A series of second chromosomes isolated from natural populations in diverse regions of the globe that, in crosses of MR-bearing males to laboratory-strain females, but not in the reciprocal crosses, produce dysgenic progeny. Such progeny transmit the MR chromosome at reduced levels compared with the homologous second chromosome; abnormalities in spermiogenesis including failure of individualization observed in dysgenic males account for 70% of the deficiency in recovery of MR (Matthews, 1981, Genetics 97: 95-111). Increased levels of gonial recombination observed in both sons (Hiraizumi, 1971, Proc. Nat. Acad. Sci. USA 68: 268-700) and daughters [demonstrated in c3G females by Sinclair and Green (Mol. Gen. Genet. 170: 219-24)]; mitotic crossing over in wing disks unaffected (Thompson and Woodruff, 1980, Genetica 49: 77-80). Both sons and daughters exhibit increased rates of spontaneous mutations, both lethal (Slatko and Hiraizumi, 1973, Genetics 75: 643-49) and at some but not all specific loci (e.g., Green, 1977, Proc. Nat. Acad. Sci. USA 74: 3490-93); the latter types of mutants usually unstable, undergoing further mutation either to more extreme alleles or back to wild type; increased mutation rates observed when combined with mei9 and mei41 (1981, Mutat. Res. 83: 191-200). All classes of chromosome rearrangements produced by dysgenic progeny, but with preferential points of breakage (Yannopoulos, Stamatis, Zacharopoulou, and Pelecanos, 1983, Mutat. Res. 108: 185-202); also shown in some cases to promote gonadal aplasia, especially at higher temperatures (Stamatis, Yannopoulos, and Pelecanos, 1981, Genet. Res. 38: 125-35); metaphase I of meiosis normal, but bridges and fragments observed in anaphase I and anaphase II in dysgenic males (Henderson, Woodruff and Thompson, 1973, Genetics 88: 93-107; Yannopoulos, 1978, Genet. Res. 239-47). Gross deletion of X-chromosome material induced by MR shown to involve an array of breakpoints, which, by in situ hybridization, are free of P-element sequences; postulated to arise through illegimate mitotic exchange (Green, Yamamoto, and Miklos, 1987, Proc. Nat. Acad. Sci. USA 84: 4533-37). The majority of the activity in several of the isolates maps to a site between Tft and pr on the left arm of chromosome two, but when that site removed residual activity remains in the genome. Mappability of the major effect to the same site in independent isolates suggests the presence of an element that is able to promote transposition but that itself is unable to transpose. Circumstantial evidence indicates that the element is P and that in addition to a functional P element, MR second chromosomes also carry defective P's. Males inheriting two doses of MR from mei-S332 fathers crossed to C(2)EN/0 females not discernably different from males with one dose; two doses of MR inherited from the mother are inactive (Green and Slatko, 1979, Mutat. Res. 62: 529-39).