Early lethality of β-1,4-galactosyltransferase V-mutant mice by growth retardation

• Published in: Biochemical and biophysical research communications 2009-02, Vol.379 (2), p.456-459
• Main Authors: Kumagai, Tadahiro, Tanaka, Minoru, Yokoyama, Minesuke, Sato, Takeshi, Shinkai, Tadashi, Furukawa, Kiyoshi
• Format: Article
• Language: English
• Subjects: Animals; Embryo Loss - genetics; Embryo, Mammalian - anatomy & histology; Embryo, Mammalian - enzymology; Embryonic Development - genetics; Embryonic lethality; Fetal Growth Retardation - genetics; Galactosyltransferases - genetics; Growth retardation; Knockout mice; Lactosylceramide; Mice; Mice, Knockout; N-glycans; O-glycans; β-1,4-Galactosyltransferase V
• ISSN: 0006-291X; 1090-2104
• DOI: 10.1016/j.bbrc.2008.12.078

The β-1,4-galactosyltransferase (β-1,4-GalT) V whose human and mouse genes were cloned by us has been suggested to be involved in the biosynthesis of N-glycans and O-glycans, and lactosylceramide. To determine its biological function, β-1,4-GalT V (B4galt5) mutant mice obtained by a gene trap method were analyzed. Analysis of pre- and post-implantation embryos revealed that the B4galt5−/− mice die by E10.5 while B4galt5+/− mice were born and grown normally. Histological study showed that most tissues are formed in B4galt5−/− embryos but their appearance at E10.5 is close to that of B4galt5+/− embryos at E9.0-9.5. The results indicate that the growth is delayed by one to one and half day in B4galt5−/− embryos when compared to B4galt5+/− embryos, which results in early death of the embryos by E10.5, probably due to hematopoietic and/or placental defects.