title: Early lethality of beta-1,4-galactosyltransferase V-mutant mice by growth retardation.
abstract: The beta-1,4-galactosyltransferase (beta-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, beta-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.
authors.affiliation: Laboratory of Glycobiology, Department of Bioengineering, Nagaoka University of Technology, Kamitomioka 1603-1, Nagaoka, Niigata 940-2188, Japan.
authors.forename: Tadahiro
authors.initials: T
authors.lastname: Kumagai
authors.forename: Minoru
authors.initials: M
authors.lastname: Tanaka
authors.forename: Minesuke
authors.initials: M
authors.lastname: Yokoyama
authors.forename: Takeshi
authors.initials: T
authors.lastname: Sato
authors.forename: Tadashi
authors.initials: T
authors.lastname: Shinkai
authors.forename: Kiyoshi
authors.initials: K
authors.lastname: Furukawa
mesh_terms: D000818:Animals; D020964:Embryo Loss / Q000235:genetics*; D004622:Embryo, Mammalian / Q000033:anatomy & histology / Q000201:enzymology*; D047108:Embryonic Development / Q000235:genetics; D005317:Fetal Growth Retardation / Q000235:genetics*; D005700:Galactosyltransferases / Q000235:genetics*; D051379:Mice; D018345:Mice, Knockout
chemical_list: D005700:Galactosyltransferases; C419408:beta-1,4-galactosyltransferase V