Dataset Information

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

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.

SUBMITTER: Young RM

PROVIDER: S-EPMC6380838 | biostudies-literature | 2019 Feb

REPOSITORIES: biostudies-literature

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

Young Rodrigo M RM Hawkins Thomas A TA Cavodeassi Florencia F Stickney Heather L HL Schwarz Quenten Q Lawrence Lisa M LM Wierzbicki Claudia C Cheng Bowie Yl BY Luo Jingyuan J Ambrosio Elizabeth Mayela EM Klosner Allison A Sealy Ian M IM Rowell Jasmine J Trivedi Chintan A CA Bianco Isaac H IH Allende Miguel L ML Busch-Nentwich Elisabeth M EM Gestri Gaia G Wilson Stephen W SW

eLife 20190219

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 <i>tcf7l1a</i> 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 neu ...[more]

PMID: 30777146

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Project description:BackgroundInsulin-producing beta cells emerge during pancreas development in two sequential waves. Recently described later-forming beta cells in zebrafish show high similarity to second wave mammalian beta cells in developmental capacity. Loss-of-function studies in mouse and zebrafish demonstrated that the homeobox transcription factors Pdx1 and Hb9 are both critical for pancreas and beta cell development and discrete stage-specific requirements for these genes have been uncovered. Previously, exocrine and endocrine cell recovery was shown to follow loss of pdx1 in zebrafish, but the progenitor cells and molecular mechanisms responsible have not been clearly defined. In addition, interactions of pdx1 and hb9 in beta cell formation have not been addressed.ResultsTo learn more about endocrine progenitor specification, we examined beta cell formation following morpholino-mediated depletion of pdx1 and hb9. We find that after early beta cell reduction, recovery occurs following loss of either pdx1 or hb9 function. Unexpectedly, simultaneous knockdown of both hb9 and pdx1 leads to virtually complete and persistent beta cell deficiency. We used a NeuroD:EGFP transgenic line to examine endocrine cell behavior in vivo and developed a novel live-imaging technique to document emergence and migration of late-forming endocrine precursors in real time. Our data show that Notch-responsive progenitors for late-arising endocrine cells are predominantly post mitotic and depend on pdx1. By contrast, early-arising endocrine cells are specified and differentiate independent of pdx1.ConclusionsThe nearly complete beta cell deficiency after combined loss of hb9 and pdx1 suggests functional cooperation, which we clarify as distinct roles in early and late endocrine cell formation. A novel imaging approach permitted visualization of the emergence of late endocrine cells within developing embryos for the first time. We demonstrate a pdx1-dependent progenitor population essential for the formation of duct-associated, second wave endocrine cells. We further reveal an unexpectedly low mitotic activity in these progenitor cells, indicating that they are set aside early in development.

Dataset Information

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

Publications

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

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