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The Fgf8 subfamily (Fgf8, Fgf17 and Fgf18) is required for closure of the embryonic ventral body wall

  1. Author:
    Boylan,Michael
    Anderson,Matthew
    Ornitz, David M
    Lewandoski,Mark [ORCID]
  2. Author Address

    Cancer and Developmental Biology Lab, National Cancer Institute, National Institutes of Health, Frederick, Maryland, USA., Department of Developmental Biology, Washington University School of Medicine, Saint Louis, Missouri, USA., Cancer and Developmental Biology Lab, National Cancer Institute, National Institutes of Health, Frederick, Maryland, USA lewandom@nih.gov.,
    1. Year: 2020
    2. Date: NOV
    3. Epub Date: 2020 09 09
  1. Journal: Development (Cambridge, England)
    1. 147
    2. 21
    3. Pages: pii: dev.189506
  2. Type of Article: Article
  3. Article Number: dev189506
  4. ISSN: 0950-1991
  1. Abstract:

    The closure of the embryonic ventral body wall in amniotes is an important morphogenetic event and is essential for life. Defects in human ventral wall closure are a major class of birth defect and a significant health burden. Despite this, very little is understood about how the ventral body wall is formed. Here we show that fibroblast growth factor (FGF) ligands FGF8, FGF17 and FGF18 are essential for this process. Conditional mutants for these genes display subtle migratory defects in the abdominal muscles of the ventral body wall and an enlarged umbilical ring, through which the internal organs are extruded. By refining where and when these genes are required using different Cre lines, we show that Fgf8 and Fgf17 are required in the presomitic mesoderm while Fgf18 is required in the somites. These studies identify complex and multifactorial origins of ventral wall defects and has important implications for understanding their origins during embryonic development. © 2020. Published by The Company of Biologists Ltd.

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External Sources

  1. DOI: 10.1242/dev.189506
  2. PMID: 32907848
  3. WOS: 000590574000017
  4. PII : dev.189506

Library Notes

  1. Fiscal Year: FY2020-2021
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