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Math5 -null mutation results in the loss of retinal ganglion cells (RGCs) and in a concurrent increase of amacrine and cone cells. However, it remains unclear whether there is a cell fate switch of  Math5 -lineage cells in the absence of  Math5  and whether MATH5 cell-autonomously regulates the differentiation of the above retinal neurons. Here, we performed a lineage analysis of  Math5 -expressing cells in developing mouse retinas using a conditional GFP reporter (Z/EG) activated by a  Math5 - Cre  knock-in allele. We show that during normal retinogenesis,  Math5 -lineage cells mostly develop into RGCs, horizontal cells, cone photoreceptors, rod photoreceptors, and amacrine cells. Interestingly, amacrine cells of  Math5 -lineage cells are predominately of GABAergic, cholinergic, and A2 subtypes, indicating that  Math5  plays a role in amacrine subtype specification. In the absence of  Math5 , more  Math5 -lineage cells undergo cell fate conversion from RGCs to the above retinal cell subtypes, and occasionally to cone-bipolar cells and Müller cells. This change in cell fate choices is accompanied by an up-regulation of NEUROD1, RXRγ and BHLHB5, the transcription factors essential for the differentiation of retinal cells other than RGCs. Additionally, loss of  Math5  causes the failure of early progenitors to exit cell cycle and leads to a significant increase of  Math5 -lineage cells remaining in cell cycle. Collectively, these data suggest that  Math5  regulates the generation of multiple retinal cell types via different mechanisms during retinogenesis.

MATH5 controls the acquisition of multiple retinal cell fates