scholarly journals Microfluidic platform for monitoring Saccharomyces cerevisiae mutation accumulation assay

Lab on a Chip ◽  
2021 ◽  
Author(s):  
Eliet H. Sipos ◽  
Adelaide Lety-Stefanska ◽  
Cyril DENBY WILKES ◽  
Julie SOUTOURINA ◽  
Florent Malloggi

Mutations in DNA have large-ranging consequences, from evolution to diseases. Many mechanisms contribute to mutational processes such as dysfunctions of DNA repair pathways and exogenous or endogenous mutagen exposures. Model...

Genetics ◽  
2006 ◽  
Vol 174 (1) ◽  
pp. 57-65 ◽  
Author(s):  
Dee R. Denver ◽  
Seth Feinberg ◽  
Catherine Steding ◽  
Matthew Durbin ◽  
Michael Lynch

Cancers ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3436
Author(s):  
Theodoros Rampias

Mutational processes constantly shape the cancer genome and defects in DNA repair pathways of tumor cells facilitate the accumulation of genomic alterations [...]


2008 ◽  
Vol 53 (5) ◽  
pp. 259-274 ◽  
Author(s):  
Margery L. Evans ◽  
Lindsey J. Bostelman ◽  
Ashley M. Albrecht ◽  
Andrew M. Keller ◽  
Natasha T. Strande ◽  
...  

2015 ◽  
Author(s):  
Weifeng She ◽  
Courtney Busch Cambouris ◽  
Nancy L. Craig

The movement of transposable elements from place to place in a genome requires both element-encoded and host-encoded factors. In DNA cut & paste transposition, the element-encoded transposase performs the DNA breakage and joining reactions that excise the element from the donor site and integrate it into the new insertion site. Host factors can influence many aspects of transposition. Notably, host DNA repair factors mediate the regeneration of intact duplex DNA necessary after transposase action by repairing the double strand break in the broken donor backbone, from which the transposon has excised, and repairing the single strand gaps that flank the newly inserted transposon. We have exploited the ability of the mammalian transposon piggyBat, a member of the piggyBac superfamily, to transpose in Saccharomyces cerevisiae and used the yeast single gene deletion collection to screen for genes encoding host factors involved in piggyBat transposition. piggyBac transposition is distinguished by the fact that piggyBac elements insert into TTAA target sites and also that the donor backbone is restored to its pre-transposon sequence after transposon excision, that is, excision is precise. We have found that repair of the broken donor backbone requires the non-homologous end-joining repair pathway (NHEJ). By contrast, NHEJ is not required for DNA repair at the new insertion site. Thus multiple DNA repair pathways are required for piggyBac transposition.


Genetics ◽  
1987 ◽  
Vol 115 (1) ◽  
pp. 83-90
Author(s):  
Friederike Eckardt-Schupp ◽  
Wolfram Siede ◽  
John C Game

ABSTRACT The moderately UV- and X-ray-sensitive mutant of Saccharomyces cerevisiae originally designated rs  1 complements all rad and mms mutants available. Therefore, the new nomination rad24-1 according to the RAD nomenclature is suggested. RAD24 maps on chromosome V, close to RAD3 (1.3 cM). In order to associate the RAD24 gene with one of the three repair pathways, double mutants of rad24 and various representative genes of each pathway were constructed. The UV and X-ray sensitivities of the double mutants compared to the single mutants indicate that RAD24 is involved in excision repair of UV damage (RAD3 epistasis group), as well as in recombination repair of UV and X-ray damage (RAD52 epistasis group). Properties of the mutant are discussed which hint at the control of late steps in the pathways.


Genetics ◽  
2001 ◽  
Vol 159 (3) ◽  
pp. 953-963 ◽  
Author(s):  
Petr Ćejka ◽  
Vladimír Vondrejs ◽  
Zuzana Storchová

Abstract The RAD6 postreplicative repair group participates in various processes of DNA metabolism. To elucidate the contribution of RAD6 to starvation-associated mutagenesis, which occurs in nongrowing cells cultivated under selective conditions, we analyzed the phenotype of strains expressing various alleles of the RAD6 gene and single and multiple mutants of the RAD6, RAD5, RAD18, REV3, and MMS2 genes from the RAD6 repair group. Our results show that the RAD6 repair pathway is also active in starving cells and its contribution to starvation-associated mutagenesis is similar to that of spontaneous mutagenesis. Epistatic analysis based on both spontaneous and starvation-associated mutagenesis and UV sensitivity showed that the RAD6 repair group consists of distinct repair pathways of different relative importance requiring, besides the presence of Rad6, also either Rad18 or Rad5 or both. We postulate the existence of four pathways: (1) nonmutagenic Rad5/Rad6/Rad18, (2) mutagenic Rad5/Rad6 /Rev3, (3) mutagenic Rad6/Rad18/Rev3, and (4) Rad6/Rad18/Rad30. Furthermore, we show that the high mutation rate observed in rad6 mutants is caused by a mutator different from Rev3. From our data and data previously published, we suggest a role for Rad6 in DNA repair and mutagenesis and propose a model for the RAD6 postreplicative repair group.


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