title: Disruption of the novel gene fad104 causes rapid postnatal death and attenuation of cell proliferation, adhesion, spreading and migration.
abstract: The molecular mechanisms at the beginning of adipogenesis remain unknown. Previously, we identified a novel gene, fad104 (factor for adipocyte differentiation 104), transiently expressed at the early stage of adipocyte differentiation. Since the knockdown of the expression of fad104 dramatically repressed adipogenesis, it is clear that fad104 plays important roles in adipocyte differentiation. However, the physiological roles of fad104 are still unknown. In this study, we generated fad104-deficient mice by gene targeting. Although the mice were born in the expected Mendelian ratios, all died within 1 day of birth, suggesting fad104 to be crucial for survival after birth. Furthermore, analyses of mouse embryonic fibroblasts (MEFs) prepared from fad104-deficient mice provided new insights into the functions of fad104. Disruption of fad104 inhibited adipocyte differentiation and cell proliferation. In addition, cell adhesion and wound healing assays using fad104-deficient MEFs revealed that loss of fad104 expression caused a reduction in stress fiber formation, and notably delayed cell adhesion, spreading and migration. These results indicate that fad104 is essential for the survival of newborns just after birth and important for cell proliferation, adhesion, spreading and migration.
authors.affiliation: Department of Molecular Biology, Graduate School of Pharmaceutical Sciences, Nagoya City University, 3-1 Tanabe-dori, Mizuho-ku, Nagoya, Aichi 467-8603, Japan.
authors.forename: Makoto
authors.initials: M
authors.lastname: Nishizuka
authors.forename: Keishi
authors.initials: K
authors.lastname: Kishimoto
authors.forename: Ayumi
authors.initials: A
authors.lastname: Kato
authors.forename: Masahito
authors.initials: M
authors.lastname: Ikawa
authors.forename: Masaru
authors.initials: M
authors.lastname: Okabe
authors.forename: Ryuichiro
authors.initials: R
authors.lastname: Sato
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Niida
authors.forename: Makoto
authors.initials: M
authors.lastname: Nakanishi
authors.forename: Shigehiro
authors.initials: S
authors.lastname: Osada
authors.forename: Masayoshi
authors.initials: M
authors.lastname: Imagawa
mesh_terms: D017667:Adipocytes / Q000378:metabolism / Q000502:physiology; D050156:Adipogenesis / Q000235:genetics / Q000502:physiology; D000818:Animals; D002448:Cell Adhesion / Q000235:genetics; D002465:Cell Movement / Q000235:genetics*; D049109:Cell Proliferation; D048429:Cell Size; D002478:Cells, Cultured; D004721:Endoplasmic Reticulum / Q000235:genetics / Q000502:physiology; D005328:Fetal Viability / Q000235:genetics*; D005353:Fibronectins / Q000235:genetics* / Q000378:metabolism / Q000502:physiology*; D018390:Gene Targeting; D051379:Mice; D018345:Mice, Knockout; D022502:Stress Fibers / Q000378:metabolism / Q000502:physiology
chemical_list: C538837:Fndc3b protein, mouse; D005353:Fibronectins