Repair of UV-induced (6–4)photoproducts measured in individual genes in the Drosophila embryonic<i>Kc</i>cell line

Cock, J.G.R. de; Hoffen, Anneke van; Wijnands, J.; Molenaar, G.J.; Lohman, P.H.M.; Eeken, J.C.J.

doi:10.1093/nar/20.18.4789

Cited by 20 publications

(7 citation statements)

References 35 publications

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“…This bias appeared strongest for TA transversions ( P < 0.0002), supporting previous results at the endogenous HPRT gene locus (22). No evidence for any transcription-coupled repair process (Figure 3C) was seen in the S2 cells, in keeping with results obtained with Drosophila Kc cells (23) and the absence of homologues of either CSA or CSB, the main TCR genes, in Drosophila (24). …”

Section: Resultssupporting

confidence: 88%

Direct, genome-wide assessment of DNA mutations in single cells

Gundry

Maqbool

et al. 2011

Nucleic Acids Research

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DNA mutations are the inevitable consequences of errors that arise during replication and repair of DNA damage. Because of their random and infrequent occurrence, quantification and characterization of DNA mutations in the genome of somatic cells has been difficult. Random, low-abundance mutations are currently inaccessible by standard high-throughput sequencing approaches because they cannot be distinguished from sequencing errors. One way to circumvent this problem and simultaneously account for the mutational heterogeneity within tissues is whole genome sequencing of a representative number of single cells. Here, we show elevated mutation levels in single cells from Drosophila melanogaster S2 and mouse embryonic fibroblast populations after treatment with the powerful mutagen N-ethyl-N-nitrosourea. This method can be applied as a direct measure of exposure to mutagenic agents and for assessing genotypic heterogeneity within tissues or cell populations.

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Section: Resultssupporting

confidence: 88%

Direct, genome-wide assessment of DNA mutations in single cells

Gundry

Maqbool

et al. 2011

Nucleic Acids Research

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“…Nevertheless, differences between vermilion and RL mutant frequencies were obtained previously for postmeiotic male germ cells with different repair backgrounds Tosal et al, 2001Tosal et al, , 2002] and attributed to differential repair of vermilion with respect to other X-chromosome genes. This conclusion was reached despite the absence of preferential repair in D. melanogaster [de Cock et al, 1991[de Cock et al, ,1992avan der Helm et al, 1997;Sekelsky et al, 2000].…”

Section: Discussionmentioning

confidence: 98%

Effect of nucleotide excision repair on ENU‐induced mutation in female germ cells of Drosophila melanogaster

Álvarez

Comendador

Sierra

2003

Environ and Mol Mutagen

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The role of nucleotide excision repair (NER) in the repair of alkylation damage in the germ cells of higher eukaryotes has been studied mainly by treating postmeiotic male germ cells. Little is known about repair in actively repairing female germ cells. In this study, we treated NER-deficient (ner(-)) mus201(D1) Drosophila females with N-ethyl-N-nitrosourea (ENU) and determined both the mutant frequencies in the multiple locus recessive lethal (RL) test and in the single locus vermilion gene and determined the ENU mutation spectrum in the vermilion gene. The results show that ENU is mutagenic in all cell stages and that the induced frequencies increase with cell maturation, from oogonia to mature oocytes. In addition, the induced spectrum consists mainly of A:T-->T:A transversions (43.8%), A:T-->G:C transitions (21.9%), and A:T-->C:G transversions (15.6%). G:C-->A:T (3.1%) transitions, other transversions (9.4%), frameshifts (3.1%), and deletions (3.1%) were also found. Comparison of these results with those previously obtained for repair-proficient (ner(+)) female germ cells reveal: 1) Differences in the RL and vermilion mutation frequencies for ner(+) and ner(-) germ cells, indicating that NER is involved in the repair of ENU-induced damage to these cells. 2) At least 15.6% of mutations in ner(-) cells may be the consequence of N-ethylation damage and mutations of this type were not detected in ner(+) cells. 3) Although differences were found in transition frequencies between ENU-treated ner(+) and ner(-) germ cells (52.2% vs. 25%), suggesting that a functional NER is involved in processing O-ethylated damage, the role of NER in repairing O-ethylated adducts is uncertain.

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“…Both pathways can remove damage throughout the genome, but in both humans and yeast damage on the template strand of actively transcribed genes is removed much more rapidly than other damage. Efforts to verify that this transcription-coupled repair (TCR) occurs in Drosophila, however, failed to find evidence for its existence, at least for the two main classes of UV-induced damage (de Cock et al, 1992;van der Helm et al, 1997). Cockayne syndrome is a hereditary disorder that results from disruption of TCR (for review see van Gool et al, 1997).…”

Section: Transcription-coupled Repairmentioning

confidence: 99%