Deletion of the imprinted gene Plagl1 activates the proliferative and regenerative capacity of mammalian Müller glia

To determine whether Plagl1 has an essential role in the postnatal retina, we used Plagl1+/-pat mice carrying a silenced maternal allele and a null mutation in the expressed paternal allele; these mice were previously confirmed to lack Plagl1 expression in various tissues, including the embryonic retina. Dysmorphologies were observed in Plagl1+/-pat retinas that phenocopied observations made in various mutant mice with underlying Müller glia defects. We thus examined Plagl1+/-pat retinas for signs of reactive gliosis, a stress-induced Müller glia response associated with cellular hypertrophy and increased expression of ERK signaling and reduced expression of Glul expression. In Figure 3 Western blots, we show the loss of Plagl1 induces Müller glia gliosis. (E) Western blotting for pERK in P14 wild-type and Plagl1+/-pat retinas showing increase in pERK protein levels. N=6 for both wild-type and Plagl1+/-pat retinas. (F) Western blotting for Glul in P14 wild-type and Plagl1+/-pat retinas showing decrease of Glul protein levels. N=6 for both wild-type and Plagl1+/-pat retinas.