Ontology highlight
ABSTRACT:
PROVIDER: PRJNA694993 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We are investigating the transcriptional response of Anc1 deficient yeast under basal and MMS exposed conditions; We used microarrays to detail the global programme of gene expression underlying the MMS response in WT and Anc1 deficient yeast Experiment Overall Design: Yeast strains either WT or Anc1 deficient were exposed or unexposed to MMS
2008-11-13 | E-GEOD-12150 | biostudies-arrayexpress
Project description:We are investigating the transcriptional response of Anc1 deficient yeast under basal and MMS exposed conditions We used microarrays to detail the global programme of gene expression underlying the MMS response in WT and Anc1 deficient yeast Keywords: dose
2008-11-01 | GSE12150 | GEO
Project description:DNA base damage is an important contributor to genome instability, but how the formation and repair of these lesions is affected by the genomic landscape is unknown. Here we describe genome-wide maps of DNA base damage, repair, and mutagenesis at single nucleotide resolution in yeast treated with the alkylating agent methyl methanesulfonate (MMS). Analysis of these maps revealed that base excision repair (BER) of alkylation damage is significantly modulated by chromatin, with faster repair in nucleosome free regions, and slower repair and higher mutation density within strongly positioned nucleosomes. Both the translational and rotational settings of lesions within nucleosomes significantly influence BER efficiency; moreover, this effect is asymmetric relative to the nucleosome dyad and is regulated by histone modifications. Our data also indicate that MMS-induced A mutations are significantly enriched on the non-transcribed strand (NTS) of yeast genes, particularly in BER-deficient strains, due to higher damage formation on the NTS and transcription-coupled repair of the transcribed strand (TS). These findings reveal the influence of chromatin on repair and mutagenesis of base lesions on a genome-wide scale, and suggest a novel mechanism for transcription-associated mutation asymmetry, which is frequently observed in human cancers.
2017-08-10 | GSE98031 | GEO
Project description:LSH/DDM1 enzymes are required for DNA methylation in higher eukaryotes and have poorly defined roles in genome maintenance in yeast, plants, and animals. The filamentous fungus Neurospora crassa is a tractable system that encodes a single LSH/DDM1 homolog (NCU06306). We report that the Neurospora LSH/DDM1 enzyme is encoded by mutagen sensitive-30 (mus-30), a locus identified in a genetic screen over 25 years ago. We show that MUS-30-deficient cells have normal DNA methylation, but are hypersensitive to the DNA damaging agent MMS (methyl methanesulfonate). MUS-30 is a nuclear protein, consistent with its predicted role as a chromatin remodeling enzyme, and levels of MUS-30 are increased following DNA damage. MUS-30 co-purifies with Neurospora WDR76, a homolog of yeast Changed Mutation Rate-1 and mammalian WD40 repeat domain 76. Deletion of wdr76 rescued MMS-hypersensitivity of Dmus-30 strains, demonstrating that the MUS-30-WDR76 interaction is functionally important. DNA damage-sensitivity of Dmus-30 is also partially suppressed by deletion of methyl adenine glycosylase-1, a component of the base excision repair machinery (BER); however, the rate of BER is not affected in Dmus-30 strains. It was reported that mammalian LSH is required for efficient double strand break (DSB) repair. We found that MUS-30-deficient cells were not defective for DSB repair, and we observed a negative genetic interaction between Dmus-30 and Dmei-3, the Neurospora RAD51 homolog required for homologous recombination. These data are consistent with a role for MUS-30 that is independent of DSB repair. Our findings demonstrate that LSH/DDM1 enzymes are key regulators of genome stability in eukaryotes. crf5-1 isolates (two replicates each from the F1 and F2 generation) were grown in Vogel's minimal medium for 48 hours. As a control, two replicates of the wildtype strain were grown under identical conditions.
2015-12-21 | E-GEOD-70518 | biostudies-arrayexpress
Project description:Mutation accumulation in mismatch repair deficient yeast
| PRJNA209500 | ENA
Project description:We catalogued and quantified the transcripts in livers of wild-type and Aag-deficient mice that had been exposed to the model alkylating agent methyl methanesulfonate (MMS). Gene expression analysis was performed for samples harvested 6 hours post-MMS treatment.
2018-06-04 | GSE115254 | GEO
Project description:Wild type and sgs1 null yeast were grown under DNA damaging (with MMS) conditions or without treatment to log phase and their transcriptional profiles compared. The human aging diseases Werner and Bloom syndromes are a result of mutation of the WRN and BLM genes, respectively. The SGS1 gene of Saccharomyces cerevisiae is homologous to the human WRN and BLM genes of the RecQ DNA helicase family. Deletion of SGS1 results in accelerated yeast aging and a reduction in life span as well as cell cycle arrest. We demonstrate that SGS1 deletion, DNA damage, and stress show similar transcriptional responses in yeast. Our comparative analysis of the genome-wide expression response of SGS1 deletion, stress and DNA damage indicates parallel transcriptional responses to cellular insult and aging in yeast.
2007-07-07 | E-GEOD-423 | biostudies-arrayexpress
Project description:We are investigating the transcriptional response of mice that are wt or null for Aag in response to alkylating agent MMS; We used microarrays to detail the global programme of gene expression response due to MMS exposure in a DNA repair proficient or deficient mouse Experiment Overall Design: Mice (WT and Aag null) were treated with MMS and livers extracted at 6, 12, 24, and 48 hours
2009-02-21 | E-GEOD-11252 | biostudies-arrayexpress
Project description:We are investigating the transcriptional response of mice that are wt or null for Aag in response to alkylating agent MMS We used microarrays to detail the global programme of gene expression response due to MMS exposure in a DNA repair proficient or deficient mouse Keywords: timepoint
2009-02-04 | GSE11252 | GEO