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Mid-gestational lethality in mice lacking keratin 8

H Baribault1, J Price, K Miyai

  • 1La Jolla Cancer Research Foundation, California 92037.

Genes & Development
|July 1, 1993
PubMed
Summary
This summary is machine-generated.

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Keratin 8 (mK8) and keratin 18 (mK18) are crucial for early mouse development. Loss of mK8 causes severe embryonic growth defects and mid-gestational lethality, highlighting its vital role in fetal liver integrity.

Area of Science:

  • Developmental Biology
  • Cell Biology
  • Molecular Biology

Background:

  • Keratin 8 (mK8) and keratin 18 (mK18) are the initial intermediate filament proteins expressed during mouse embryogenesis.
  • These keratins are present in various extraembryonic and embryonic simple epithelia, including trophectoderm, visceral yolk sac, and developing organs like the gastrointestinal tract, lungs, mammary glands, and uterus.

Purpose of the Study:

  • To investigate the function of keratin 8 (mK8) during mouse embryogenesis.
  • To determine the consequences of a targeted null mutation in the mK8 gene on embryonic development and survival.

Main Methods:

  • Generation of a targeted null mutation in the mouse keratin 8 (mK8) gene.
  • Analysis of embryonic development, including growth, survival, and internal organ morphology at mid-gestation.

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Main Results:

  • Targeted deletion of the mK8 gene resulted in mid-gestational lethality in mutant embryos.
  • Mutant embryos exhibited growth retardation and significant internal bleeding, with abnormal erythrocyte accumulation in fetal livers.
  • The mK8- phenotype demonstrated high penetrance (94%), with a small number of mice surviving to adulthood.

Conclusions:

  • Keratin 8 (mK8) and keratin 18 (mK18) filaments are essential for maintaining the integrity of the fetal liver during mouse development.
  • The function of mK8 in mouse development differs from simple epithelium keratins in Xenopus at the gastrulation stage, underscoring a vital role for mK8 at 12 days postcoitum in mice.