Disease relevance of mei-P22

• Strong mei-P22 mutations eliminate meiotic crossing over and suppress the sterility of DSB repair-defective mutants [1].

High impact information on mei-P22

• Electron microscopy of oocytes from females homozygous for either of two meiotic mutants (mei-W68 and mei-P22), which eliminate both meiotic crossing over and gene conversion, revealed normal synaptonemal complex formation [2].
• Consistent with a direct role in DSB formation, mei-P22 encodes a basic 35.7-kD protein, which, when examined by immunofluorescence, localizes to foci on meiotic chromosomes [1].
• Interestingly, crossing over in mei-P22 mutants can be restored to almost 50% of wild-type by X irradiation [1].
• Here we present genetic evidence that the mei-P22 gene is required for the induction of DSBs during meiotic prophase in Drosophila females [1].
• Similarly, we found that MEI-P22 foci did not appear in a c(3)G mutant in which SC does not form, suggesting that DSB formation is dependent on SC formation in Drosophila [1].

Physical interactions of mei-P22

• We propose that MEI-P22 interacts with meiosis-specific chromosome proteins to facilitate DSB creation by MEI-W68 [1].

Other interactions of mei-P22

• Our screen identified two new recombination-deficient mutations: mei-P22, which fully eliminates meiotic recombination, and mei-P26, which decreases meiotic exchange by 70% in a polar fashion [3].

References