Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1117860 | ENA |
REPOSITORIES: ENA
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Project description:Gene expression was quantified in S. cerevisiae cells after 40 hours of LiCl treatment or control conditions. Cells expressing wild type (WT) Hcm1, a stable Hcm1 mutant (Hcm1-3N), or a consitutitvely active, phosphomimetic mutant (Hcm1-8E) were compared to allow the identification of genes whose expression depends upon dynamic phosphorylation of Hcm1. We found that dynamic phosphorylation of Hcm1 is required for expression of Hcm1 target genes in LiCl stress.
2024-09-18 | GSE276435 | GEO
Project description:Analysis of gene expression across the cell cycle from wild type cells, and cells expressing alleles of Yox1, Yhp1, Hcm1, and Tos4 that cannot be phosphorylated by Cdk1. Expression of S-phase and M/G1 transcripts are downregulated when phosphorylation of these factors is blocked, demonstrating that Cdk1 promotes expression of late cell cycle genes.
2014-04-10 | GSE55121 | GEO
Project description:In S. cerevisiae, the forkhead transcription factor Hcm1 has been involved in chromosome segregation, spindle pole dynamics and budding. We found that, in response to oxidative stress stimuli, Hcm1 shifts from cytoplasm to the nucleus, interacting with the histone deacetylase Sir2, which regulates Hcm1 localization. Hcm1-overexpressing cells showed increased resistance to oxidative stress which can be attributed to increased catalase and Sod2 activities. Microarray analysis revealed that genes corresponding to mitochondrial function and transition from exponential to stationary phase are clearly induced in these cells which consistently showed higher rates of oxygen consumption due to an increase in mitochondria – possibly triggered by higher amounts of Abf2, a protein involved in mitochondrial biogenesis. In wild-type cells, when glucose levels decreased by 50%, we observed Hcm1 translocation to the nucleus and increased Hcm1 levels. We conclude that Hcm1 may act as an early regulator to respond to nutrient limitation, increasing stress resistance and mitochondrial function and thereby allowing the cells to adapt to nutrient limitations by shifting from fermentative to respiratory metabolism.
2010-10-04 | GSE20420 | GEO
Project description:Regulation of gene expression by Hcm1 in chronic LiCl stress
| PRJNA1157366 | ENA
Project description:Here we show that ?-catenin mediates pro-resilient and anxiolytic effects in mice in the nucleus accumbens (NAc), a key brain reward region, an effect that is mediated by ?-catenin signaling in D2-type medium spiny neurons (MSNs) specifically. Conversely, blocking ?-catenin function in NAc promotes susceptibility to chronic stress, and we show evidence of robust suppression of ?-catenin transcriptional activity in the NAc both of depressed humans examined postmortem as well as of mice that display a susceptible phenotype after chronic stress, with a converse upregulation in mice that are stress resilient. Using ChIP-seq, we demonstrate a global, genome-wide enrichment of ?-catenin in the NAc of resilient mice, and specifically identify Dicer1—important in small RNA (e.g., microRNA [miRNA]) biogenesis—as a critical ?-catenin target gene involved in mediating a resilient phenotype. Small RNA-seq after excising ?-catenin from the NAc in the context of chronic stress reveals dynamic ?-catenin-dependent miRNA regulation associated with resilience. Control: 2 samples, Resilient: 2 samples, Susceptible: 2 samples; DNA input: 1 sample.
2014-11-13 | E-GEOD-61294 | biostudies-arrayexpress
Project description:Analysis of gene expression across the cell cycle from wild type cells, and cells expressing alleles of Yox1, Yhp1, Hcm1, and Tos4 that cannot be phosphorylated by Cdk1. Expression of S-phase and M/G1 transcripts are downregulated when phosphorylation of these factors is blocked, demonstrating that Cdk1 promotes expression of late cell cycle genes. These experiments are two-color hybridizations of RNA isolated from synchronized wild type (WT) or phosphomutant (4P) cells, compared to RNA from asyncrhonous wild type cells in mid-log phase. Wild type and mutant cells were synchronized in G1 phase, released into the cell cycle and samples collected at 15 minute intervals. Each time course was carried out in duplicate, the replicate experiment was performed as a dye swap.
2014-04-10 | E-GEOD-55121 | biostudies-arrayexpress
Project description:Here we show that ?-catenin mediates pro-resilient and anxiolytic effects in mice in the nucleus accumbens (NAc), a key brain reward region, an effect that is mediated by ?-catenin signaling in D2-type medium spiny neurons (MSNs) specifically. Conversely, blocking ?-catenin function in NAc promotes susceptibility to chronic stress, and we show evidence of robust suppression of ?-catenin transcriptional activity in the NAc both of depressed humans examined postmortem as well as of mice that display a susceptible phenotype after chronic stress, with a converse upregulation in mice that are stress resilient. Using ChIP-seq, we demonstrate a global, genome-wide enrichment of ?-catenin in the NAc of resilient mice, and specifically identify Dicer1—important in small RNA (e.g., microRNA [miRNA]) biogenesis—as a critical ?-catenin target gene involved in mediating a resilient phenotype. Small RNA-seq after excising ?-catenin from the NAc in the context of chronic stress reveals dynamic ?-catenin-dependent miRNA regulation associated with resilience. GFP_Control: 12 samples, GFP_Resilient: 12 samples, GFP_Susceptible: 4 samples; CRE_Control: 12 samples, CRE_Susceptible: 8 samples.
2014-11-13 | E-GEOD-61295 | biostudies-arrayexpress
Project description:Obesity is a chronic organismal stress that disrupts multiple systemic and tissue-specific functions. Here, we describe the effects of established obesity on the activity of the hematopoietic stem cell (HSC) compartment. We show that obesity promotes the selection of a quiescent HSC subset primed for activation, leading to aberrant hematopoietic stress responses. We establish that the transcription factor Gfi1 is a key regulator of the HSC fate in obesity as its increased expression in obesity induces their abnormal activity. We demonstrate that these dysregulations are initially triggered by the chronic oxidative stress associated with obesity. Once acquired, we show that the impact of obesity on HSCs is long lasting and cannot be reversed by weight loss or transplantation. These results demonstrated that obesity promotes irreversible changes on the long-term fitness of the HSC compartment, a phenomenon that is likely to contribute to the hematopoietic dysregulations observed in obese patients.
2019-12-02 | GSE94087 | GEO
Project description:Obesity is a chronic organismal stress that disrupts multiple systemic and tissue-specific functions. Here, we describe the effects of established obesity on the activity of the hematopoietic stem cell (HSC) compartment. We show that obesity promotes the selection of a quiescent HSC subset primed for activation, leading to aberrant hematopoietic stress responses. We establish that the transcription factor Gfi1 is a key regulator of the HSC fate in obesity as its increased expression in obesity induces their abnormal activity. We demonstrate that these dysregulations are initially triggered by the chronic oxidative stress associated with obesity. Once acquired, we show that the impact of obesity on HSCs is long lasting and cannot be reversed by weight loss or transplantation. These results demonstrated that obesity promotes irreversible changes on the long-term fitness of the HSC compartment, a phenomenon that is likely to contribute to the hematopoietic dysregulations observed in obese patients.
2017-11-23 | GSE90725 | GEO