Developmental changes in the accessible chromatin, transcriptome and Ascl1-binding correlate with the loss in Müller Glial regenerative potential.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
12 08 2020
Historique:
received: 13 03 2020
accepted: 16 07 2020
entrez: 14 8 2020
pubmed: 14 8 2020
medline: 12 1 2021
Statut: epublish

Résumé

Diseases and damage to the retina lead to losses in retinal neurons and eventual visual impairment. Although the mammalian retina has no inherent regenerative capabilities, fish have robust regeneration from Müller glia (MG). Recently, we have shown that driving expression of Ascl1 in adult mouse MG stimulates neural regeneration. The regeneration observed in the mouse is limited in the variety of neurons that can be derived from MG; Ascl1-expressing MG primarily generate bipolar cells. To better understand the limits of MG-based regeneration in mouse retinas, we used ATAC- and RNA-seq to compare newborn progenitors, immature MG (P8-P12), and mature MG. Our analysis demonstrated developmental differences in gene expression and accessible chromatin between progenitors and MG, primarily in neurogenic genes. Overexpression of Ascl1 is more effective in reprogramming immature MG, than mature MG, consistent with a more progenitor-like epigenetic landscape in the former. We also used ASCL1 ChIPseq to compare the differences in ASCL1 binding in progenitors and reprogrammed MG. We find that bipolar-specific accessible regions are more frequently linked to bHLH motifs and ASCL1 binding. Overall, our analysis indicates a loss of neurogenic gene expression and motif accessibility during glial maturation that may prevent efficient reprogramming.

Identifiants

pubmed: 32788677
doi: 10.1038/s41598-020-70334-1
pii: 10.1038/s41598-020-70334-1
pmc: PMC7423883
doi:

Substances chimiques

Ascl1 protein, mouse 0
Basic Helix-Loop-Helix Transcription Factors 0
Chromatin 0

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

13615

Subventions

Organisme : NICHD NIH HHS
ID : T32 HD007183
Pays : United States
Organisme : NIGMS NIH HHS
ID : T32 GM007270
Pays : United States
Organisme : NEI NIH HHS
ID : R01 EY021482
Pays : United States

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Auteurs

Leah S VandenBosch (LS)

Department of Biological Structure, University of Washington, Box 357420, Seattle, WA, 98195, USA.
Molecular and Cellular Biology Program, University of Washington, Seattle, WA, USA.

Stefanie G Wohl (SG)

Department of Biological Structure, University of Washington, Box 357420, Seattle, WA, 98195, USA.
Department of Biological and Vision Sciences, College of Optometry, The State University of New York, New York, NY, USA.

Matthew S Wilken (MS)

Department of Biological Structure, University of Washington, Box 357420, Seattle, WA, 98195, USA.
Molecular and Cellular Biology Program, University of Washington, Seattle, WA, USA.

Marcus Hooper (M)

Department of Biological Structure, University of Washington, Box 357420, Seattle, WA, 98195, USA.

Connor Finkbeiner (C)

Department of Biological Structure, University of Washington, Box 357420, Seattle, WA, 98195, USA.

Kristen Cox (K)

Department of Biological Structure, University of Washington, Box 357420, Seattle, WA, 98195, USA.

Laura Chipman (L)

Department of Biological Structure, University of Washington, Box 357420, Seattle, WA, 98195, USA.

Thomas A Reh (TA)

Department of Biological Structure, University of Washington, Box 357420, Seattle, WA, 98195, USA. tomreh@uw.edu.
Institute for Stem Cells and Regenerative Medicine, University of Washington, Box 358056, Seattle, WA, 98109, USA. tomreh@uw.edu.

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