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Gene regulatory networks controlling vertebrate retinal regeneration
Author(s) -
Thanh Hoang,
Jie Wang,
Patrick Boyd,
Fang Wang,
Clayton P. Santiago,
Lizhi Jiang,
Sooyeon Yoo,
Manuela Lahne,
Levi Todd,
Meng Jia,
Cristian Saez Gonzalez,
Casey Keuthan,
Isabella Palazzo,
Natalie Squires,
Warren A. Campbell,
Fatemeh Rajaii,
Trisha Parayil,
Vickie Trinh,
Dong Won Kim,
Guohua Wang,
Leah J. Campbell,
John D. Ash,
Andy J. Fischer,
David R. Hyde,
Jiang Qian,
Seth Blackshaw
Publication year - 2020
Publication title -
science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 12.556
H-Index - 1186
eISSN - 1095-9203
pISSN - 0036-8075
DOI - 10.1126/science.abb8598
Subject(s) - muller glia , neurogenesis , biology , zebrafish , retinal regeneration , regeneration (biology) , microbiology and biotechnology , vertebrate , retinal , chromatin , progenitor cell , transcription factor , retina , gene regulatory network , neuroscience , gene , stem cell , gene expression , genetics , biochemistry
Unlocking retinal regeneration in mice Zebrafish can regenerate damaged retinal tissue, but mice cannot. Hoanget al. found that tracking changes in gene expression and chromatin accessibility upon injury revealed clues as to why retinal glial cells in zebrafish could generate new neurons but the same cell type in mice could not. In zebrafish, activated Müller glial cells shift into a proliferative phase, whereas in mice, a genetic network returns the glial cells to quiescence. A few transcription factors enforce quiescence in the mouse, and disruption of these allowed Müller glia to proliferate and generate new neurons after retinal injury.Science , this issue p.eabb8598

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