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Comparative transcriptomic and epigenomic analysis identifies key regulators of injury response and neurogenic competence in retinal glia

By Thanh Hoang, Jie Wang, Patrick Boyd, Fang Wang, Clayton Santiago, Lizhi Jiang, Manuela Lahne, Levi J. Todd, Cristian Saez, Sooyeon Yoo, Casey Keuthan, Isabella Palazzo, Natalie Squires, Warren A. Campbell, Meng Jia, Fatemeh Rajaii, Trisha Payail, Guohua Wang, John Ash, Andy J. Fischer, David R Hyde, Jiang Qian, Seth Blackshaw

Posted 30 Jul 2019
bioRxiv DOI: 10.1101/717876

Injury induces retinal Muller glia of cold-blooded, but not mammalian, vertebrates to generate neurons. To identify gene regulatory networks that control neurogenic competence in retinal glia, we comprehensively profiled injury-dependent changes in gene expression and chromatin conformation in Muller glia from zebrafish, chick and mice using bulk RNA and ATAC-Seq, as well as single-cell RNA-Seq. Integration of these data, together with functional analysis of candidate genes, identified evolutionarily conserved and species-specific gene networks controlling glial quiescence, gliosis, and neurogenic competence. In zebrafish and chick, transition from quiescence to gliosis is a critical stage in acquisition of neurogenic competence, while in mice a dedicated network suppresses this transition and rapidly restores quiescence. Selective disruption of NFI family transcription factors in mice, which maintain and restore quiescence, confers injury-dependent proliferative and neurogenic competence on Muller glia. These findings may help guide the design of cell-based therapies aimed at restoring retinal neurons lost in disease.

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