The ATR-Chk1 pathway plays a role in the generation of centrosome aberrations induced by Rad51C dysfunction.

Rad51C is a central component of two complexes formed by five Rad51 paralogs in vertebrates. These complexes are involved in repairing DNA double-strand breaks through homologous recombination. Despite accumulating evidence suggesting that the paralogs may prevent aneuploidy by controlling centrosome integrity, Rad51C's role in maintaining chromosome stability remains unclear.

XRCC3 deficiency results in a defect in recombination and increased endoreduplication in human cells.

XRCC3 was inactivated in human cells by gene targeting. Consistent with its role in homologous recombination, XRCC3(-/-) cells showed a two-fold sensitivity to DNA cross-linking agents, a mild reduction in sister chromatid exchange, impaired Rad51 focus formation and elevated chromosome aberrations. Furthermore, endoreduplication was increased five- seven-fold in the mutants.

Ocular development-associated gene (ODAG), a novel gene highly expressed in ocular development.

Complementary DNA (cDNA) arrays were used to detect highly expressed messenger RNA (mRNA) at postnatal day 2 (P2) and P10 in the mouse eye, and several clones highly expressed at P2 were isolated. We focused among them on a novel gene, the ocular development-associated gene (ODAG), which was down regulated at P10. The expression around birth was subsequently confirmed by reverse transcription-polymerase chain reaction.

A role for RAD54B in homologous recombination in human cells.

In human somatic cells, homologous recombination is a rare event. To facilitate the targeted modification of the genome for research and gene therapy applications, efforts should be directed toward understanding the molecular mechanisms of homologous recombination in human cells. Although human genes homologous to members of the RAD52 epistasis group in yeast have been identified, no genes have been demonstrated to play a role in homologous recombination in human cells.