RT Journal Article
SR Electronic
T1 Compensatory mechanisms render Tcf7l1a dispensable for eye formation despite its cell-autonomous requirement in eye field specification
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 377119
DO 10.1101/377119
A1 Rodrigo M. Young
A1 Florencia Cavodeassi
A1 Thomas A. Hawkins
A1 Heather L. Stickney
A1 Quenten Schwarz
A1 Lisa M. Lawrence
A1 Claudia Wierzbicki
A1 Gaia Gestri
A1 Elizabeth Ambrosio
A1 Allison Klosner
A1 Jasmine Rowell
A1 Isaac H. Bianco
A1 Miguel L. Allende
A1 Stephen W. Wilson
YR 2018
UL http://biorxiv.org/content/early/2018/08/25/377119.abstract
AB 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.