SWI/SNF senses carbon starvation with a pH-sensitive low complexity sequence
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA731118 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14585768.fastq.gz | Fastqsanger.gz | |||
| SRR14585769.fastq.gz | Fastqsanger.gz | |||
| SRR14585770.fastq.gz | Fastqsanger.gz | |||
| SRR14585771.fastq.gz | Fastqsanger.gz | |||
| SRR14585772.fastq.gz | Fastqsanger.gz |
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Project description:It is increasingly appreciated that intracellular pH changes are important biological signals. This motivates the elucidation of molecular mechanisms of pH sensing. We determined that a nucleocytoplasmic pH oscillation was required for the transcriptional response to carbon starvation in Saccharomyces cerevisiae. The SWI/SNF chromatin remodeling complex is a key mediator of this transcriptional response. A glutamine-rich low-complexity domain (QLC) in the SNF5 subunit of this complex, and histidines within this sequence, was required for efficient transcriptional reprogramming. Furthermore, the SNF5 QLC mediated pH-dependent recruitment of SWI/SNF to an acidic transcription factor in a reconstituted nucleosome remodeling assay. Simulations showed that protonation of histidines within the SNF5 QLC leads to conformational expansion, providing a potential biophysical mechanism for regulation of these interactions. Together, our results indicate that pH changes are a second messenger for transcriptional reprogramming during carbon starvation and that the SNF5 QLC acts as a pH sensor.
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Project description:Purpose: It is increasingly appreciated that intracellular pH changes are important biological signals. This motivates the elucidation of molecular mechanisms of pH-sensing. We determined that a nucleocytoplasmic pH oscillation was required for the transcriptional response to carbon starvation in S. cerevisiae. Methods: We performed RNA sequencing analysis to determine the extent of the requirement for theSNF5 QLC in the activation of glucose-repressed genes. Total RNA was extracted from WT, ΔQ-snf5 and HtoA-snf5 strains during exponentially growth (+Glu) and after 4 hours of glucose starvation. Next, Poly-A selection was performed using Dynabeads and libraries were performed following manufactures indications. Sequencing of the 32 samples was performed on an Illumina Hi-seq on two lanes. RNA-seq data were aligned to the University of California, Santa Cruz (UCSC), sacCer2 genome using Kallisto (0.43.0,http://www.nature.com/nbt/journal/v34/n5/full/nbt.3519.html) and downstream visualization and analysis was done using R (3.2.2). Differential gene expression analysis, heat maps and volcano plots were created using DESeq2 where a wald test was used to determine differentially expressed genes and Euclidean distance to calculate clustering for heat maps. Conclusions: We found that pH changes and the SNF5 QLC are required for correct transcriptional reprogramming upon carbon starvation, but the dependencies are nuanced.
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Project description:Fluctuating environments that consist of regular cycles of co-occurring stress are a common challenge faced by cellular populations. For a population to thrive in constantly changing conditions, an ability to coordinate a rapid cellular response is essential. Here, we identify a mutation conferring an arginine-to-histidine (Arg to His) substitution in the transcription terminator Rho. The rho R109H mutation frequently arose in E. coli populations experimentally evolved under repeated long-term starvation conditions, during which feast and famine result in drastic environmental pH fluctuations. Metagenomic sequencing revealed that populations containing the rho mutation also possess putative loss-of-function mutations in ydcI, which encodes a recently characterized transcription factor associated with pH homeostasis. Genetic reconstructions of these mutations show that the rho allele confers a plastic alkaline-induced reduction of Rho function that, when found in tandem with a ΔydcI allele, leads to intracellular alkalinization and genetic assimilation of Rho mutant function. We further identify Arg to His substitutions at analogous sites in rho alleles from species originating from fluctuating alkaline environments. Our results suggest that Arg to His substitutions in global regulators of gene expression can serve to rapidly coordinate complex responses through pH sensing and shed light on how cellular populations across the tree of life use environmental cues to coordinate rapid responses to complex, fluctuating environments.
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Project description:In eukaryotes, ATP-dependent chromatin remodelers regulate gene expression in response to nutritional and metabolic stimuli. The Swi-Snf complex is one such remodeler that has been implicated in disease, where loss of Swi-Snf function leads to dysregulated gene transcription. However, altered transcription of metabolic genes may have consequences for entire pathways that remain poorly understood. In this study, we use genetic and molecular approaches to uncover a role for Swi-Snf as a critical regulator of metabolism. We find that Δsnf mutants are cysteine-deficient, despite growth in nutrient-rich media. This cysteine deficiency causes widespread perturbations in sulfur metabolic gene transcription. This includes global alteration and redistribution of the transcription factor Met4 which senses cysteine deficiency and also has roles in heavy metal stress response and cell cycle progression. Additionally, we show that in its role as a metabolic regulator, Swi-Snf is a critical determinant of survival following oxidative stress. Our findings show how a chromatin remodeler can have a significant impact on a whole metabolic pathway by directly regulating an important gene subset and demonstrate an emerging role for chromatin remodeling complexes as key determinants of metabolic control.
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Project description:In eukaryotes, ATP-dependent chromatin remodelers regulate gene expression in response to nutritional and metabolic stimuli. The Swi-Snf complex is one such remodeler that has been implicated in disease, where loss of Swi-Snf function leads to dysregulated gene transcription. However, altered transcription of metabolic genes may have consequences for entire pathways that remain poorly understood. In this study, we use genetic and molecular approaches to uncover a role for Swi-Snf as a critical regulator of metabolism. We find that Δsnf mutants are cysteine-deficient, despite growth in nutrient-rich media. This cysteine deficiency causes widespread perturbations in sulfur metabolic gene transcription. This includes global alteration and redistribution of the transcription factor Met4 which senses cysteine deficiency and also has roles in heavy metal stress response and cell cycle progression. Additionally, we show that in its role as a metabolic regulator, Swi-Snf is a critical determinant of survival following oxidative stress. Our findings show how a chromatin remodeler can have a significant impact on a whole metabolic pathway by directly regulating an important gene subset and demonstrate an emerging role for chromatin remodeling complexes as key determinants of metabolic control.
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Project description:In eukaryotes, ATP-dependent chromatin remodelers regulate gene expression in response to nutritional and metabolic stimuli. The Swi-Snf complex is one such remodeler that has been implicated in disease, where loss of Swi-Snf function leads to dysregulated gene transcription. However, altered transcription of metabolic genes may have consequences for entire pathways that remain poorly understood. In this study, we use genetic and molecular approaches to uncover a role for Swi-Snf as a critical regulator of metabolism. We find that Δsnf mutants are cysteine-deficient, despite growth in nutrient-rich media. This cysteine deficiency causes widespread perturbations in sulfur metabolic gene transcription. This includes global alteration and redistribution of the transcription factor Met4 which senses cysteine deficiency and also has roles in heavy metal stress response and cell cycle progression. Additionally, we show that in its role as a metabolic regulator, Swi-Snf is a critical determinant of survival following oxidative stress. Our findings show how a chromatin remodeler can have a significant impact on a whole metabolic pathway by directly regulating an important gene subset and demonstrate an emerging role for chromatin remodeling complexes as key determinants of metabolic control.
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Project description:In eukaryotes, ATP-dependent chromatin remodelers regulate gene expression in response to nutritional and metabolic stimuli. The Swi-Snf complex is one such remodeler that has been implicated in disease, where loss of Swi-Snf function leads to dysregulated gene transcription. However, altered transcription of metabolic genes may have consequences for entire pathways that remain poorly understood. In this study, we use genetic and molecular approaches to uncover a role for Swi-Snf as a critical regulator of metabolism. We find that Δsnf mutants are cysteine-deficient, despite growth in nutrient-rich media. This cysteine deficiency causes widespread perturbations in sulfur metabolic gene transcription. This includes global alteration and redistribution of the transcription factor Met4 which senses cysteine deficiency and also has roles in heavy metal stress response and cell cycle progression. Additionally, we show that in its role as a metabolic regulator, Swi-Snf is a critical determinant of survival following oxidative stress. Our findings show how a chromatin remodeler can have a significant impact on a whole metabolic pathway by directly regulating an important gene subset and demonstrate an emerging role for chromatin remodeling complexes as key determinants of metabolic control.
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