Maf1 controls retinal neuron number by both RNA Pol III- and Pol II-dependent mechanisms.

ABSTRACT: The generation of appropriate numbers and types of neurons is a prerequisite for assembling functional neural circuits. However, the molecular basis regulating retinal neuron number remains poorly understood. Here, we report that inactivation of the RNA polymerase (Pol) III inhibitor gene Maf1 in mice results in decreased retinal thickness and neuron number that cause attenuated electroretinogram (ERG) responses. Its absence causes aberrant differentiation of all retinal neuron types primarily by an RNA Pol II-dependent mechanism while promoting retinal progenitor cell proliferation via both Pol III- and Pol II-dependent mechanisms. Chromatin profiling and transcription assay reveal that Maf1 binds widely to the genome to regulate the expression of a large set of Pol II-transcribed

SUBMITTER: Li Y 

PROVIDER: S-EPMC10711482 | biostudies-literature | 2023 Dec

REPOSITORIES: biostudies-literature