A dominant, recombination-defective allele of Dmc1 causing male-specific sterility.
Document Type
Article
Publication Date
2007
Keywords
Animals, Cell-Cycle-Proteins, DNA-Binding-Proteins, Female, Infertility-Female, Infertility-Male, Male, Meiosis, Mice, Nuclear-Proteins, Oocytes, Ovary, Recombination-Genetic
JAX Source
PLoS Biol 2007 May; 5(5):e105.
Abstract
DMC1 is a meiosis-specific homolog of bacterial RecA and eukaryotic RAD51 that can catalyze homologous DNA strand invasion and D-loop formation in vitro. DMC1-deficient mice and yeast are sterile due to defective meiotic recombination and chromosome synapsis. The authors identified a male dominant sterile allele of Dmc1, Dmc1(Mei11), encoding a missense mutation in the L2 DNA binding domain that abolishes strand invasion activity. Meiosis in male heterozygotes arrests in pachynema, characterized by incomplete chromosome synapsis and no crossing-over. Young heterozygous females have normal litter sizes despite having a decreased oocyte pool, a high incidence of meiosis I abnormalities, and susceptibility to premature ovarian failure. Dmc1(Mei11) exposes a sex difference in recombination in that a significant portion of female oocytes can compensate for DMC1 deficiency to undergo crossing-over and complete gametogenesis. Importantly, these data demonstrate that dominant alleles of meiosis genes can arise and propagate in populations, causing infertility and other reproductive consequences due to meiotic prophase I defects.
Recommended Citation
Bannister LA,
Pezza RJ,
Donaldson JR,
de RD,
Schimenti KJ,
Camerini OR,
Schimenti JC.
A dominant, recombination-defective allele of Dmc1 causing male-specific sterility. PLoS Biol 2007 May; 5(5):e105.