| Literature DB >> 33004674 |
Thanh Hoang1, Jie Wang2, Patrick Boyd3,4,5, Fang Wang2, Clayton Santiago1, Lizhi Jiang1, Sooyeon Yoo1, Manuela Lahne3,4,5, Levi J Todd6, Meng Jia3,4,5, Cristian Saez1, Casey Keuthan7, Isabella Palazzo6, Natalie Squires6, Warren A Campbell6, Fatemeh Rajaii2, Trisha Parayil1, Vickie Trinh1, Dong Won Kim1, Guohua Wang2, Leah J Campbell3,4,5, John Ash7, Andy J Fischer6, David R Hyde8,4,5, Jiang Qian9, Seth Blackshaw10,2,11,12,13,14.
Abstract
Injury induces retinal Müller glia of certain cold-blooded vertebrates, but not those of mammals, to regenerate neurons. To identify gene regulatory networks that reprogram Müller glia into progenitor cells, we profiled changes in gene expression and chromatin accessibility in Müller glia from zebrafish, chick, and mice in response to different stimuli. We identified evolutionarily conserved and species-specific gene networks controlling glial quiescence, reactivity, and neurogenesis. In zebrafish and chick, the transition from quiescence to reactivity is essential for retinal regeneration, whereas in mice, a dedicated network suppresses neurogenic competence and restores quiescence. Disruption of nuclear factor I transcription factors, which maintain and restore quiescence, induces Müller glia to proliferate and generate neurons in adult mice after injury. These findings may aid in designing therapies to restore retinal neurons lost to degenerative diseases.Entities:
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Year: 2020 PMID： 33004674 PMCID： PMC7899183 DOI： 10.1126/science.abb8598
Source DB: PubMed Journal: Science ISSN： 0036-8075 Impact factor: 63.714