutations, we have isolated 285 mutations affecting all
aspects of zebrafish larval pigmentation, By complementation analysis, we define
94 genes, We show here that comparison of their phenotypes permits classification
of these mutations according to the types of defects they cause, and these suggest
which process of neural crest development is probably affected, Mutations in eight
genes affect the number of chromatophores: these include strong candidates for
genes necessary for the processes of pigment cell specification and proliferation,
Mutations in five genes remove part of the wild-type pigment pattern, and suggest
a role in larval pigment pattern formation, Mutations in five genes show ectopic
chromatophores in distinct sites, and may have implications for chromatophore
patterning and proliferation, 76 genes affect pigment or morphology of one or
more chromatophore types: these mutations include strong candidates for genes
important in various aspects of chromatophore differentiation and survival, In
combination with the embryological advantages of zebrafish, these mutations should
permit cellular and molecular dissection of many aspects of neural crest development.'
acknowledgement: We wish to thank Drs Judith Eisen, Steve Johnson, Dave Raible and
Jim Weston for valuable comments. R. N. K. was supported by a NATO Postdoctoral
Fellowship.
article_processing_charge: No
article_type: original
author:
- first_name: Robert
full_name: Kelsh, Robert
last_name: Kelsh
- first_name: Michael
full_name: Brand, Michael
last_name: Brand
- first_name: Yunjin
full_name: Jiang, Yunjin
last_name: Jiang
- 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: Shuo
full_name: Lin, Shuo
last_name: Lin
- first_name: Pascal
full_name: Haffter, Pascal
last_name: Haffter
- first_name: Jörg
full_name: Odenthal, Jörg
last_name: Odenthal
- first_name: Mary
full_name: Mullins, Mary
last_name: Mullins
- first_name: Fredericus
full_name: Van Eeden, Fredericus
last_name: Van Eeden
- first_name: Makoto
full_name: Furutani Seiki, Makoto
last_name: Furutani Seiki
- first_name: Michael
full_name: Granato, Michael
last_name: Granato
- first_name: Matthias
full_name: Hammerschmidt, Matthias
last_name: Hammerschmidt
- first_name: Donald
full_name: Kane, Donald
last_name: Kane
- first_name: Rachel
full_name: Warga, Rachel
last_name: Warga
- first_name: Dirk
full_name: Beuchle, Dirk
last_name: Beuchle
- first_name: Lisa
full_name: Vogelsang, Lisa
last_name: Vogelsang
- first_name: Christiane
full_name: Nüsslein Volhard, Christiane
last_name: Nüsslein Volhard
citation:
ama: Kelsh R, Brand M, Jiang Y, et al. Zebrafish pigmentation mutations and the
processes of neural crest development. Development. 1996;123(1):369-389.
doi:10.1242/dev.123.1.369
apa: Kelsh, R., Brand, M., Jiang, Y., Heisenberg, C.-P. J., Lin, S., Haffter, P.,
… Nüsslein Volhard, C. (1996). Zebrafish pigmentation mutations and the processes
of neural crest development. Development. Company of Biologists. https://doi.org/10.1242/dev.123.1.369
chicago: Kelsh, Robert, Michael Brand, Yunjin Jiang, Carl-Philipp J Heisenberg,
Shuo Lin, Pascal Haffter, Jörg Odenthal, et al. “Zebrafish Pigmentation Mutations
and the Processes of Neural Crest Development.” Development. Company of
Biologists, 1996. https://doi.org/10.1242/dev.123.1.369.
ieee: R. Kelsh et al., “Zebrafish pigmentation mutations and the processes
of neural crest development,” Development, vol. 123, no. 1. Company of
Biologists, pp. 369–389, 1996.
ista: Kelsh R, Brand M, Jiang Y, Heisenberg C-PJ, Lin S, Haffter P, Odenthal J,
Mullins M, Van Eeden F, Furutani Seiki M, Granato M, Hammerschmidt M, Kane D,
Warga R, Beuchle D, Vogelsang L, Nüsslein Volhard C. 1996. Zebrafish pigmentation
mutations and the processes of neural crest development. Development. 123(1),
369–389.
mla: Kelsh, Robert, et al. “Zebrafish Pigmentation Mutations and the Processes of
Neural Crest Development.” Development, vol. 123, no. 1, Company of Biologists,
1996, pp. 369–89, doi:10.1242/dev.123.1.369.
short: R. Kelsh, M. Brand, Y. Jiang, C.-P.J. Heisenberg, S. Lin, P. Haffter, J.
Odenthal, M. Mullins, F. Van Eeden, M. Furutani Seiki, M. Granato, M. Hammerschmidt,
D. Kane, R. Warga, D. Beuchle, L. Vogelsang, C. Nüsslein Volhard, Development
123 (1996) 369–389.
date_created: 2018-12-11T12:07:28Z
date_published: 1996-12-01T00:00:00Z
date_updated: 2022-08-05T11:16:49Z
day: '01'
doi: 10.1242/dev.123.1.369
extern: '1'
external_id:
pmid:
- '9007256 '
intvolume: ' 123'
issue: '1'
language:
- iso: eng
month: '12'
oa_version: None
page: 369 - 389
pmid: 1
publication: Development
publication_identifier:
issn:
- 0950-1991
publication_status: published
publisher: Company of Biologists
publist_id: '1933'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Zebrafish pigmentation mutations and the processes of neural crest development
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 123
year: '1996'
...
---
_id: '4188'
abstract:
- lang: eng
text: 'Epiboly, the enveloping of the yolk cell by the blastoderm, is the first
zebrafish morphogenetic movement, We isolated four mutations that affect epiboly:
half baked, avalanche, lawine and weg, Homozygous mutant embryos arrest the vegetal
progress of the deep cells of the blastoderm; only the yolk syncytial layer of
the yolk cell and the enveloping layer of the blastoderm reach the vegetal pole
of the embryo, The mutations half baked, avalanche and lawine produce a novel
dominant effect, termed a zygotic-maternal dominant effect: heterozygous embryos
produced from heterozygous females slow down epiboly and accumulate detached cells
over the neural tube; a small fraction of these mutant individuals are viable,
Heterozygous embryos produced from heterozygous males crossed to homozygous wild-type
females complete epiboly normally and are completely viable. Additionally, embryos
heterozygous for half baked have an enlarged hatching gland, a partial dominant
phenotype, The phenotypes of these mutants demonstrate that, for the spreading
of cells during epiboly, the movement of the deep cells of the blastoderm require
the function of genes that are not necessary for the movement of the enveloping
layer or the yolk cell, Furthermore, the dominant zygotic-maternal effect phenotypes
illustrate the maternal and zygotic interplay of genes that orchestrate the early
cell movements of the zebrafish.'
acknowledgement: We thank Drs John Postlethwait and Sigfreid Roth for their helpful
comments on earlier drafts of this paper. This work was supported in part by a grant
from the National Institutes of Health to D. A. K.
article_processing_charge: No
article_type: original
author:
- first_name: Donald
full_name: Kane, Donald
last_name: Kane
- first_name: Matthias
full_name: Hammerschmidt, Matthias
last_name: Hammerschmidt
- first_name: Mary
full_name: Mullins, Mary
last_name: Mullins
- first_name: Hans
full_name: Maischein, Hans
last_name: Maischein
- first_name: Michael
full_name: Brand, Michael
last_name: Brand
- first_name: Fredericus
full_name: Van Eeden, Fredericus
last_name: Van Eeden
- first_name: Makoto
full_name: Furutani Seiki, Makoto
last_name: Furutani Seiki
- first_name: Michael
full_name: Granato, Michael
last_name: Granato
- first_name: Pascal
full_name: Haffter, Pascal
last_name: Haffter
- 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: Yunjin
full_name: Jiang, Yunjin
last_name: Jiang
- first_name: Robert
full_name: Kelsh, Robert
last_name: Kelsh
- first_name: Jörg
full_name: Odenthal, Jörg
last_name: Odenthal
- first_name: Rachel
full_name: Warga, Rachel
last_name: Warga
- first_name: Christiane
full_name: Nüsslein Volhard, Christiane
last_name: Nüsslein Volhard
citation:
ama: Kane D, Hammerschmidt M, Mullins M, et al. The zebrafish epiboly mutants. Development.
1996;123(1):47-55. doi:10.1242/dev.123.1.47
apa: Kane, D., Hammerschmidt, M., Mullins, M., Maischein, H., Brand, M., Van Eeden,
F., … Nüsslein Volhard, C. (1996). The zebrafish epiboly mutants. Development.
Company of Biologists. https://doi.org/10.1242/dev.123.1.47
chicago: Kane, Donald, Matthias Hammerschmidt, Mary Mullins, Hans Maischein, Michael
Brand, Fredericus Van Eeden, Makoto Furutani Seiki, et al. “The Zebrafish Epiboly
Mutants.” Development. Company of Biologists, 1996. https://doi.org/10.1242/dev.123.1.47 .
ieee: D. Kane et al., “The zebrafish epiboly mutants,” Development,
vol. 123, no. 1. Company of Biologists, pp. 47–55, 1996.
ista: Kane D, Hammerschmidt M, Mullins M, Maischein H, Brand M, Van Eeden F, Furutani
Seiki M, Granato M, Haffter P, Heisenberg C-PJ, Jiang Y, Kelsh R, Odenthal J,
Warga R, Nüsslein Volhard C. 1996. The zebrafish epiboly mutants. Development.
123(1), 47–55.
mla: Kane, Donald, et al. “The Zebrafish Epiboly Mutants.” Development, vol.
123, no. 1, Company of Biologists, 1996, pp. 47–55, doi:10.1242/dev.123.1.47 .
short: D. Kane, M. Hammerschmidt, M. Mullins, H. Maischein, M. Brand, F. Van Eeden,
M. Furutani Seiki, M. Granato, P. Haffter, C.-P.J. Heisenberg, Y. Jiang, R. Kelsh,
J. Odenthal, R. Warga, C. Nüsslein Volhard, Development 123 (1996) 47–55.
date_created: 2018-12-11T12:07:29Z
date_published: 1996-12-01T00:00:00Z
date_updated: 2022-08-05T09:22:40Z
day: '01'
doi: '10.1242/dev.123.1.47 '
extern: '1'
external_id:
pmid:
- '9007228 '
intvolume: ' 123'
issue: '1'
language:
- iso: eng
month: '12'
oa_version: None
page: 47 - 55
pmid: 1
publication: Development
publication_identifier:
issn:
- 0950-1991
publication_status: published
publisher: Company of Biologists
publist_id: '1930'
quality_controlled: '1'
scopus_import: '1'
status: public
title: The zebrafish epiboly mutants
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 123
year: '1996'
...
---
_id: '4189'
abstract:
- lang: eng
text: 'This report describes mutants of the zebrafish having phenotypes causing
a general arrest in early morphogenesis. These mutants identify a group of loci
making up about 20% of the loci identified by mutants with visible morphological
phenotypes within the first day of development. There are 12 Class I mutants,
which fall into 5 complementation groups and have cells that lyse before morphological
defects are observed. Mutants at three loci, speed bump, ogre and zombie, display
abnormal nuclei. The 8 Class II mutants, which fall into 6 complementation groups,
arrest development before cell lysis is observed. These mutants seemingly stop
development in the late segmentation stages, and maintain a body shape similar
to a 20 hour embryo. Mutations in speed bump, ogre, zombie, specter, poltergeist
and troll were tested for cell lethality by transplanting mutant cells into wild-type
hosts. With poltergeist, transplanted mutant cells all survive. The remainder
of the mutants tested were autonomously but conditionally lethal: mutant cells,
most of which lyse, sometimes survive to become notochord, muscles, or, in rare
cases, large neurons, all cell types which become postmitotic in the gastrula.
Some of the genes of the early arrest group may be necessary for progression though
the cell cycle; if so, the survival of early differentiating cells may be based
on having their terminal mitosis before the zygotic requirement for these genes.'
acknowledgement: We thank Dr Adam Felsenfeld for his careful comments on earlier drafts
of this manuscript, D. A. K. also thanks the two anonymous referees who patiently
pointed out a number of ‘speed bumps’ in the first submitted draft of this manuscript.
This work was supported in part by a grant from the National Institutes of Health
to D. A. K.
article_processing_charge: No
article_type: original
author:
- first_name: Donald
full_name: Kane, Donald
last_name: Kane
- first_name: Hans
full_name: Maischein, Hans
last_name: Maischein
- first_name: Michael
full_name: Brand, Michael
last_name: Brand
- first_name: Fredericus
full_name: Van Eeden, Fredericus
last_name: Van Eeden
- first_name: Makoto
full_name: Furutani Seiki, Makoto
last_name: Furutani Seiki
- first_name: Michael
full_name: Granato, Michael
last_name: Granato
- first_name: Pascal
full_name: Haffter, Pascal
last_name: Haffter
- first_name: Matthias
full_name: Hammerschmidt, Matthias
last_name: Hammerschmidt
- 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: Yunjin
full_name: Jiang, Yunjin
last_name: Jiang
- first_name: Robert
full_name: Kelsh, Robert
last_name: Kelsh
- first_name: Mary
full_name: Mullins, Mary
last_name: Mullins
- first_name: Jörg
full_name: Odenthal, Jörg
last_name: Odenthal
- first_name: Rachel
full_name: Warga, Rachel
last_name: Warga
- first_name: Christiane
full_name: Nüsslein Volhard, Christiane
last_name: Nüsslein Volhard
citation:
ama: Kane D, Maischein H, Brand M, et al. The zebrafish early arrest mutants. Development.
1996;123(1):57-66. doi:10.1242/dev.123.1.57
apa: Kane, D., Maischein, H., Brand, M., Van Eeden, F., Furutani Seiki, M., Granato,
M., … Nüsslein Volhard, C. (1996). The zebrafish early arrest mutants. Development.
Company of Biologists. https://doi.org/10.1242/dev.123.1.57
chicago: Kane, Donald, Hans Maischein, Michael Brand, Fredericus Van Eeden, Makoto
Furutani Seiki, Michael Granato, Pascal Haffter, et al. “The Zebrafish Early Arrest
Mutants.” Development. Company of Biologists, 1996. https://doi.org/10.1242/dev.123.1.57 .
ieee: D. Kane et al., “The zebrafish early arrest mutants,” Development,
vol. 123, no. 1. Company of Biologists, pp. 57–66, 1996.
ista: Kane D, Maischein H, Brand M, Van Eeden F, Furutani Seiki M, Granato M, Haffter
P, Hammerschmidt M, Heisenberg C-PJ, Jiang Y, Kelsh R, Mullins M, Odenthal J,
Warga R, Nüsslein Volhard C. 1996. The zebrafish early arrest mutants. Development.
123(1), 57–66.
mla: Kane, Donald, et al. “The Zebrafish Early Arrest Mutants.” Development,
vol. 123, no. 1, Company of Biologists, 1996, pp. 57–66, doi:10.1242/dev.123.1.57 .
short: D. Kane, H. Maischein, M. Brand, F. Van Eeden, M. Furutani Seiki, M. Granato,
P. Haffter, M. Hammerschmidt, C.-P.J. Heisenberg, Y. Jiang, R. Kelsh, M. Mullins,
J. Odenthal, R. Warga, C. Nüsslein Volhard, Development 123 (1996) 57–66.
date_created: 2018-12-11T12:07:29Z
date_published: 1996-12-01T00:00:00Z
date_updated: 2022-08-05T09:43:44Z
day: '01'
doi: '10.1242/dev.123.1.57 '
extern: '1'
external_id:
pmid:
- '9007229 '
intvolume: ' 123'
issue: '1'
language:
- iso: eng
month: '12'
oa_version: None
page: 57 - 66
pmid: 1
publication: Development
publication_identifier:
issn:
- 0950-1991
publication_status: published
publisher: Company of Biologists
publist_id: '1931'
quality_controlled: '1'
scopus_import: '1'
status: public
title: The zebrafish early arrest mutants
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 123
year: '1996'
...