Transcriptional profiling of pH-dependent cell cycle progression
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA608468 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11172945.fastq.gz | Fastqsanger.gz | |||
| SRR11172946.fastq.gz | Fastqsanger.gz | |||
| SRR11172947.fastq.gz | Fastqsanger.gz | |||
| SRR11172948.fastq.gz | Fastqsanger.gz | |||
| SRR11172949.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
Similar Datasets
Project description:Cells have evolved a complex network of signaling cascades that mediate cellular adaptation to availability of nutrients, growth factors or stress. In these networks, cellular information flow is mostly mediated by posttranslational modifications, most notably phosphorylation, or signaling molecules such as GTPases. However, genetic analysis has also implicated a number of proton transporters in regulating cellular signaling processes. Here, we report the transcriptional response of starved cells upon stimulation with serum and glucose upon inhibition of Sodium Hydrogen Exchangers and compare these responses to inhibition of cycle progression with the p300/CBP inhibitor C646.
2020-08-11 | GSE145833 | GEO
Project description:Intracellular pH (pHi) dynamics regulates diverse cell processes such as proliferation, dysplasia, and differentiation, often mediated by the protonation state of a functionally critical histidine residue in endogenous pH sensing proteins. How pHi dynamics can directly regulate gene expression and whether transcription factors can function as pH sensors has received limited attention. We tested the prediction that transcription factors with a histidine in their DNA binding domain (DBD) that forms hydrogen bonds with nucleotides can have pH-regulated activity, which is relevant to more than 85 transcription factors in distinct families, including FOX, KLF, SOX and MITF/Myc. Focusing on FOX family transcription factors, we used unbiased SELEX-seq to identify pH-dependent DNA binding motif preferences, then confirm pH-regulated binding affinities for FOXC2, FOXM1, and FOXN1 to a canonical FkhP DNA motif that are 2.5 to 7.5 greater at pH 7.0 compared with pH 7.5. For FOXC2, we also find greater activity for an FkhP motif at lower pHi in cells and that pH-regulated binding and activity are dependent on a conserved histidine (His122) in the DBD. RNA-seq with FOXC2 also reveals pH-dependent differences in enriched promoter motifs. Our findings identify pH-regulated transcription factor-DNA binding selectivity with relevance to how pHi dynamics can regulate gene expression for myriad cell behaviours.
2024-06-24 | GSE270316 | GEO
Project description:Cell cycle-dependent chromatin and transcriptional changes
| PRJNA705689 | ENA
Project description:Intracellular pH (pHi) dynamics regulates diverse cell processes such as proliferation, dysplasia, and differentiation, often mediated by the protonation state of a functionally critical histidine residue in endogenous pH sensing proteins. How pHi dynamics can directly regulate gene expression and whether transcription factors can function as pH sensors has received limited attention. We tested the prediction that transcription factors with a histidine in their DNA binding domain (DBD) that forms hydrogen bonds with nucleotides can have pH-regulated activity, which is relevant to more than 85 transcription factors in distinct families, including FOX, KLF, SOX and MITF/Myc. Focusing on FOX family transcription factors, we used unbiased SELEX-seq to identify pH-dependent DNA binding motif preferences, then confirm pH-regulated binding affinities for FOXC2, FOXM1, and FOXN1 to a canonical FkhP DNA motif that are 2.5 to 7.5 greater at pH 7.0 compared with pH 7.5. For FOXC2, we also find greater activity for an FkhP motif at lower pHi in cells and that pH-regulated binding and activity are dependent on a conserved histidine (His122) in the DBD. RNA-seq with FOXC2 also reveals pH-dependent differences in enriched promoter motifs. Our findings identify pH-regulated transcription factor-DNA binding selectivity with relevance to how pHi dynamics can regulate gene expression for myriad cell behaviours.
2025-04-04 | GSE293822 | GEO
Project description:Intracellular pH (pHi) dynamics regulates diverse cell processes such as proliferation, dysplasia, and differentiation, often mediated by the protonation state of a functionally critical histidine residue in endogenous pH sensing proteins. How pHi dynamics can directly regulate gene expression and whether transcription factors can function as pH sensors has received limited attention. We tested the prediction that transcription factors with a histidine in their DNA binding domain (DBD) that forms hydrogen bonds with nucleotides can have pH-regulated activity, which is relevant to more than 85 transcription factors in distinct families, including FOX, KLF, SOX and MITF/Myc. Focusing on FOX family transcription factors, we used unbiased SELEX-seq to identify pH-dependent DNA binding motif preferences, then confirm pH-regulated binding affinities for FOXC2, FOXM1, and FOXN1 to a canonical FkhP DNA motif that are 2.5 to 7.5 greater at pH 7.0 compared with pH 7.5. For FOXC2, we also find greater activity for an FkhP motif at lower pHi in cells and that pH-regulated binding and activity are dependent on a conserved histidine (His122) in the DBD. RNA-seq with FOXC2 also reveals pH-dependent differences in enriched promoter motifs. Our findings identify pH-regulated transcription factor-DNA binding selectivity with relevance to how pHi dynamics can regulate gene expression for myriad cell behaviours.
2024-06-24 | GSE270232 | GEO
Project description:FOXC2-HIS122 and pH-dependent gene expression
| PRJNA1125484 | ENA
Project description:The purpose of this study was to examine how Mtb integrates acidic pH and available carbon sources as environmental cues to regulate its metabolism and growth rate. RNA-seq transcriptional profiling of M. tuberculosis growing at acidic or neutral pH, in pyruvate or glycerol, was examined. These studies identified carbon source-dependent and -independent pH-dependent adaptations.
2014-07-07 | GSE52020 | GEO
Project description:Amino acid homeostasis is critical for many cellular processes. It is well established that amino acids are compartmentalized using pH gradients generated between organelles and the cytoplasm; however, the dynamics of this partitioning has not been explored. We have developed a highly sensitive pH reporter, and we find that the major amino acid storage compartment in Saccharomyces cerevisiae, the lysosome-like vacuole, alkalinizes prior to cell division and re-acidifies as cells divide. The vacuolar pH dynamics require the uptake of extracellular amino acids and activity of TORC1, the v-ATPase and the cycling of the vacuolar specific lipid, PI3,5P2 which is regulated by the cyclin-dependent kinase, CDK5/Pho85. Vacuolar pH regulation enables amino acid sequestration and mobilization from the organelle, which is important for mitochondrial function, ribosome homeostasis and cell size control. Collectively, our data provide a new paradigm for the use of dynamic pH-dependent amino acid compartmentalization during cell growth/division.
2023-07-10 | GSE236913 | GEO
Project description:Polymerase II pausing licenses cell-cycle progression
| PRJNA393887 | ENA
Project description:Entry into the cell cycle requires activation of G1 cyclin-dependent kinases (CDKs) and the initiation of the G1/S transcriptional program. Unregulated transcription of this gene expression program can lead to genomic instability and aneuploidy. In fission yeast, the MBF complex is the key transcription factor that drives early cell-cycle gene expression. MBF-dependent transcription is triggered in metaphase and is suppressed at the end of S phase by a robust feedback mechanism involving the cyclin Cig2 and the co-repressors Nrm1 and Yox1. Under replicative stress, Yox1 is phosphorylated to release its repressive activity; however, the precise mechanism activating MBF in an unperturbed cell cycle remains unclear. Here, we identify Nrm1 as the primary target of the cell cycle machinery in regulating MBF activity through a two-step control mechanism. We demonstrate that CDK1-mediated phosphorylation of Nrm1 initiates its release, along with Yox1, from chromatin in metaphase. This mechanism overlaps with the irreversible degradation of unphosphorylated Nrm1 (which originates from de novo synthesis or by dephosphorylation of pre-existing Nrm1 during anaphase), preventing its re-association with MBF until the end of the following S phase. These parallel mechanisms, which sense cell cycle status, create a regulated window in which MBF-dependent transcription is relieved from repression, supporting orderly cell cycle progression.
2025-07-23 | GSE287772 | GEO