[대학원 생명과학과 세미나 안내]
연사 : 김진우 교수(KAIST 생명과학과)
연제 : Conventional and unconventional pathways of retinal regeneration
일시 : 2022년 10월 28일 (금) 오후 4시 30분
장소 : 하나과학관 A동 109호
초청교수 : 지성욱 교수
Abstract
Retinal neurons are generated during development and degenerate during lifetime. Degenerated cells can be replaced by new cells in many animal tissues that contain stem cells. However, given the absence of residual retinal stem cells, degenerated retinal neurons cannot be regenerated in the retina. However, retinal neurons can be regenerated from Müller glia (MG) in cold-blooded vertebrates upon the injury but not in in mammalian retina, highlighting the incompetency of mammalian MG for retinal regeneration. Previous studies have proposed the factors, which induce mammalian MG to proliferate after the retinal injury. Those include ß-catenin, Yes-associated protein (Yap), and achaete-scute homolog 1 (Ascl1), which however have limited capability to boost MG proliferation. We found that prospero-related homeobox (Prox1) accumulated in MG and suppresses injury-induced MG reprograming and proliferation in the injured mouse retina, but not in the regenerating zebrafish retina. Consistent with this, we succeeded in inducing proliferation of MG in the injured mouse retina by blocking the accumulation of Prox1. Conversely, we could suppress MG proliferation in the injured zebrafish retina by providing Prox1 externally. Collectively, our study suggests that MG proliferation and subsequent retinal neurogenesis in the injured mammalian retina can be recovered by eliminating PROX1 in MG by various therapeutic strategies.