Targeted disruption of the gene encoding the proteolipid subunit of mouse vacuolar H+-ATPase leads to early embryonic lethality

Hiroki Inoue, Takato Noumi, Mitsuo Nagata, Hiroshi Murakami, Hiroshi Kanazawa

Research output: Contribution to journalArticle

64 Citations (Scopus)

Abstract

Vacuolar H+-ATPase (V-ATPase) is responsible for acidification of intracellular compartments in eukaryotic cells. Its 16-kDa subunit (proteolipid, PL16) plays a central role in V-ATPase function, forming the principal channel via which protons are translocated. To elucidate physiological roles of V-ATPase in mammalian cell function and embryogenesis, we attempted to generate a PL16 null mutant mouse by gene-targeting. Mice heterozygous (PL16(+/-)) for the proteolipid mutation were intercrossed and their offspring were classified according to genotype. There were no homozygous (PL16(-/-)) pups among 69 neonates examined, but a few PL16(-/-) embryos were found during the pre-implantation stages of embryonic development, up to day 3.5 post-coitum. These results suggested that PL16 (and hence V-ATPase) may play an essential role in cell proliferation and viability during early embryogenesis. PL16(+/-) mice were indistinguishable from their wild-type littermates and displayed no discernible abnormalities, although the PL16 mRNA level in PL16(+/-) mice decreased to about one-half of wild-type levels. Copyright (C) 1999 Elsevier Science B.V.

Original languageEnglish
Pages (from-to)130-138
Number of pages9
JournalBiochimica et Biophysica Acta - Bioenergetics
Volume1413
Issue number3
DOIs
Publication statusPublished - Nov 10 1999

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Cell Biology

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