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Early Embryonic Lethality of Mice Lacking the Essential Protein SNEV
Author(s) -
Klaus Fortschegger,
Bettina Wagner,
Regina Voglauer,
Hermann Katinger,
Maria Sibilia,
Regina GrillariVoglauer
Publication year - 2007
Publication title -
molecular and cellular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.14
H-Index - 327
eISSN - 1067-8824
pISSN - 0270-7306
DOI - 10.1128/mcb.01188-06
Subject(s) - biology , gene targeting , microbiology and biotechnology , embryonic stem cell , blastocyst , homologous recombination , embryo , nuclear protein , gene , genetics , embryogenesis , transcription factor
SNEV (Prp19, Pso4, NMP200) is a nuclear matrix protein known to be involved in pre-mRNA splicing, ubiquitylation, and DNA repair. In human umbilical vein endothelial cells, SNEV overexpression delayed the onset of replicative senescence. Here we analyzed the function of the mouseSNEV gene in vivo by employing homologous recombination in mice and conclude that SNEV is indispensable for early mouse development. Mutant preimplantation embryos initiated blastocyst formation but died shortly thereafter. Outgrowth ofSNEV -null blastocysts showed a lack of proliferation of cells of the inner cell mass, which subsequently underwent cell death. WhileSNEV -heterozygous mice showed no overt phenotype, heterozygous mouse embryonic fibroblast cell lines with reduced SNEV levels displayed a decreased proliferative potential in vitro. Our experiments demonstrate that the SNEV protein is essential, functionally nonredundant, and indispensable for mouse development.

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