Eye Pigmentation Changes in Drosophila Melanogaster as a Sensitive Test for Mutagenicity

Rasmuson, Bertil; Rasmuson, Åsa; Nygren, Jan

doi:10.1016/b978-0-444-80519-5.50032-8

Cited by 8 publications

(7 citation statements)

References 18 publications

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“…This instability is especially remarkable in the w +Uz strain, which reverts in both somatic and germ-line cells. This instability has been useful in developing a somatic mutagenicity assay (the UZ test) for detection of genotoxic damage (Rasmuson et al, 1978;Rasmuson, Rasmuson & Nygren, 1984;Rasmuson, 1984a). Somatic mutations within the w +Uz allele induced during embryonic or early larval development give rise to wildtype pigmented or white sectors in the yellow eye (Rasmuson, 1985a).…”

Section: Introductionmentioning

confidence: 99%

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

Rasmuson-Lestander

Ekström

1996

Genetica

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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: Introductionmentioning

confidence: 99%

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

Rasmuson-Lestander

Ekström

1996

Genetica

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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: Methodsmentioning

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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“…The unstable-zeste (UZ) system has been widely used as a genotoxicity test (Rasmuson et al 1984;Xamena et al 1984;Fujikawa et al 1985;Vogel 1989;BatisteAlentorn et al 1991;Rasmuson and Larsson 1992). This is a simple and fast in vivo bioassay used to detect somatic genetic changes, but it may also be used to detect germ-line changes (Rasmuson et al 1984).…”

Section: Introductionmentioning

confidence: 99%

An FB-NOF mediated duplication of the white gene is responsible for the zeste 1 phenotype in some Drosophila melanogaster unstable strains

et al. 2005

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The males of the Drosophila melanogaster M115 mutant strain and of its spontaneous revertant strain RM115 are phenotypically similar to those carrying the w(+UZ) and w(+UR) alleles. The molecular description of these mutant strains could be extended to the unstable-zeste system, which has been used as a genotoxicity test, and could be of use for a better understanding of the assay. An FB element in the 3' vicinity of the white gene, actually into the second intron of the newly predicted CG32795 gene, was found and precisely located in our M115 and RM115 strains, and also in w(+UZ) as expected. We demonstrate the presence of NOF sequences in the M115 and w(+UZ) insertions. However, we found that the z1 phenotype in these males might not be due to the FB-NOF interference on the zeste-white interaction but to a duplication of the white gene unnoticed in previous studies. The reversion of RM115 correlates with the loss of the duplication, probably by a complex recombination event. Furthermore, a FISH experiment suggests that the two copies of white are nearby or tandemly duplicated.

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Eye Pigmentation Changes in Drosophila Melanogaster as a Sensitive Test for Mutagenicity

Cited by 8 publications

References 18 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

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

An FB-NOF mediated duplication of the white gene is responsible for the zeste 1 phenotype in some Drosophila melanogaster unstable strains

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