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
  • Zygote/metabolism
  • Animals
  • Male
  • Kinetics
  • Morphogenesis*
  • Phenotype
  • Transcription Factor 7-Like 1 Protein/genetics
  • Transcription Factor 7-Like 1 Protein/metabolism*
  • Cell Proliferation
  • Female
  • Prosencephalon/embryology
  • Mutation/genetics
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
  • Neural Plate/embryology
  • Neurogenesis
  • Eye/growth & development*
  • Eye/pathology
  • Gene Expression Regulation, Developmental
  • Up-Regulation/genetics
  • Zebrafish/embryology
  • Zebrafish/genetics
  • Zebrafish/growth & development*
  • Penetrance
  • Genetic Loci
  • Embryo, Nonmammalian/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)
Show all Figures
Expression
Phenotype
Fish Conditions Stage Phenotype Figure
WTresection: optic vesiclePrim-25
WTresection: optic vesiclePrim-25
WTresection: optic vesicleDay 4
WT + MO4-tcf7l1astandard conditionsBud
WT + MO4-tcf7l1astandard conditionsPrim-15
WT + MO4-tcf7l1a + MO5-tcf7l1bstandard conditionsLong-pec
WT + MO4-tcf7l1a + MO5-tcf7l1bstandard conditionsLong-pec
cct5u762/u762standard conditionsPrim-25
cct5u762/u762standard conditionsLong-pec
cct5u762/u762; rw021Tgstandard conditionsLong-pec
1 - 10 of 67
Show
Mutations / Transgenics
Allele Construct Type Affected Genomic Region
cu2TgTransgenic Insertion
    hi2972bTgTransgenic Insertion
    m881
      		Point Mutation
      rw021TgTransgenic Insertion
        u762
          		Point Mutation
          u768
            		Point Mutation
            u910
              		Small Deletion
              w32TgTransgenic Insertion
                zf157TgTransgenic Insertion
                zf460TgTransgenic Insertion
                  1 - 10 of 10
                  Show
                  Human Disease / Model
                  No data available
                  Sequence Targeting Reagents
                  Target Reagent Reagent Type
                  tcf7l1aMO4-tcf7l1aMRPHLNO
                  tcf7l1bMO5-tcf7l1bMRPHLNO
                  1 - 2 of 2
                  Show
                  Fish
                  Fish
                  cct5u762/u762
                  cct5u762/u762; rw021Tg
                  cct5u762/u762; tcf7l1am881/m881
                  cct5u762/u762; tcf7l1am881/m881; rw021Tg
                  cu2Tg
                  gdf6au768/u768
                  gdf6au768/u768; tcf7l1am881/m881
                  hesx1u910/u910
                  rw021Tg
                  tcf7l1am881/m881
                  1 - 10 of 19
                  Show
                  Antibodies
                  Orthology
                  No data available
                  Engineered Foreign Genes
                  Marker Marker Type Name
                  GFPEFGGFP
                  RFPEFGRFP
                  1 - 2 of 2
                  Show
                  Mapping
                  No data available
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                  Citation
                  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. (2019) Compensatory growth renders Tcf7l1a dispensable for eye formation despite its requirement in eye field specification. eLIFE. 8:.