Bre1 vs WT transcriptional profile
Ontology highlight
ABSTRACT:
ORGANISM(S): Saccharomyces cerevisiae
PROVIDER: GSE13701 | GEO | 2009/11/19
SECONDARY ACCESSION(S): PRJNA109429
REPOSITORIES: GEO
Similar Datasets
Project description:Relative mRNA abundance of all S. cerevisiae genes was measured in bre1 compared to wild-type. Arrays done in quadruplicate with dye-swaps.
2010-06-19 | E-GEOD-13701 | biostudies-arrayexpress
Project description:Histone modification affects life span in various organisms. The loss of Histone H3K36 methylation can shorten replicative life span in Saccharomyces cerevisiae. However, budding yeast, as a model organism for aging research, has replicative life span (RLS) and chronological life span (CLS). In this study, we showed that the loss of Histone H3K36 methylation can shorten CLS in Saccharomyces cerevisiae. We identified Ubc3/Bre1 mediates polyubiquitination of Set2 K25 and K530 at log phase and stationary phase, and Bre1 interacts with Ubc3 and Rad6 simultaneously. BRE1 knockout can stabilize Set2 protein to maintain H3K36me3 and regulate the transcription of aging related genes, such as DSE1/DSE2/SUN4/EGT2/SCW11. We also proved that Gcn5-mediated Set2 acetylation regulates Set2 protein stability and chronological aging. Altogether, our study showed that knockout of BRE1 and GCN5 regulate Set2 protein level by mediating the polyubiquitination of Set2 to influence the level of H3K36me3 and the transcription level of aging related genes enriched by H3K36me3, thereby extending the chronological life span.
2023-09-29 | GSE221025 | GEO
Project description:Histone modification affects life span in various organisms. The loss of Histone H3K36 methylation can shorten replicative life span in Saccharomyces cerevisiae. However, budding yeast, as a model organism for aging research, has replicative life span (RLS) and chronological life span (CLS). In this study, we showed that the loss of Histone H3K36 methylation can shorten CLS in Saccharomyces cerevisiae. We identified Ubc3/Bre1 mediates polyubiquitination of Set2 K25 and K530 at log phase and stationary phase, and Bre1 interacts with Ubc3 and Rad6 simultaneously. BRE1 knockout can stabilize Set2 protein to maintain H3K36me3 and regulate the transcription of aging related genes, such as DSE1/DSE2/SUN4/EGT2/SCW11. We also proved that Gcn5-mediated Set2 acetylation regulates Set2 protein stability and chronological aging. Altogether, our study showed that knockout of BRE1 and GCN5 regulate Set2 protein level by mediating the polyubiquitination of Set2 to influence the level of H3K36me3 and the transcription level of aging related genes enriched by H3K36me3, thereby extending the chronological life span.
2023-09-29 | GSE221024 | GEO
Project description:Relative mRNA abundance of all S. cerevisiae genes was measured in various mutants, compared to wild-type Keywords: quadruplicate mutant:WT analysis, with dye-swapping
2006-06-01 | GSE4934 | GEO
Project description:Relative mRNA abundance of all S. cerevisiae genes was measured in various mutants, compared to wild-type Keywords: quadruplicate mutant:WT analysis, with dye-swapping
2006-05-17 | GSE4826 | GEO
Project description:These paired RIP experiments were designed to determine specific ncRNAs that associated with either Lsd1 (Lysine specific demethylase 1) complex or Bre1.
2024-05-01 | GSE244906 | GEO
Project description:Relative mRNA abundance of all S. cerevisiae genes was measured in various mutants, compared to wild-type mutant and wild-type grown to log phase, YPAD, 30C, purified mRNA, reverse-transcribed to cDNA, labelled with Cy5/Cy3, hybridized to whole genome ORF microarrays
2010-06-11 | E-GEOD-4826 | biostudies-arrayexpress
Project description:Mammalian Bre1 complexes (BRE1A/B (RNF20/40) in humans and Bre1a/b (Rnf20/40) in mice) function similarly to their yeast homolog Bre1 as ubiquitin ligases in monoubiquitination of histone H2B. This ubiquitination facilitates methylation of histone H3 at K4 and K79, and accounts for the roles of Bre1 and its homologs in transcriptional regulation. Recent studies by others suggested that Bre1 acts as a tumor suppressor, augmenting expression of select tumor suppressor genes and suppressing select oncogenes. In this study we present an additional mechanism of tumor suppression by Bre1 through maintenance of genomic stability. We track the evolution of genomic instability in Bre1-deficient cells from replication-associated double-strand breaks (DSBs) to specific genomic rearrangements that explain a rapid increase in DNA content and trigger breakage-fusion-bridge cycles. We show that aberrant RNA-DNA structures (R-loops) constitute a significant source of DSBs in Bre1-deficient cells. Combined with a previously reported defect in homologous recombination, generation of R-loops is a likely initiator of replication stress and genomic instability in Bre1-deficient cells. We propose that genomic instability triggered by Bre1 deficiency may be an important early step that precedes acquisition of an invasive phenotype, as we find decreased levels of BRE1A/B and dimethylated H3K79 in testicular seminoma and in the premalignant lesion in situ carcinoma. A cellular modification design type is where a modification of the transcriptome, proteome (not genome) is made, for example RNAi, antibody targeting. Knock down by RNA interference: gene knocked down in RIF-1 cell line cellular_modification_design
2013-01-09 | E-GEOD-34977 | biostudies-arrayexpress
Project description:An analysis of purified Cx32 wt, W3S and R22G mutations. The three different proteins were expressed, digested and measured in DIA.
2023-08-08 | PXD033848 | Pride
Project description:Mammalian Bre1 complexes (BRE1A/B (RNF20/40) in humans and Bre1a/b (Rnf20/40) in mice) function similarly to their yeast homolog Bre1 as ubiquitin ligases in monoubiquitination of histone H2B. This ubiquitination facilitates methylation of histone H3 at K4 and K79, and accounts for the roles of Bre1 and its homologs in transcriptional regulation. Recent studies by others suggested that Bre1 acts as a tumor suppressor, augmenting expression of select tumor suppressor genes and suppressing select oncogenes. In this study we present an additional mechanism of tumor suppression by Bre1 through maintenance of genomic stability. We track the evolution of genomic instability in Bre1-deficient cells from replication-associated double-strand breaks (DSBs) to specific genomic rearrangements that explain a rapid increase in DNA content and trigger breakage-fusion-bridge cycles. We show that aberrant RNA-DNA structures (R-loops) constitute a significant source of DSBs in Bre1-deficient cells. Combined with a previously reported defect in homologous recombination, generation of R-loops is a likely initiator of replication stress and genomic instability in Bre1-deficient cells. We propose that genomic instability triggered by Bre1 deficiency may be an important early step that precedes acquisition of an invasive phenotype, as we find decreased levels of BRE1A/B and dimethylated H3K79 in testicular seminoma and in the premalignant lesion in situ carcinoma. A cellular modification design type is where a modification of the transcriptome, proteome (not genome) is made, for example RNAi, antibody targeting. Knock down by RNA interference: gene knocked down in RIF-1 cell line
2013-01-09 | GSE34977 | GEO