How many loci on the X‐chromosome of drosophila melanogaster can mutate to recessive lethals?

Abrahamson, S.; Würgler, Friedrich E.; DeJongh, C.; Meyer, Heiko

doi:10.1002/em.2860020403

Cited by 57 publications

(9 citation statements)

References 8 publications

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“…Analysis of vermilion mutation frequencies in both sexes indicate (Table III): 1) whereas in male cells F 1 mutation frequencies increased with maturation, in female cells mutation frequencies decreased; 2) in general, F 1 mutation frequencies were higher in female than in male germ cells; and 3) F 2 mutation frequencies were much higher in male than in female germ cells. Furthermore, while the postmeiotic male germ cell vermilion mutation frequencies and RL per locus frequencies (calculated by assuming 700 loci on the X-chromosome can mutate to a lethal phenotype [Abrahamson et al, 1980]) were similar (1.75 ϫ 10 -4 vs. 1.95 ϫ 10 -4 ), this was not the case for premeiotic cells from both males and females.…”

Section: Mutation Frequencies In Rl Test and At The Vermilion Locusmentioning

confidence: 88%

O‐ethylthymidine adducts are the most relevant damages for mutation induced by N‐ethyl‐N‐nitrosourea in female germ cells of Drosophila melanogaster

Álvarez¹,

Comendador²,

Sierra³

2002

Environ and Mol Mutagen

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Responses to genotoxic agents vary not only among organisms, test systems, and cellular stages, but also between sexes; little, however, is known about the mutagenic consequences of chemical exposures to female germ cells. In this study, the mutagenicity of N-ethyl-N-nitrosourea (ENU) was analyzed in female germ cells of Drosophila melanogaster using the recessive-lethal test and the vermilion system, which simultaneously generates information on induced mutation frequency and mutation spectrum. ENU was mutagenic in all stages of oogenesis, although there were differences among the stages. In mature and immature oocytes, ENU-induced mutations in the vermilion locus were 43.5% A:T-->G:C transitions, 39.1% A:T-->T:A transversions, 8.7% G:C-->A:T transitions, and 8.7% A:T-->C:G transversions, indicating that the most important premutagenic lesions induced by this chemical are O(4)-ethylthymine and O(2)-ethylthymine. The low frequency of mutation involving O(6)-ethylguanine (i.e., G:C-->A:T transitions) could be a consequence of the repair of these lesions by O(6)-methylguanine DNA methyltransferase. Comparison of these results with those previously obtained in male germ cells stresses the importance of the repair activity of the analyzed cells, because the mutation spectrum in female germ cells was similar to the spectrum obtained with repair-proficient spermatogonial cells and different from repair-deficient postmeiotic cells. The results also indicate that studies with female germ cells could be an alternative to the use of premeiotic male germ cells, especially when the analysis of these cells is difficult or almost impossible and when studies of in vivo DNA repair in premeiotic germ cells are performed.

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Section: Mutation Frequencies In Rl Test and At The Vermilion Locusmentioning

confidence: 88%

O‐ethylthymidine adducts are the most relevant damages for mutation induced by N‐ethyl‐N‐nitrosourea in female germ cells of Drosophila melanogaster

Álvarez¹,

Comendador²,

Sierra³

2002

Environ and Mol Mutagen

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“…However, the only available data for the RL frequency in ner + conditions are those obtained in this work, because Pastink et al (1989) did not present this kind of data in their work. Nevertheless, a RL frequency may be estimated for that work based on the frequency of vermilion mutations in the F 1 , and assuming that there are 700 loci on the X chromosome that can mutate to a recessive lethal phenotype (Abrahamson et al 1980). This is possible because from most of the spectra induced with dierent chemicals in the vermilion system under repair-pro®cient conditions, it is clear that the RL frequency per locus gives a good estimate of the F 1 vermilion mutation frequency .…”

Section: Rl Frequency and Mutability Indexmentioning

confidence: 99%

In vivo repair of ENU-induced oxygen alkylation damage by the nucleotide excision repair mechanism in Drosophila melanogaster

Tosal

Sierra

2001

Mol Gen Genomics

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DNA damage caused by oxygen alkylation of bases (mainly at O6-G, O4-T and O2-T positions in DNA) has been correlated with the mutagenic and carcinogenic potency of monofunctional alkylating agents. In all kinds of organisms, repair of O6-alkylG is carried out mainly by the enzyme O6-methyl guanine-DNA methyltransferase (MGMT). However, little is known about the repair of the O-alkylT adducts or about the contribution of nucleotide excision repair (NER) to this process, especially in higher eukaryotes. To study the influence of the NER system on the repair of O-alkylation damage, the molecular mutation spectrum induced by N-ethyl-N-nitrosourea (ENU) in an NER-deficient Drosophila strain, carrying a mutation at the mus201 locus, was obtained and compared with a previously published spectrum for NER-proficient conditions. This comparison reveals a clear increase in the frequency of base pair changes, including GC --> AT and AT --> GC transitions and AT --> TA transversions. In addition, one deletion and two frameshift mutations, not found under NER-proficient conditions, were isolated in the NER-deficient mutant. The results demonstrate that: (1) N-alkylation damage contributes considerably (more than 20%) to the mutagenic activity of ENU under NER-deficient conditions, confirming that the NER system repairs this kind of damage; and (2) that in germ cells of Drosophila in vivo, NER seems to repair O6-ethylguanine and/or O2-ethylcytosine, O4-ethylthymine, and possibly also O2-ethylthymine.

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“…However, exact values for hypermutability at the vermilion locus cannot be provided, in the absence of data for the rate of spontaneous mutation at the vermilion locus. Nevertheless, the average RL frequency per locus on the X chromosome (2.14´10 )6 ) may be taken as the spontaneous mutation rate at the vermilion locus, assuming that there are 700 mutable loci on the X chromosome (Abrahamson et al 1980). This is possible because ± based on data from most of the spectra induced with dierent chemicals ± in the vermilion system, it is clear that the RL frequency per locus represents a good estimate of the F 1 vermilion mutation frequency (reviewed in Nivard et al 1999).…”

Section: Induction Of Vermilion Mutations and Determination Of The Momentioning

confidence: 99%

The mus308 locus of Drosophila melanogaster is implicated in the bypass of ENU-induced O-alkylpyrimidine adducts

Tosal¹,

Comendador²,

Sierra³

2000

Mol Gen Genet

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The mus308 locus of D. melanogaster was originally characterized by virtue of a mutant phenotype that resulted in specific hypersensitivity to cross-linking agents. However, the gene product has also been implicated in the repair of lesions other than cross-links. The gene was recently sequenced, and it encodes a protein with motifs characteristic of both DNA polymerases and helicases. We present mutability studies, using the recessive lethal (RL) test, which show that N-ethyl-N-nitrosourea (ENU) induces hypermutability in mus308-deficient conditions, although only in early broods. Further studies elucidated the role of MUS308 in repair processes by characterizing the spectrum of molecular mutations induced by in vivo ENU in postmeiotic germ cells, in mus308 conditions. These revealed that, in comparison to repair-proficient conditions, there is an increase in the frequency of GC --> AT and AT --> GC transitions, and AT --> TA transversions. Moreover, frameshift mutations, which have not previously been reported to form part of the ENU spectrum, were also found. These results indicate that MUS308 is needed to process ENU-induced lesions, and support the hypothesis that the mus308 gene plays a role in post-replication bypass of O-alkylpyrimidines, probably mediated by recombination, which serves to increase the time available for error-free repair of these persistent and highly mutagenic lesions.

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How many loci on the X‐chromosome of drosophila melanogaster can mutate to recessive lethals?

Cited by 57 publications

References 8 publications

O‐ethylthymidine adducts are the most relevant damages for mutation induced by N‐ethyl‐N‐nitrosourea in female germ cells of Drosophila melanogaster

O‐ethylthymidine adducts are the most relevant damages for mutation induced by N‐ethyl‐N‐nitrosourea in female germ cells of Drosophila melanogaster

In vivo repair of ENU-induced oxygen alkylation damage by the nucleotide excision repair mechanism in Drosophila melanogaster

The mus308 locus of Drosophila melanogaster is implicated in the bypass of ENU-induced O-alkylpyrimidine adducts

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