TheAtoh1-CreKnock-In Allele Ectopically Labels a Subpopulation of Amacrine Cells and Bipolar Cells in Mouse Retina

Abstract

AbstractThe retina has diverse neuronal cell types derived from a common pool of retinal progenitors. Many molecular drivers, mostly transcription factors, have been identified to promote different cell fates. InDrosophila,atonalis required for specifying photoreceptors. In mice, there are two closely relatedatonalhomologs,Atoh1andAtoh7. WhileAtoh7is known to promote the genesis of retinal ganglion cells, there is no study on the function ofAtoh1in retinal development. Here, we crossedAtoh1Cre/+mice to mice carrying a Cre-dependent TdTomato reporter to track potentialAtoh1-lineage neurons in retinas. We characterized a heterogeneous group of TdTomato+retinal neurons that were detected at the postnatal stage, including glutamatergic amacrine cells, AII amacrine cells, and BC3b bipolar cells. Unexpectedly, we did not observe TdTomato+retinal neurons in the mice with anAtoh1-FlpOknock-in allele and a Flp-dependent TdTomato reporter, suggestingAtoh1is not expressed in the mouse retina. Consistent with these data, conditional removal ofAtoh1in the retina did not cause any observable phenotypes. Importantly, we did not detectAtoh1expression in the retina at multiple ages using mice withAtoh1-GFPknock-in allele. Therefore, we conclude thatAtoh1Cre/+mice have ectopic Cre expression in the retina and thatAtoh1is not required for retinal development.