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Modification of MR mutator activity in repair-deficient strains of Drosophila melanogaster
Abstract:
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.
Insights
Male recombination (MR) in Drosophila enhances mutation rates, especially when DNA repair pathways like excision (mei-9a) and post-replication repair (mei-41D5) are deficient. Combined deficiencies significantly boost MR
Area of Science:
- Genetics
- Molecular Biology
- Drosophila melanogaster research
Background:
- Drosophila melanogaster male recombination (MR) second chromosomes are known mutators and recombination inducers.
- MR is hypothesized to cause DNA breaks, facilitating insertion sequence integration.
- DNA repair pathways are crucial for maintaining genomic integrity.
Purpose of the Study:
- To investigate how DNA repair pathways influence MR-induced DNA sequence excision and incorporation.
- To determine the role of excision repair (mei-9a) and post-replication repair (mei-41D5) in MR activity.
Main Methods:
- MR-carrying second chromosomes were introduced into Drosophila melanogaster males with specific DNA repair deficiencies (mei-9a, mei-41D5, or both).
- MR activity was quantified by measuring visible mutation frequencies at the singed (sn) and raspberry (ras) loci.
- Spontaneous mutation frequencies were used as a baseline for comparison.
Main Results:
- In repair-proficient males, MR significantly increased sn and ras mutation frequencies compared to spontaneous rates.
- Males deficient in both mei-9a and mei-41D5 exhibited a substantial enhancement of MR-induced mutation frequencies for both loci.
- Single deficiencies in mei-9a or mei-41D5 also showed an enhancement of mutation frequencies, though this effect was of borderline statistical significance.
Conclusions:
- Deficiencies in DNA repair pathways, particularly combined defects in excision and post-replication repair, significantly potentiate the mutator activity of Drosophila melanogaster male recombination chromosomes.
- The results suggest that MR-induced DNA breaks are processed by repair pathways, and impaired repair leads to increased mutation accumulation.
- This study highlights the interplay between recombination machinery and DNA repair systems in shaping genome stability.