Compensatory mechanisms render Tcf7l1a dispensable for eye formation despite its cell-autonomous requirement in eye field specification
Year: 2018
Type: preprint
Abstract: The vertebrate eye originates from the eyefield, a domain of cells specified by a small number of transcription factors. In this study, we show that Tcf7la is one such transcription factor that acts cell-autonomously to specify the eye field in zebrafish. Despite the much reduced eyefield 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 compensation by paralogous genes; 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.
DOI: 10.1101/377119
Authors: Rodrigo M. Young, Florencia Cavodeassi, Thomas A. Hawkins, Heather L. Stickney, Quenten Schwarz, Lisa M. Lawrence, Claudia Wierzbicki, Gaia Gestri, Elizabeth Ambrosio, Allison Klosner, Jasmine Rowell, Isaac H. Bianco, Miguel L. Allende, Stephen W. Wilson
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: green
OpenAlex ID: W2883177597