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Genetic background-dependent role of Egr1 for eyelid development.

  1. Author:
    Oh, Jangsuk
    Wang, Yujuan
    Chen, Shida
    Li, Peng
    Du, Ning
    Yu, Zu-Xi
    Butcher, Donna
    Gebregiorgis, Tesfay
    Strachan, Erin
    Lehmann, Ordan J
    Brooks, Brian P
    Chan, Chi-Chao
    Leonard, Warren J

  2. Author Address

    Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892., Immunology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892., Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892., Pathology Core, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892., Pathology/Histotechnology Laboratory, Leidos Biomedical Research, Inc., Frederick, MD 21702., Department of Medical Genetics, University of Alberta, Edmonton AB, Canada T6G 2H7., Ophthalmic Genetics and Visual Function Branch, National Eye Institute, National Institutes of Health, Bethesda, MD 20892., Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892; wjl@helix.nih.gov chanc@nei.nih.gov., Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892; wjl@helix.nih.gov chanc@nei.nih.gov.,
    1. Year: 2017
    2. Date: Aug 04
    3. Epub Date: 2017 Aug 04
  2. Journal: Proceedings of the National Academy of Sciences of the United States of America
    1. 114
    2. 34
    3. Pages: E7131-E7139
  4. Type of Article: Article
  5. ISSN: 0027-8424
  1. Abstract:

    EGR1 is an early growth response zinc finger transcription factor with broad actions, including in differentiation, mitogenesis, tumor suppression, and neuronal plasticity. Here we demonstrate that Egr1(-/-) mice on the C57BL/6 background have normal eyelid development, but back-crossing to BALB/c background for four or five generations resulted in defective eyelid development by day E15.5, at which time EGR1 was expressed in eyelids of WT mice. Defective eyelid formation correlated with profound ocular anomalies evident by postnatal days 1-4, including severe cryptophthalmos, microphthalmia or anophthalmia, retinal dysplasia, keratitis, corneal neovascularization, cataracts, and calcification. The BALB/c albino phenotype-associated Tyr(c) tyrosinase mutation appeared to contribute to the phenotype, because crossing the independent Tyr(c-2J) allele to Egr1(-/-) C57BL/6 mice also produced ocular abnormalities, albeit less severe than those in Egr1(-/-) BALB/c mice. Thus EGR1, in a genetic background-dependent manner, plays a critical role in mammalian eyelid development and closure, with subsequent impact on ocular integrity.

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External Sources

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  2. DOI: 10.1073/pnas.1705848114
  3. PMID: 28778995
  4. View record in Web of Science®
  5. WOS: 000408095300013

Library Notes

  1. Fiscal Year: FY2016-2017
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