Targeted disruption of fad24, a regulator of adipogenesis, causes pre-implantation embryonic lethality due to the growth defect at the blastocyst stage

Natsuki Ochiai, Makoto Nishizuka, Tomomi Miyamoto, Ichiro Miyoshi, Masahito Ikawa, Shigehiro Osada, Masayoshi Imagawa

Research output: Contribution to journalArticlepeer-review

2 Citations (Scopus)

Abstract

In previous studies, we identified a novel gene, factor for adipocyte differentiation 24 (fad24), which plays an important role during the early stages of adipogenesis in mouse 3T3-L1 cells. Moreover, overexpression of fad24 increased the number of smaller adipocytes in white adipose tissue and improved glucose metabolic activity in mice, thus indicating that fad24 functions as a regulator of adipogenesis in vivo. However, the physiological roles of fad24 in vivo are largely unknown. In this study, we attempted to generate fad24-deficient mice by gene targeting. No fad24-null mutants were recovered after embryonic day 9.5 (E9.5). Although fad24-null embryos were detected in an expected Mendelian ratio of genotypes at E3.5, none of the homozygous mutants developed into blastocysts. In vitro culture experiments revealed that fad24-null embryos develop normally to the morula stage but acquire growth defects during subsequent stages. The number of nuclei decreased in fad24-deficient morulae compared with that in wild-type ones. These results strongly suggested that fad24 is essential for pre-implantation in embryonic development, particularly for the progression to the blastocyst stage.

Original languageEnglish
Pages (from-to)301-305
Number of pages5
JournalBiochemical and biophysical research communications
Volume438
Issue number2
DOIs
Publication statusPublished - 2013 Aug 23
Externally publishedYes

Keywords

  • Adipogenesis
  • Blastocyst
  • Embryonic development
  • Embryonic lethality
  • Fad24
  • Morula

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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