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Notch signaling via Hey1 and Id2b regulates Müller glia’s regenerative response to retinal injury

dc.contributor.authorSahu, Aresh
dc.contributor.authorDevi, Sulochana
dc.contributor.authorJui, Jonathan
dc.contributor.authorGoldman, Daniel
dc.date.accessioned2021-11-02T00:46:44Z
dc.date.available2023-01-01 20:46:41en
dc.date.available2021-11-02T00:46:44Z
dc.date.issued2021-12
dc.identifier.citationSahu, Aresh; Devi, Sulochana; Jui, Jonathan; Goldman, Daniel (2021). "Notch signaling via Hey1 and Id2b regulates Müller glia’s regenerative response to retinal injury." Glia 69(12): 2882-2898.
dc.identifier.issn0894-1491
dc.identifier.issn1098-1136
dc.identifier.urihttps://hdl.handle.net/2027.42/170858
dc.description.abstractZebrafish Müller glia (MG) respond to retinal injury by suppressing Notch signaling and producing progenitors for retinal repair. A certain threshold of injury‐derived signal must be exceeded in order to engage MG in a regenerative response (MG’s injury‐response threshold). Pan‐retinal Notch inhibition expands the zone of injury‐responsive MG at the site of focal injury, suggesting that Notch signaling regulates MG’s injury‐response threshold. We found that Notch signaling enhanced chromatin accessibility and gene expression at a subset of regeneration‐associated genes in the uninjured retina. Two Notch effector genes, hey1 and id2b, were identified that reflect bifurcation of the Notch signaling pathway, and differentially regulate MG’s injury‐response threshold and proliferation of MG‐derived progenitors. Furthermore, Notch signaling component gene repression in the injured retina suggests a role for Dll4, Dlb, and Notch3 in regulating Notch signaling in MG and epistasis experiments confirm that the Dll4/Dlb‐Notch3‐Hey1/Id2b signaling pathway regulates MG’s injury‐response threshold and proliferation.Main PointsNotch represses chromatin accessibility & the expression of regeneration‐associated genes in the uninjured retina.Hey1 regulates Müller glia’s injury‐response threshold; Hey1 & id2b regulate proliferation of Müller glia‐derived progenitors.
dc.publisherJohn Wiley & Sons, Inc.
dc.subject.otherAscl1
dc.subject.otherdll4
dc.subject.othernotch3
dc.subject.otherreprogramming
dc.subject.otherstem cell
dc.subject.otherzebrafish
dc.titleNotch signaling via Hey1 and Id2b regulates Müller glia’s regenerative response to retinal injury
dc.typeArticle
dc.rights.robotsIndexNoFollow
dc.subject.hlbsecondlevelMolecular, Cellular and Developmental Biology
dc.subject.hlbsecondlevelNeurosciences
dc.subject.hlbsecondlevelPublic Health
dc.subject.hlbtoplevelHealth Sciences
dc.subject.hlbtoplevelScience
dc.description.peerreviewedPeer Reviewed
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/170858/1/glia24075_am.pdf
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/170858/2/glia24075.pdf
dc.identifier.doi10.1002/glia.24075
dc.identifier.sourceGlia
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