James Patton, Ph.D.
Professor of Biological Sciences, Cell and Developmental
Biology and Ophthalmology and Visual Sciences
Stevenson Chair of Biological Sciences


Record History
Added on August 31, 2018 at 2:12 PM by Uttz, Pam
Modified on October 5, 2018 at 10:27 AM by Uttz, Pam
Shared with (contributions)
Public: SPRING Meeting

Meeting Details

Start Date / Time October 10, 2018 at 9:00 AM
End Date / Time October 10, 2018 at 10:00 AM
Duration 1 hour(s)
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

Meeting Agenda/Notes

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.


Document Fall_2019_Email_Notice_Patton.pdf - Added on October 5, 2018 at 10:27 AM by Pam Uttz