Delayed embryonic development and impaired cell growth and survival in Actg1 null mice

Tina M. Bunnell, James M. Ervasti

Research output: Contribution to journalArticlepeer-review

54 Scopus citations


10.1002/cm.20467.absActins are among the most highly expressed proteins in eukaryotes and play a central role in nearly all aspects of cell biology. While the intricate process of development undoubtedly requires a properly regulated actin cytoskeleton, little is known about the contributions of different actin isoforms during embryogenesis. Of the six actin isoforms, only the two cytoplasmic actins, βcyto- and γcyto-actin, are ubiquitously expressed. We found that γcyto-actin null (Actg1-/-) mice were fully viable during embryonic development, but most died within 48 h of birth due to respiratory failure and cannibalization by the parents. While no morphogenetic defects were identified, Actg1-/- mice exhibited stunted growth during embryonic and postnatal development as well as delayed cardiac outflow tract formation that resolved by birth. Using primary mouse embryonic fibroblasts, we confirm that γcyto-actin is not required for cell migration. The Actg1-/- cells, however, exhibited growth impairment and reduced cell viability, defects which perhaps contribute to the stunted growth and developmental delays observed in Actg1-/- embryos. Since the total amount of actin protein was maintained in Actg1-/- cells, our data suggests a distinct requirement for γcyto-actin in cell growth and survival.

Original languageEnglish (US)
Pages (from-to)564-572
Number of pages9
Issue number9
StatePublished - Sep 2010


  • Actin isoforms
  • Cell migration
  • Cell viability
  • Murine embryonic development


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