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Zic5 stabilizes Gli3 via a non-transcriptional mechanism during retinal development

  1. Author:
    Sun,Jian
    Yoon,Jaeho
    Lee,Moonsup
    Lee,Hyun Kyung
    Hwang,Rich Yooseok
    Daar,Ira

  2. Author Address

    Cancer and Developmental Biology Laboratory, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Frederick, MD 21702, USA., Cancer and Developmental Biology Laboratory, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Frederick, MD 21702, USA. Electronic address: daari@mail.nih.gov.,
    1. Year: 2022
    2. Date: Feb 01
  2. Journal: Cell Reports
    1. 38
    2. 5
  4. Type of Article: Article
  5. Article Number: 110312
  1. Abstract:

    The Zic family of zinc finger transcription factors plays a critical role in multiple developmental processes. Using loss-of-function studies, we find that Zic5 is important for the differentiation of retinal pigmented epithelium (RPE) and the rod photoreceptor layer through suppressing Hedgehog (Hh) signaling. Further, Zic5 interacts with the critical Hh signaling molecule, Gli3, through the zinc finger domains of both proteins. This Zic5-Gli3 interaction disrupts Gli3/Gli3 homodimerization, resulting in Gli3 protein stabilization via a reduction in Gli3 ubiquitination. During embryonic Hh signaling, the activator form of Gli is normally converted to a repressor form through proteosome-mediated processing of Gli3, and the ratio of Gli3 repressor to full-length (activator) form of Gli3 determines the Gli3 repressor output required for normal eye development. Our results suggest Zic5 is a critical player in regulating Gli3 stability for the proper differentiation of RPE and rod photoreceptor layer during Xenopus eye development. Copyright © 2022. Published by Elsevier Inc.

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External Sources

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  2. DOI: 10.1016/j.celrep.2022.110312
  3. PMID: 35108539
  4. PII : S2211-1247(22)00024-9

Library Notes

  1. Fiscal Year: FY2021-2022
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