| Popis: |
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 intcf7l1amutants, 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 oftcf7l1amutants 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 inhesx1, cct5andgdf6a, which give synthetically enhanced eye specification or growth phenotypes when in combination with thetcf7l1amutation. |
