Modification of MR mutator activity in repair-deficient strains of Drosophila melanogaster.

In drosophila, MR (male recombination) second chromosomes are known to act as mutators and recombination-inducers in males. One explanation of MR- induced effects is that MR causes breaks at specific sites where, subsequently, insertion sequences become integrated. To examine the extent to which excision and incorporation of DNA sequences by MR is affected by enzymatic pathways involved in DNA repair, the following experiments were carried out. MR-chromosomes were introduced into males deficient for excision (mei-9a) or post-replication repair (mei-41D5) or into males carrying both repair-deficient mutations. MR activity was recorded by the occurrence of visible mutations at the sn (singed) and ras (raspberry) loci. The spontaneous mutation frequency for sn is 0.2 . 10-5 (1/490 000) and for ras, 0.4 . 10-5 (2/490 000). When MR is introduced into repair-proficient males the frequency of sn mutations is 51 . 10-5 (16/30 795) and of ras mutations is 19. 10-5 (6/30 795). In MR males deficient for both excision and post-replication repair (mei-9a mei-41D5) mutator activity is significantly enhanced; the frequency of sn mutations amounts to 225 . 10-5 (174/77 219) and of ras mutations to 135 . 10-5 (104/77 219). mei-9a or mei-41D5 alone also leads to an enhancement of the mutation frequencies, but this effect is of borderline significance.