Transpositions, Mutable Genes, and the Dispersed Gene Family Dm225 in Drosophila melanogaster

Rasmuson, Bertil; Westerberg, B. M.; Rasmuson, Åsa; Гвоздев, В. А.; Belyaeva, E. S.; Ilyin, Yu. V.

doi:10.1101/sqb.1981.045.01.070

Cited by 17 publications

(15 citation statements)

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“…Attempts to correlate the white instability with other transposable elements was reported in a previous study (Rasmuson et al, 1981). It was proposed that mdgl (Dm225) was a possible candidate element, since in situ hybridisation analyses revealed the presence of homologous DNA at 3C.…”

Section: The White Deletions and Transpositionsmentioning

confidence: 98%

Genetic and molecular analysis of a set of unstable white mutants in Drosophila melanogaster

Rasmuson-Lestander

Ekström

1996

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Two related unstable mutants at the white locus of Drosophila melanogaster show different interactions with the zeste1 mutant: one mutated white gene becomes repressed in males, whereas the other is unaffected by z1. By use of Southern blot techniques and by constructing genomic lambda-libraries, molecular analyses of the white regions of these two strains were performed. The results showed a single difference at a site 2.5 kb (kilobases) downstream of the white transcription unit. In both strains, FB (foldback) elements were integrated at this site, but the repressed strain also harboured a 4 kb NOF (Nofretete) element. No other restriction site polymorphisms between the two strains were observed within a 120 kb region surrounding the white gene. The extent of twelve white deletions and twelve white transpositions deriving from these unstable strains was analysed by in situ hybridisation and Southern blot techniques. The results revealed that the distal breakpoint of all aberrations coincided with the insertion site of the mobile elements, but that the centromere proximal breakpoints varied. The mechanisms for the instability and the interaction with the zeste1 mutant are discussed.

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Section: The White Deletions and Transpositionsmentioning

confidence: 98%

Genetic and molecular analysis of a set of unstable white mutants in Drosophila melanogaster

Rasmuson-Lestander

Ekström

1996

Genetica

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“…3, the equilibrium copy number of an element is strongly dependent on the relative rates of transposition and loss; if selection is involved in its maintenance, equation (29) shows that the strength of selection against additional copies is of the order of u -v at equilibrium. The available evidence for Drosophila suggests that transposition and loss typically occur at rates of the order of 10~4 to 10~5 per generation (Rasmuson et al 1981;Ising & Block, 1981). Any hope of directly detecting selection effectsby comparing the fitnesses of individuals with different copy numbers seems to be futile.…”

Section: B C H a B L B S W O R T H And D E B O R A H Charlesworthmentioning

confidence: 99%

The population dynamics of transposable elements

1983

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This paper describes analytical and simulation models of the population dynamics of transposable elements in randomly mating populations. The models assume a finite number of chromosomal sites that are occupable by members of a given family of elements. Element frequencies can change as a result of replicative transposition, loss of elements from occupied sites, selection on copy number per individual, and genetic drift. It is shown that, in an infinite population, an equilibrium can be set up such that not all sites in all individuals are occupied, allowing variation between individuals in both copy number and identity of occupied sites, as has been observed for several element families in Drosophila melanogaster. Such an equilibrium requires either regulation of transposition rate in response to copy number per genome, a sufficiently strongly downwardly curved dependence of individual fitness on copy number, or both. The probability distributions of element frequencies, generated by the effects of finite population size, are derived on the assumption of independence between different loci, and compared with simulation results. Despite some discrepancies due to violation of the independence assumption, the general pattern seen in the simulations agrees quite well with theory.Data from Drosophila population studies are compared with the theoretical models, and methods of estimating the relevant parameters are discussed.

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“…x-irradiation than after UV-irradiation can be explained by the assumption that a hypermutable "hot spot" structure of DNA similar to the double loop mentioned above is formed by the transposable element thought to be responsible for the unstable mutant phenotype of w+(TE) (21,22).…”

Section: Discussionmentioning

confidence: 99%

“…As previously reported (20), to assay somatic mutation, we used two strains: one bears the genetic markers z' (zeste mutant) and w+(TE) (a genetically unstable white allele, presumably caused by a transposable element) (21,22), and the second bears the white-ivory mutation w' (23).…”

Section: Introductionmentioning

confidence: 99%

“…It is defective in the capacity of postreplication repair of UV-induced DNA damage (16). The loci mus2OJDl and muslO4Dl map to chromosome 2 and the X chromosome, respectively (19).As previously reported (20), to assay somatic mutation, we used two strains: one bears the genetic markers z' (zeste mutant) and w+(TE) (a genetically unstable white allele, presumably caused by a transposable element) (21,22), and the second bears the white-ivory mutation w' (23).Abbreviations: kb, kilobase(s); bp, base pair(s). …”

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confidence: 99%

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Photoreactivation rescue and hypermutability of ultraviolet-irradiated excisionless Drosophila melanogaster larvae

Ryo¹,

Kondo²

1986

Proc. Natl. Acad. Sci. U.S.A.

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There is accumulating evidence suggesting that expression of genes for repair of UV damage to DNA in mammals and fish is regulated developmentally. Therefore, the activity of excision repair and photoreactivation in vivo in young larvae of Drosophila melanogaster was examined in a strain carrying the mutation mus201 that was unable to carry out excision repair. The photoreactivation activity in firstinstar larvae was so high that UV-induced lethality in excisionless larvae was almost completely rescued by posttreatment with fluorescent light. Excision repair activity in first-instar repair-proficient larvae was so high that UV irradiation was scarcely able to produce somatic eye-color mutations. In contrast, excisionless larvae showed a high incidence of somatic eye-color mutation after UV-irradiation, and this incidence was reduced to the spontaneous level by posttreatment with fluorescent light. Incorporation of a postreplication repair-defective mutation into the excisionless strain decreased the incidence of UV-induced somatic mutations by a factor of 3. The analogous repair dependence of UV mutagenesis in Drosophila and Escherichia coli is discussed. It is proposed that UVinduced somatic mutations in excisionless Drosophila larvae are caused primarily by pyrimidine dimers and that a constitutive, error-prone pathway for filling daughter-strand gaps opposite dimers is, at least partly, responsible for the fixation of mutations.The ability of living organisms to recover from lethal damage caused by external agents was first convincingly demonstrated in 1949 by Kelner (1) (4,8). Photoreactivation of UV-induced pyrimidine dimers occurs in the skin (only in the dermis) of neonatal mice but not in that of adult mice of the same inbred strain (9). In mouse embryo fibroblasts, excision-repair activity decreases abruptly during progressive passage of the cells in culture (10). Cultured mouse fibroblasts have only low activity of excision repair (11). In adult mice, repair in the dark of DNA damage caused by UV and UV-mimetic chemicals, as measured by unscheduled DNA synthesis in vivo in skin, is considerably less active in fibroblastic cells than in epithelial cells (12, 13). Dark repair activity for UV-induced DNA damage is absent in cultured fish cells (14,15) but present in fish embryos (15).The above cited findings strongly suggest that the expression of repair genes in animals is regulated developmentally (4). Much information is available on both the developmental biology and genetics of D. melanogaster. In this species, about 30 DNA repair-defective mutations have been reported (16), and two mutant strains, referred to by the mutations mei-9 and mus201 that they respectively carry, are unable to excise UV-induced pyrimidine dimers (16,17). Survival to eclosion of larvae of the mus201 strain is drastically reduced after UV-irradiation as compared with parallel irradiation of repair-proficient larvae (17). In the present study, we used this excisionless strain in studies on photoreactivation and dark ...

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Transpositions, Mutable Genes, and the Dispersed Gene Family Dm225 in Drosophila melanogaster

Cited by 17 publications

References 0 publications

Genetic and molecular analysis of a set of unstable white mutants in Drosophila melanogaster

Genetic and molecular analysis of a set of unstable white mutants in Drosophila melanogaster

The population dynamics of transposable elements

Photoreactivation rescue and hypermutability of ultraviolet-irradiated excisionless Drosophila melanogaster larvae

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