Separating the impact of flocculation upon global gene transcription in a yeast Cyc8 mutant
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ABSTRACT:
PROVIDER: PRJNA1044767 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26941200_1.fastq.gz | Fastqsanger.gz | |||
| SRR26941200_2.fastq.gz | Fastqsanger.gz | |||
| SRR26941201_1.fastq.gz | Fastqsanger.gz | |||
| SRR26941201_2.fastq.gz | Fastqsanger.gz | |||
| SRR26941202_1.fastq.gz | Fastqsanger.gz |
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Project description:The transcriptome from a S. cerevisiae tup1 deletion mutant was one of the first comprehensive yeast transcriptomes published. Subsequent transcriptomes from tup1 and cyc8 mutants firmly established the Tup1-Cyc8 complex as predominantly acting as a repressor of gene transcription. However, transcriptomes from tup1/cyc8 gene deletion or conditional mutants would all have been influenced by the striking flocculation phenotypes that these mutants display. In this study, we have separated the impact of flocculation from the transcriptome in a cyc8 conditional mutant to reveal those genes (i) subject solely to Cyc8p dependent regulation, (ii) regulated by flocculation only, and (iii) regulated by Cyc8p and further influenced by flocculation. We reveal an improved Cyc8p transcriptome that includes newly identified Cyc8p-regulated genes that were masked by the flocculation phenotype and excludes genes which were indirectly influenced by flocculation and not regulated by Cyc8p. Furthermore, we show evidence to suggest that flocculation exerts a complex and potentially dynamic influence upon global gene transcription. These data should be of interest to future studies into the mechanism of action of the Tup1-Cyc8 complex and to those involved in understanding the development of flocculation and its impact upon cell function.
2023-12-05 | GSE248550 | GEO
Project description:The Saccharomyces cerevisiae Swi-Snf co-activator complex was the first ATP-dependent chromatin remodelling complex discovered which functions by altering promoter chromatin structure to enable gene transcription. Conversely, the yeast Tup1-Cyc8 complex was identified as the first global co-repressor which can repress transcription by establishing ordered arrays of hypoacetylated nucleosomes across gene promoters. Although studies have indicated potential cooperation between these archetypal complexes upon transcription regulation, the precise mechanism and global extent of this antagonistic interplay remains unclear. We have identified all of the genes subject to repression by Tup1-Cyc8 and activation by Swi-Snf in glucose-grown yeast. These antagonistically regulated genes are enriched for those involved in cell wall structure and sugar metabolism. The data reveals that some co-regulated genes are kept inactive by Tup1-Cyc8 in wt and are de-repressed in the absence of CYC8 in a SNF2-dependent manner. Conversely, other co-regulated genes are actively transcribed in wt at levels mediated by the net negative influence of CYC8 and the positive influence of SNF2. In all cases, co-regulated genes located nearest to telomeres are subject to the most robust regulation by Swi-Snf and Tup1-Cyc8. ChIP analysis suggests that Snf2p and Cyc8p are present at both the active and inactive co-regulated genes in wt, where SNF2 is required for full Tup1p occupancy. We show that Snf2p and Cyc8p can directly interact with each other, most likely in the context of their respective complexes, suggesting that Swi-Snf and Tup1-Cyc8 are present together at co-regulated genes. We demonstrate that the nucleosome remodelling activities by Swi-Snf and Tup1-Cyc8 are specific to each target gene and extend over the available upstream intergenic region, the length of which is dependent upon the genes chromosomal context. Together, these data/ provide a deeper insight into the interplay between Tup1-Cyc8 and Swi-Snf upon transcription regulation and /suggest their occupancy and activity are intimately intertwined to yield the target gene transcriptional outcome via chromosomal location-dependent chromatin remodelling covering the available upstream gene regions.
2026-06-04 | GSE327900 | GEO
Project description:The Saccharomyces cerevisiae Swi-Snf co-activator complex was the first ATP-dependent chromatin remodelling complex discovered which functions by altering promoter chromatin structure to enable gene transcription. Conversely, the yeast Tup1-Cyc8 complex was identified as the first global co-repressor which can repress transcription by establishing ordered arrays of hypoacetylated nucleosomes across gene promoters. Although studies have indicated potential cooperation between these archetypal complexes upon transcription regulation, the precise mechanism and global extent of this antagonistic interplay remains unclear. We have identified all of the genes subject to repression by Tup1-Cyc8 and activation by Swi-Snf in glucose-grown yeast. These antagonistically regulated genes are enriched for those involved in cell wall structure and sugar metabolism. The data reveals that some co-regulated genes are kept inactive by Tup1-Cyc8 in wt and are de-repressed in the absence of CYC8 in a SNF2-dependent manner. Conversely, other co-regulated genes are actively transcribed in wt at levels mediated by the net negative influence of CYC8 and the positive influence of SNF2. In all cases, co-regulated genes located nearest to telomeres are subject to the most robust regulation by Swi-Snf and Tup1-Cyc8. ChIP analysis suggests that Snf2p and Cyc8p are present at both the active and inactive co-regulated genes in wt, where SNF2 is required for full Tup1p occupancy. We show that Snf2p and Cyc8p can directly interact with each other, most likely in the context of their respective complexes, suggesting that Swi-Snf and Tup1-Cyc8 are present together at co-regulated genes. We demonstrate that the nucleosome remodelling activities by Swi-Snf and Tup1-Cyc8 are specific to each target gene and extend over the available upstream intergenic region, the length of which is dependent upon the genes chromosomal context. Together, these data/ provide a deeper insight into the interplay between Tup1-Cyc8 and Swi-Snf upon transcription regulation and /suggest their occupancy and activity are intimately intertwined to yield the target gene transcriptional outcome via chromosomal location-dependent chromatin remodelling covering the available upstream gene regions.
2026-06-04 | GSE302848 | GEO
Project description:The Saccharomyces cerevisiae Swi-Snf co-activator complex was the first ATP-dependent chromatin remodelling complex discovered which functions by altering promoter chromatin structure to enable gene transcription. Conversely, the yeast Tup1-Cyc8 complex was identified as the first global co-repressor which can repress transcription by establishing ordered arrays of hypoacetylated nucleosomes across gene promoters. Although studies have indicated potential cooperation between these archetypal complexes upon transcription regulation, the precise mechanism and global extent of this antagonistic interplay remains unclear. We have identified all of the genes subject to repression by Tup1-Cyc8 and activation by Swi-Snf in glucose-grown yeast. These antagonistically regulated genes are enriched for those involved in cell wall structure and sugar metabolism. The data reveals that some co-regulated genes are kept inactive by Tup1-Cyc8 in wt and are de-repressed in the absence of CYC8 in a SNF2-dependent manner. Conversely, other co-regulated genes are actively transcribed in wt at levels mediated by the net negative influence of CYC8 and the positive influence of SNF2. In all cases, co-regulated genes located nearest to telomeres are subject to the most robust regulation by Swi-Snf and Tup1-Cyc8. ChIP analysis suggests that Snf2p and Cyc8p are present at both the active and inactive co-regulated genes in wt, where SNF2 is required for full Tup1p occupancy. We show that Snf2p and Cyc8p can directly interact with each other, most likely in the context of their respective complexes, suggesting that Swi-Snf and Tup1-Cyc8 are present together at co-regulated genes. We demonstrate that the nucleosome remodelling activities by Swi-Snf and Tup1-Cyc8 are specific to each target gene and extend over the available upstream intergenic region, the length of which is dependent upon the genes chromosomal context. Together, these data/ provide a deeper insight into the interplay between Tup1-Cyc8 and Swi-Snf upon transcription regulation and /suggest their occupancy and activity are intimately intertwined to yield the target gene transcriptional outcome via chromosomal location-dependent chromatin remodelling covering the available upstream gene regions.
2026-05-31 | GSE305763 | GEO
Project description:The Tup1-Cyc8 complex in Saccharomyces cerevisiae was one of the first global co-repressors of gene transcription discovered. The model for Tup1-Cyc8 function proposes that Tup1p mediates the repression activity, whilst Cyc8p recruits the complex to target genes. However, despite years of study, a full understanding of the contribution of Tup1p and Cyc8p to complex function is lacking. We examined TUP1 and CYC8 single and double deletion mutants and show that CYC8 represses more genes than TUP1, and there are genes subject to (i) unique repression by TUP1 or CYC8, (ii) redundant repression by TUP1 and CYC8, and (iii) there are genes at which de-repression in a cyc8 mutant is dependent upon TUP1, and vice-versa. We also reveal that Tup1p and Cyc8p can make distinct contributions to commonly repressed genes possibly via specific interactions with histone deacetylases. Furthermore, we show that Tup1p and Cyc8p can be found independently of each other to negatively regulate gene transcription and can persist at active genes to negatively regulate on-going transcription. Together, these data suggest that Tup1p and Cyc8p can associate with inactive and active genes to mediate distinct negative and positive regulatory roles when functioning within, and possibly out with the complex.
2023-07-05 | GSE230732 | GEO
Project description:The Saccharomyces cerevisiae Swi-Snf co-activator complex was the first ATP-dependent chromatin remodelling complex discovered which functions by altering promoter chromatin structure to enable gene transcription. Conversely, the yeast Tup1-Cyc8 complex was identified as the first global co-repressor which can repress transcription by establishing ordered arrays of hypoacetylated nucleosomes across gene promoters. Although studies have indicated potential cooperation between these archetypal complexes upon transcription regulation, the precise mechanism and global extent of this antagonistic interplay remains unclear. We have identified all of the genes subject to repression by Tup1-Cyc8 and activation by Swi-Snf in glucose-grown yeast. These antagonistically regulated genes are enriched for those involved in cell wall structure and sugar metabolism. The data reveals that some co-regulated genes are kept inactive by Tup1-Cyc8 in wt and are de-repressed in the absence of CYC8 in a SNF2-dependent manner. Conversely, other co-regulated genes are actively transcribed in wt at levels mediated by the net negative influence of CYC8 and the positive influence of SNF2. In all cases, co-regulated genes located nearest to telomeres are subject to the most robust regulation by Swi-Snf and Tup1-Cyc8. ChIP analysis suggests that Snf2p and Cyc8p are present at both the active and inactive co-regulated genes in wt, where SNF2 is required for full Tup1p occupancy. We show that Snf2p and Cyc8p can directly interact with each other, most likely in the context of their respective complexes, suggesting that Swi-Snf and Tup1-Cyc8 are present together at co-regulated genes. We demonstrate that the nucleosome remodelling activities by Swi-Snf and Tup1-Cyc8 are specific to each target gene and extend over the available upstream intergenic region, the length of which is dependent upon the genes chromosomal context. Together, these data/ provide a deeper insight into the interplay between Tup1-Cyc8 and Swi-Snf upon transcription regulation and /suggest their occupancy and activity are intimately intertwined to yield the target gene transcriptional outcome via chromosomal location-dependent chromatin remodelling covering the available upstream gene regions.
2026-05-31 | GSE304974 | GEO
Project description: Not available
| S-EPMC10995634 | biostudies-literature
Project description:Chronologically aging yeast cells are prone to adaptive regrowth, whereby mutants with a survival advantage spontaneously appear and re-enter the cell cycle in stationary phase cultures. Adaptive regrowth is especially noticeable with short-lived strains, including those defective for SNF1, the homolog of mammalian AMP-activated protein kinase (AMPK). SNF1 becomes active in response to multiple environmental stresses that occur in chronologically aging cells, including glucose depletion and oxidative stress. SNF1 is also required for the extension of chronological lifespan (CLS) by caloric restriction (CR) as defined as limiting glucose at the time of culture inoculation. To identify specific downstream SNF1 targets responsible for CLS extension during CR, we screened for adaptive regrowth mutants that restore chronological longevity to a short-lived snf1∆ parental strain. Whole genome sequencing of the adapted mutants revealed missense mutations in TPR motifs 9 and 10 of the transcriptional co-repressor Cyc8 that specifically mediate repression through the transcriptional repressor Mig1. Another mutation occurred in MIG1 itself, thus implicating the activation of Mig1-repressed genes as a key function of SNF1 in maintaining CLS. Consistent with this conclusion, the cyc8 TPR mutations partially restored growth on alternative carbon sources and significantly extended CLS compared to the snf1∆ parent. Furthermore, cyc8 TPR mutations reactivated multiple Mig1-repressed genes, including the transcription factor gene CAT8, which is responsible for activating genes of the glyoxylate and gluconeogenesis pathways. Deleting CAT8 completely blocked CLS extension by the cyc8 TPR mutations on CLS, identifying these pathways as key Snf1-regulated CLS determinants.
2018-03-28 | GSE110409 | GEO
Project description:Saccharomyces cerevisiae normally cannot assimilate mannitol, a promising brown macroalgal carbon source for bioethanol production. To date, the molecular mechanisms underlying this inability remain unknown. Here, we found that cells acquiring mannitol-assimilating ability appeared from wild-type S. cerevisiae strain during prolonged culture in mannitol medium. Our microarray analysis revealed that genes for putative mannitol dehydrogenase and hexose transporters were up-regulated in cells acquiring mannitol-assimilating ability. Take account of our other results including complementation analysis and cell growth data, we demonstrated that this acquisition of mannitol-assimilating ability was due to the spontaneous mutation in the gene encoding Tup1 or Cyc8. Tup1-Cyc8 is the general corepressor complex involved in the repression of many kinds of genes. Thus, it is suggested that the inability of wild-type S. cerevisiae to assimilate mannitol can be attributed to the transcriptional repression of a set of genes involved in mannitol utilization by Tup1-Cyc8 corepressor. In other words, Tup1-Cyc8 is a key regulator of mannitol metabolism in S. cerevisiae. We also showed that S. cerevisiae strain which carries mutant allele of TUP1 or CYC8 produced ethanol from mannitol efficiently. Especially, strain carrying mutant allele of CYC8 showed high tolerance to salt, which is superior to other ethanologenic microorganisms. This characteristic is highly beneficial to produce bioethanol from marine biomass. Taken together, Tup1-Cyc8 can be an ideal target to develop a yeast-algal bioethanol production system. To figure out how Mtl+ strains (cells acquiring ability to grow in mannitol medium) had acquired the ability to assimilate mannitol, we performed genome-wide analysis by using Nimblegen microarrays. Yeast Saccharomyces cerevisiae cells (wild-type BY4742 strain and two Mtl+ strains, MK3619 and MK3683) were grown at 30°C to the logarithmic phase in SC or SM media. Total RNA was purified and the 4 RNA samples (BY4742 cells in SC as control, MK3619 cells in SM, MK3683 cells in both SC and SM) were analyzed with Nimblegen microarrays.
2014-12-04 | E-GEOD-55755 | biostudies-arrayexpress
Project description: Not available
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