Midgestation lethality in mice deficient for the RecA-related gene, Rad51d/Rad51l3

• Published in: Genesis (New York, N.Y. : 2000) N.Y. : 2000), 2000-03, Vol.26 (3), p.167-173
• Main Authors: Pittman, Douglas L., Schimenti, John C.
• Format: Article
• Language: English
• Subjects: Animals; Base Sequence; Culture Techniques; DNA Primers; DNA repair; DNA-Binding Proteins - genetics; double-strand break repair; Fetal Death - genetics; Genes, Lethal; Genotype; Mice; Mutagenesis; Rad51; Rad5113 gene; Rad51d gene; Rec A Recombinases - genetics; RecA; recombination; Recombination, Genetic
• ISSN: 1526-954X; 1526-968X
• DOI: 10.1002/(SICI)1526-968X(200003)26:3<167::AID-GENE1>3.0.CO;2-M

Homologous recombination (HR) occurs in all organisms, and is important for repair of DNA damage, chromosome segregation during meiosis, and genetic diversification. Genes critical for recombinational DNA repair and meiotic recombination include members of the RecA/RAD51 family, of which seven have been identified in mammals. Here, we describe the disruption of Rad51d (recently designated Rad51l3) in mice and its phenotypic consequences. Rad51d‐deficient mice die between 8.5 and 11.5 dpc. The affected embryos are smaller than littermates, posteriorly truncated, and developmentally delayed. Embryonic fibroblasts from mutant embryos could not be propagated more than one generation in culture. Rad51d‐deficient blastocysts were not sensitive to gamma radiation or methylmethanesulfonate (MMS) in blastocyst outgrowth experiments. The variable and generalized developmental progression defects in Rad51d‐deficient embryos suggests that mutant cells may undergo delayed or suboptimal repair of DNA damage, resulting in accumulated degrees of mutation and/or cell cycle perturbation that are incompatible with normal embryonic development. genesis 26:167–173, 2000. © 2000 Wiley‐Liss, Inc.