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.
Highlights
The paired optic vesicles originate from the eye field, a single, coherent group of cells located in the anterior neural plate (Cavodeassi, 2018)
Given that the wildtype splice site in intron seven is still present in tcf7l1a mutants, we assessed whether the lack of phenotype in MZtcf7l1a-/- mutants could be due to
We show that Tcf7l1a is required for cells to adopt eye field identity and express rx3, tcf7l1a mutants form normal, functional eyes
Summary
The paired optic vesicles originate from the eye field, a single, coherent group of cells located in the anterior neural plate (Cavodeassi, 2018). The specification and relative sizes of prospective forebrain territories, including the eye field, depend on the activity of the Wnt/b-Catenin and other signalling pathways (Beccari et al, 2013; Cavodeassi, 2014; Wilson and Houart, 2004). A number of genes have been identified as encoding a transcription factor network that specifies the eye field (Beccari et al, 2013; Zuber et al, 2003) These genes have been defined based on conserved cross species expression patterns in the anterior neuroectoderm and on phenotypes observed when overexpressed or when function is compromised (Beccari et al, 2013).
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