The nrl and tbx2b share an epistatic relationship governing rod versus UV cone fate. Schematic of putative interaction of tbx2b repressing activation of nrl in otherwise UV cone fated cells. (A) In wildtype zebrafish, nrl is sufficient to induce the rod fate but is repressed by tbx2b in UV fated cells. (B) Loss of nrl expression leads to failure to develop rods and increase in UV cone production (N = 4), as cells fail to adopt the rod fate and instead take on a default UV cone program. (C) Loss of tbx2b releases nrl from repression, driving an excess of rod development in otherwise UV cone fated cells (N = 3). (D) Double mutants recapitulate the single nrl mutant phenotype, producing excess UV cones at the expense of rods (N = 5) as tbx2b is not needed to act on an already non-functional nrl. Together these results indicate that tbx2b is not required for UV cone development, but instead likely prevents nrl expression from imposing the rod fate on UV fated cells. Rods and UV cones detected with antibodies 4C12 and 10C9.1, respectively, label an unknown rod epitope and Sws1 opsin. * = P < 0.05, ** = P < 0.005, *** = P < 0.0005 significance as determined by unpaired t-test. Significance markers denote differences in abundance of each photoreceptor cell type relative to wildtype.
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