Genetic recombination and DNA transpositions induced by pteridines and extracts of pteridine-treated diapausing chrysalids and mutants injected in Drosophila melanogaster.

This paper presents the results of two different treatments using pteridines in Drosophila melanogaster larvae: injection of pteridines alone; and injection of extracts from diapaused Pieris brassicae chrysalids treated with pteridines. Genetic analysis reveals first the induction of lethal or visible recessive mutations that give rise mostly to developmental mutants with variable phenotypes, and second the induction of genetic recombinations. Both treatments disturb genetic recombination in F1 female female issued from the treated larvae. This disturbance is evidenced by the increase in the rate of recombination particularly in the centromere region, and induces in F1 female female and male male clusters of mitotic recombinations of premeiotic origin. These two observations present an analogy with hybrid dysgenesis in the P-M system. This suggests that the treatments either promote the mobility of transposons in female and male larvae and their progeny, or affect the system controlling transposon mobility and integration at specific chromosomal sites. We used in situ hybridization to test our hypotheses, using P, I and copia-like probes. P yields a positive response both at the level of gonadal sterility (gonadal dysgenesis test) and in situ hybridization: after treatment, Oregon K and the wing-altered mutant bspw exhibit a normal number of P elements whereas the maternal strain Oregon K is totally devoid of P. This mutant bspw carries the neutral strain Q (a variant of P), which cannot produce P-M dysgenesis. The implication of these findings for understanding the mode of action of pteridines is twofold: (1) pteridines may be mutagenic agents which perturb meiotic and mitotic recombination; and (2) pteridines disturb the system regulating the mobility and insertion of P elements.