MAPK14 Governs Mammalian Müller glia Fate Determination between Gliosis and Reprogramming [scRNA-Seq]
Irreversible loss of retinal neurons is the leading cause of blindness. Harnessing the latent stem cell potential of mammalian Müller glia offers a promising strategy for endogenous retinal regeneration. Shifting the Müller glia response from gliosis to regeneration after retinal injury is a critical step in promoting the orderly entry of Müller glia into a regenerative program. However, the molecular switch governing this divergent fate decision remains elusive. Here, through RNA-seq and scRNA-seq, we confirm the upstream determinant of Müller glia fate after retinal injury. Overall design: RNA sequencing was performed on MIO-M1 cells following MAPK14 or control siRNA treatment, as well as MAPK8+9 or control siRNA treatment, according to the manufacturer's instructions, to identify downstream signaling changes. To characterize the types of neurons regenerated in Adezmapimod-treated mice, we performed scRNA-seq) on fluorescence-activated cell sorting (FACS)-purified MG and their neuronal progeny 1 month after NMDA and Adezmapimod treatment.