Plagl1 is part of the mammalian retinal injury response and a critical regulator of Muller glial cell quiescence
Touahri, Y.; David, L. A.; Ilnytskyy, Y.; van Oosten, E.; Hanna, J.; Tachibana, N.; Adnani, L.; Zhao, J.; Hoffman, M.; Dixit, R.; Journot, L.; Sauve, Y.; Kovalchuk, I.; Aubert, I.; Biernaskie, J.; Schuurmans, C.
Show abstract
Retinal damage triggers reactive gliosis in Muller glia across vertebrate species, but only in regenerative animals, such as teleost fish, do Muller glia initiate repair; proliferating and undergoing neurogenesis to replace lost cells. By mining scRNA-seq and bulk RNA-seq datasets, we found that Plagl1, a maternally imprinted gene, is dynamically regulated in reactive Muller glia post-insult, with transcript levels transiently increasing before stably declining. To study Plagl1 retinal function, we examined Plagl1+/-pat null mutants postnatally, revealing defects in retinal architecture, visual signal processing and a reactive gliotic phenotype. Plagl1+/-pat Muller glia proliferate ectopically and give rise to inner retinal neurons and photoreceptors. Transcriptomic and ATAC-seq profiles revealed similarities between Plagl1+/-pat retinas and neurodegenerative and injury models, including an upregulation of pro-gliogenic and pro-proliferative pathways, such as Notch, not observed in wild-type retinas Plagl1 is thus an essential component of the transcriptional regulatory networks that retain mammalian Muller glia in quiescence.
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