DNA damage and repair in somatic and germ cells in vivo

Vogel, E.; Natarajan, A. T.

doi:10.1016/0027-5107(95)00040-p

Cited by 87 publications

(33 citation statements)

References 95 publications

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“…Sensitivity differences to mutagen/carcinogen exposure among the various germ-cell stages may result from several different factors, such as the presence and efficiency of repair enzymes, the capacity of cells for xenobiotic metabolism, the existence of selection mechanisms due to the low viability of damaged cells, and the applied mutagen dose. The repair capacity is high in oocytes and oogonia [Vogel, 1989;Vogel and Natarajan, 1995;Ashwood-Smith and Edwards, 1996]; it is possible that DNA damage induced in oogonia or in growing, metabolically active oocytes is repaired, while similar damage is not as efficiently repaired in mature oocytes. It has been reported that metabolic activity declines markedly in mature oocytes as compared to growing oocytes [Oakberg, 1968;Baker et al, 1969], which require a greater number of active genes for gamete viability.…”

Section: Discussionmentioning

confidence: 99%

“…3) DNA repair activity: efficient repair of premutational damage takes place in female germ cells [Ashwood-Smith and Edwards, 1996], as well as in immature male germ cells. The latest stages of spermatogenesis, that is, late spermatids and spermatozoa, are deficient in DNA repair [Sega and Sotomayor, 1982;Lee and Kelley, 1986;Vogel, 1989;Vogel and Natarajan, 1995;Sotomayor et al, 1999].…”

Section: Introductionmentioning

confidence: 99%

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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: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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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“…Compounds such as EMS (ethyl methanesulfonate) and MNU (N-Nitroso-N-methylurea)-induced single nucleotide changes by alkylation of specific nucleotides [16,17], giving mutations that were high in density and essentially randomly distributed [18]. Therefore, a relatively small population of rice can provide variety of missense changes with differing effects on protein function [19].…”

Section: Introductionmentioning

confidence: 99%

Identification of Phenotypic Variation and Genetic Diversity in Rice (Oryza sativa L.) Mutants

Anh

Khanh

Dat³

et al. 2018

Agriculture

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Abstract:In this study, phenotypic variation and genetic diversity, important factors to decide germplasm for rice breeding, were evaluated among 15 rice mutants attained from the MNU (N-Nitroso-N-methylurea) mutation. The correlation coefficient values among these phenotypic characteristics were calculated. The results showed that full grain number per plant was the most relevant factor contributing to grain yield per plant, and grain length to width ratio was the key parameter affected to amylose content. Furthermore, the genetic variation among mutants was estimated by Simple Sequence Repeat (SSR) markers related to amylose content trait. Fifty-six polymorphism markers covering across eleven rice chromosomes were recorded with an average of 3.02 alleles per locus. The average value of polymorphism information content was 0.47. By using the unweighted pair group method with arithmetic mean (UPGMA) clustering, four clusters were generated with the genetic similarities ranging from 0.52 to 0.91. The variation among groups was 34%, while the variation among individuals within groups was 66%. Findings of this study provided useful genetic background and phenotypic information of collected rice mutants to breed rice cultivars with improved quality.

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“…В рамках данного иссле-дования дилудин снижал уровень повреждений хромосом, индуцированных алкилирующим агентом ЭМС. ЭМС от-носится к мутагенам прямого действия и вызывает разры-вы и перестройки хромосом благодаря алкилированию N-7 гуанина с последующим ослаблением гликозидных связей, выпадением модифицированного основания и образовани-ем AP-сайтов (Beranek, 1990;Vogel, Natarajan, 1995). Один из механизмов хемопротекторного эффекта производных 1,4-ДГП связан с модуляцией процессов репарации ДНК.…”

Section: таблица 6 влияние цереброкраста (цк) на частоту эмс-индуцироunclassified

“…Следует упомянуть, что механизмы становления этих событий различаются, и му-тации, в том числе РСПЛМ, возникают преимуществен-но в результате алкилирования O 6 гуанина и ошибочного спаривания модифицированного основания с образова-нием транзиции GC→AT (Beranek, 1990). Частота ЭМС-индуцированных РСПЛМ зависит от функционирования систем эксцизионной репарации (Vogel, Natarajan, 1995). Не исключено влияние ферментов, осуществляющих репарацию неспаренных оснований или формирующих адаптивный ответ, который в половых клетках личинок дрозофилы может быть обусловлен индукцией глутатион-S-трансферазы (Кужир, 1999;Savina et al, 2003).…”

Section: таблица 6 влияние цереброкраста (цк) на частоту эмс-индуцироunclassified

Diludine and cerebrocrast as bioprotectors in the model test-systems in vivo

Savina

Nikitchenko

Dalivelya

et al. 2009

Ecological genetics

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An influence of two 1,4-dihydropyridine derivatives (diludine and cerebrocrast) on Drosophiladevelopment and germ cell mutability was studied. It was revealed the concentration range, within which the compounds manifest their bio-stimulating effects increasing individual survival by 50-80 % as well as the protective action against the alkylating agent ethyl methanesulfonate reducing the level of induced mutations by 30-50 %. The pattern and presumable mechanisms of the bioprotective action of these compounds are considered.

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DNA damage and repair in somatic and germ cells in vivo

Cited by 87 publications

References 95 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

Identification of Phenotypic Variation and Genetic Diversity in Rice (Oryza sativa L.) Mutants

Diludine and cerebrocrast as bioprotectors in the model test-systems in vivo

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