Abdu et al., 2003, Genetics 165(1): 197--204

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Abdu et al., 2003, Genetics 165(1): 197--204
FlyBase Identifier FBrf0162153
FlyBase URL http://flybase.org/reports/FBrf0162153.html
Publication Type paper
Publication Year 2003
PubMed ID 14504227
PubMed URL http://www.ncbi.nlm.nih.gov/pubmed/14504227


The Drosophila spn-D gene encodes a RAD51C-like protein that is required exclusively during meiosis.


In Drosophila, mutations in double-strand DNA break (DSB) repair enzymes, such as spn-B, activate a meiotic checkpoint leading to dorsal-ventral patterning defects in the egg and an abnormal appearance of the oocyte nucleus. Mutations in spn-D cause an array of ovarian phenotypes similar to spn-B. We have cloned the spn-D locus and found that it encodes a protein of 271 amino acids that shows significant homology to the human RAD51C protein. In mammals the spn-B and spn-D homologs, XRCC3 and RAD51C, play a role in genomic stability in somatic cells. To test for a similar role for spn-B and spn-D in double-strand DNA repair in mitotic cells, we analyzed the sensitivity of single and double mutants to DSBs induced by exposure to X rays and MMS. We found that neither singly mutant nor doubly mutant animals were significantly sensitized to MMS or X rays. These results suggest that spn-B and spn-D act in meiotic recombination but not in repair of DSBs in somatic cells. As there is no apparent ortholog of the meiosis-specific DMC1 gene in the Drosophila genome, and given their meiosis-specific requirement, we suggest that spn-B and spn-D may have a function comparable to DMC1.

Genes from Reference

Gene(s) Dmel\w
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