PUBLICATION

Compensatory growth renders Tcf7l1a dispensable for eye formation despite its requirement in eye field specification

Authors
Young, R.M., Hawkins, T.A., Cavodeassi, F., Stickney, H.L., Schwarz, Q., Lawrence, L.M., Wierzbicki, C., Cheng, B.Y., Luo, J., Ambrosio, E.M., Klosner, A., Sealy, I.M., Rowell, J., Trivedi, C.A., Bianco, I.H., Allende, M.L., Busch-Nentwich, E.M., Gestri, G., Wilson, S.W.
ID
ZDB-PUB-190220-2
Date
2019
Source
eLIFE   8: (Journal)
Registered Authors
Allende, Miguel L., Bianco, Isaac, Busch-Nentwich, Elisabeth, Cavodeassi, Florencia, Gestri, Gaia, Hawkins, Tom, Stickney, Heather, Trivedi, Chintan, Wierzbicki, Claudia, Wilson, Steve, Young, Rodrigo
Keywords
development, developmental biology, eye, genetics, tcf7l1, zebrafish
MeSH Terms
  • Morphogenesis*
  • Eye/growth & development*
  • Eye/pathology
  • Prosencephalon/embryology
  • Neurogenesis
  • Male
  • Cell Proliferation
  • Mutation/genetics
  • Phenotype
  • Female
  • Gene Expression Regulation, Developmental
  • Genetic Loci
  • Transcription Factor 7-Like 1 Protein/genetics
  • Transcription Factor 7-Like 1 Protein/metabolism*
  • Embryo, Nonmammalian/metabolism
  • Up-Regulation/genetics
  • Animals
  • Neural Plate/embryology
  • Kinetics
  • Zebrafish/embryology
  • Zebrafish/genetics
  • Zebrafish/growth & development*
  • Penetrance
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
  • Zygote/metabolism
(all 26)
PubMed
30777146 Full text @ Elife
Abstract
The vertebrate eye originates from the eye field, a domain of cells specified by a small number of transcription factors. In this study, we show that Tcf7l1a is one such transcription factor that acts cell-autonomously to specify the eye field in zebrafish. Despite the much-reduced eye field in tcf7l1a mutants, these fish develop normal eyes revealing a striking ability of the eye to recover from a severe early phenotype. This robustness is not mediated through genetic compensation at neural plate stage; instead, the smaller optic vesicle of tcf7l1a mutants shows delayed neurogenesis and continues to grow until it achieves approximately normal size. Although the developing eye is robust to the lack of Tcf7l1a function, it is sensitised to the effects of additional mutations. In support of this, a forward genetic screen identified mutations in hesx1, cct5 and gdf6a, which give synthetically enhanced eye specification or growth phenotypes when in combination with the tcf7l1a mutation.
Genes / Markers
Figures
Figure Gallery (9 images)
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
No data available
Sequence Targeting Reagents
Target Reagent Reagent Type
tcf7l1aMO4-tcf7l1aMRPHLNO
tcf7l1bMO5-tcf7l1bMRPHLNO
1 - 2 of 2
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Fish
Antibodies
Orthology
No data available
Engineered Foreign Genes
Marker Marker Type Name
GFPEFGGFP
RFPEFGRFP
1 - 2 of 2
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Mapping
No data available