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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.

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