|Start Date / Time||October 10, 2018 at 9:00 AM|
|End Date / Time||October 10, 2018 at 10:00 AM|
|Location||9455 MRB IV|
|Presenter Name||James Patton, Ph.D.|
|Presentation Title||The miR-216a-Dot1l regulatory axis is necessary and sufficient for Müller glia reprogramming during retina regeneration|
|Status||This meeting has already occurred|
Unlike the adult mammalian retina, Müller glia (MG) in the adult zebrafish retina are able to dedifferentiate into a ‘stem cell’-like state and give rise to multipotent progenitor cells upon retinal damage. We show that miR-216a is downregulated in MG after constant intense light lesioning and that miR-216a suppression is necessary and sufficient for MG dedifferentiation and proliferation during retina regeneration. miR-216a targets the H3K79 methyltransferase Dot1l which is upregulated in proliferating MG after retinal damage. Loss-of-function experiments show that Dot1l is necessary for MG reprogramming and mediates MG proliferation downstream of miR-216a. We further demonstrate that miR-216a and Dot1l regulate MG-mediated retina regeneration through canonical Wnt signaling. Together, our study reports a novel regulatory mechanism upstream of Wnt signaling during retina regeneration and provides potential targets for enhancing regeneration in the adult mammalian retina.