Expression data from yeast with modulated expression of base excision repair players
Ontology highlight
ABSTRACT:
ORGANISM(S): Saccharomyces cerevisiae
PROVIDER: GSE9295 | GEO | 2007/11/30
SECONDARY ACCESSION(S): PRJNA102937
REPOSITORIES: GEO
Similar Datasets
Project description:We are investigating the transcriptional response of yeast to modulation of the expression of base excision repair players, these generate different dna lesions of abasic sites of strand breaks; We used microarrays to detail the global programme of gene expression underlying the DNA damage response in yeast Experiment Overall Design: Yeaststrains with different expression levels of players in base excision repair (in biological triplicate) were grown to mid log phase. The expression responses were compared to each other and we have deciphered a gene expression profile that is specific for DNA damage in yeast.
2008-06-16 | E-GEOD-9295 | biostudies-arrayexpress
Project description:Nucleosomes are a significant barrier to the repair of UV damage because they impede damage recognition by nucleotide excision repair (NER). The RSC and SWI/SNF chromatin remodelers function in cells to promote DNA access by moving or evicting nucleosomes and both have been linked to NER in yeast. Here, we report genome-wide repair maps of UV-induced cyclobutane pyrimidine dimers (CPDs) in yeast cells lacking RSC or SWI/SNF activity. Our data indicate that SWI/SNF is not generally required for NER, but instead promotes repair of CPD lesions at specific yeast genes. In contrast, mutation or depletion of RSC subunits causes a general defect in NER across the yeast genome. Our data indicate that RSC is required for repair not only in nucleosomal DNA, but also neighboring linker DNA and nucleosome-free regions (NFRs). Intriguingly, while depletion of the RSC catalytic subunit also affects base excision repair (BER) of N-methylpurine (NMP) lesions, RSC activity is less important for BER in linker DNA and NFRs. Furthermore, our data indicate that RSC plays a direct role in transcription coupled-NER (TC-NER) of transcribed DNA. These findings help to define the specific genomic and chromatin contexts in which each chromatin remodeler functions in DNA repair, and indicate that RSC plays a unique function in facilitating repair by both NER subpathways.
2021-04-12 | GSE161929 | GEO
Project description:Data from Excision-seq experiments to map deoxyuridine and pyrimidine dimers in S. cerevisiae and E. coli For uracil mapping in pre-digestion Excision-seq, uracil was excised from genomic DNA from dut ung yeast and bacteria yielding double-stranded DNA fragments. Adapters were ligated to these fragments for Illumina library preparation. Using this method, the number of reads at a genomic location corresponds to the quantity of dU at that location. In post-digestion Excision-seq, uracil-containing library fragments are destroyed by UDG treatment, thus coverage is inversely proportional to uracil content. For pyrimidine dimer Excision-seq, yeast were irradiated with high doses of UVC light to generate a large number of DNA modifications. Using the excision repair enzyme UVDE from S. pombe, we excised pyrimidine dimers, cutting the phosphodieseter bond to release small double stranded fragments. These fragments were repaired with either CPD photolyase or 6-4 photolyase to generate independent libraries for each modification type. Illumina adapters were ligated to these fragments for library preparation. Using this method the number of reads at a genomic location corresponds to the quantity of the 3' pyrimidine of the dimer.
2014-05-15 | E-GEOD-51361 | biostudies-arrayexpress
Project description:Nucleosomes are a significant barrier to the repair of UV damage because they impede damage recognition by nucleotide excision repair (NER). The RSC chromatin remodeler functions in cells to promote DNA access by moving or evicting nucleosomes and has been linked to NER in yeast. Here, we report genome-wide repair maps of UV-induced cyclobutane pyrimidine dimers (CPDs) in yeast cells lacking Rsc2.
2021-04-12 | GSE168369 | GEO
Project description:Lamin A/C promotes DNA base excision repair
| PRJNA512097 | ENA
Project description:We recapitulated two main, cellular base excision repair (BER) complexes (herein termed Complex A, comprised of POLB and XRCC1 and Complex B, XRCC1-devoid complexes) by exploiting a separation-of-function mutant of POLB that does not bind to XRCC1, the V303-loop mutant POLB(TM). Cell lines were developed that expressed Flag-tagged-POLB(WT) and Flag-tagged-POLB(TM). To screen for binding partners of POLB or the POLB/XRCC1 complex, anti-Flag M2 affinity gel was used to immunoprecipitate proteins from cell lysates of LN428/Flag-POLB(WT), LN428/Flag-POLB(TM) or LN428/EGFP cells. The immunoprecipitates were loaded on SDS-PAGE gels and proteins were separated from low molecular weight reagents using short gel (~1cm) fractionation. The gels were stained by Coomassie blue. Gel regions were excised as indicated and processed for tryptic digestion. Liquid-chromatography Fourier transform mass spectrometry was used to measure the mass-to-charge (m/z) ratio, retention time, and intensity of more than 100,000 peptide signals that are detected in high-resolution full-scan mass spectra.
2024-04-24 | MSV000094615 | MassIVE
Project description:Base excision repair (BER) corrects DNA damage from oxidation, deamination and alkylation. Such base lesions cause little distortion to the DNA helix structure. BER is initiated by a DNA glycosylase that recognizes and removes the damaged base, leaving an abasic site that is further processed by short-patch repair or long-patch repair that largely uses different proteins to complete BER. At least 11 distinct mammalian DNA glycosylases are known, each recognizing a few related lesions, frequently with some overlap in specificities. Impressively, the damaged bases are rapidly identified in a vast excess of normal bases, without a supply of energy. BER protects against cancer, aging, and neurodegeneration and takes place both in nuclei and mitochondria. More recently, an important role of uracil-DNA glycosylase UNG2 in adaptive immunity was revealed. Furthermore, other DNA glycosylases may have important roles in epigenetics, thus expanding the repertoire of BER proteins.
| S-EPMC3683898 | biostudies-literature
Project description:Repair of UV damage from the transcribed strand (TS) of yeast genes is rapid due to the transcription coupled nucleotide excision repair (TC-NER) pathway. TC-NER is triggered when RNA polymerase stalls at UV damage, such as a UV-induced cyclobutane pyrimidine dimer (CPD). During transcription, the histone methyltransferase Set2 methylates histone H3K36, but it is not known if Set2 regulates TC-NER. Here, we report genome-wide repair maps of UV-induced cyclobutane pyrimidine dimers (CPDs) in yeast cells lacking Set2.
2022-02-21 | GSE179794 | GEO
Project description:p62, a well-known adaptor of autophagy, plays multiple functions in response to various stresses. Here, we report a function for p62 in base excision repair that is distinct from its known functions. Loss of p62 impairs BER capacity and increases the sensitivity of cancer cells to alkylating and oxidizing agents. In response to alkylative and oxidative damage, p62 is accumulated in the nucleus，acetylated by hMOF， deacetylated by SIRT7, and acetylated p62 is recruited to chromatin. The chromatin-enriched p62 directly interacts with APE1, a key enzyme of the BER pathway, and promotes its endonuclease activity, which facilitates BER and cell survival. Collectively, our findings demonstrate that p62 is a regulator of BER, and provide further rationale for targeting p62 as a cancer therapeutic strategy.
2022-07-19 | PXD034901 | Pride
Project description:p62, a well-known adaptor of autophagy, plays multiple functions in response to various stresses. Here, we report a function for p62 in base excision repair that is distinct from its known functions. Loss of p62 impairs BER capacity and increases the sensitivity of cancer cells to alkylating and oxidizing agents. In response to alkylative and oxidative damage, p62 is accumulated in the nucleus，acetylated by hMOF， deacetylated by SIRT7, and acetylated p62 is recruited to chromatin. The chromatin-enriched p62 directly interacts with APE1, a key enzyme of the BER pathway, and promotes its endonuclease activity, which facilitates BER and cell survival. Collectively, our findings demonstrate that p62 is a regulator of BER, and provide further rationale for targeting p62 as a cancer therapeutic strategy.
2022-07-19 | PXD034899 | Pride