Model for the role of Yap during zebrafish retina regeneration. (A) Relative gene expression of progenitor markers at 1 and 2 dpl (n = 4 biological replicates for 1 dpl; n = 7 biological replicates for 2 dpl) in DN-Yap+ versus DN-Yap− controls. ns, non-significant; *p < 0.05, **p < 0.01. Paired t-test for the relative gene expression of progenitor markers. (B) In the zebrafish model system, in response to a light-induced lesion, photoreceptors start to degenerate, and quiescent Müller glial cells (MGs) become activated in response to the insult. Activated MGs then undergo a reprogramming event, reentering the cell cycle, and dividing and producing a pool of progenitor cells that migrate to the lesion site and differentiate into new photoreceptors. Based on our findings, we propose a model for the role of Yap during MG reprogramming after photoreceptor damage. Our data suggest that Yap is required to regulate MG reprogramming possibly via a lin28a–ascl1a-dependent mechanism, being necessary for correct Sox2 + progenitor proliferation and photoreceptor differentiation. We suggest that Yap regulates lin28a expression; however, if ascl1a is also regulated by Yap or Lin28a, it still needs further investigation.
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