Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Cellular responses to long-term phosphate starvation of fission yeast: Maf1 determines fate choice between quiescence and death associated with aberrant tRNA biogenesis (CHX experiments)

ABSTRACT: Cellular responses to long-term phosphate starvation of fission yeast: Maf1 determines fate choice between quiescence and death associated with aberrant tRNA biogenesis (CHX experiments)

PROVIDER: PRJNA901456 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR22280603_1.fastq.gz	Fastqsanger.gz
	SRR22280603_2.fastq.gz	Fastqsanger.gz
	SRR22280604_1.fastq.gz	Fastqsanger.gz
	SRR22280604_2.fastq.gz	Fastqsanger.gz
	SRR22280605_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 42

Similar Datasets

Cellular responses to long-term phosphate starvation of fission yeast: Maf1 determines fate choice between quiescence and death associated with aberrant tRNA biogenesis

Project description:Inorganic phosphate is an essential nutrient acquired by cells from their environment. Here we characterize the adaptative responses of fission yeast to chronic phosphate starvation, during which cells enter a state of quiescence, initially fully reversible upon replenishing phosphate after 2 days but resulting in gradual loss of viability during 4 weeks of starvation. Time-resolved analyses of changes in mRNA levels revealed a coherent transcriptional program in which phosphate dynamics and autophagy were upregulated, while the machineries for rRNA synthesis and ribosome assembly, and for tRNA synthesis and maturation, were downregulated in tandem with global repression of genes encoding ribosomal proteins and translation factors. Consistent with the transcriptome changes, proteome analysis highlighted global depletion of 102 ribosomal proteins. Concomitant with this ribosomal protein deficit, 28S and 18S rRNAs became vulnerable to site-specific cleavages that generated temporally stable rRNA fragments. The finding that Maf1, a repressor of RNA polymerase III transcription, was upregulated during phosphate starvation prompted a hypothesis that its activity might prolong lifespan of the quiescent cells by limiting production of tRNAs. Indeed, we found that deletion of maf1 results in precocious death of phosphate-starved cells via a distinctive starvation-induced pathway associated with tRNA overproduction and dysfunctional tRNA biogenesis.

2023-02-18 | PXD038988 | Pride

Cellular responses to long-term phosphate starvation of fission yeast: Maf1 determines fate choice between quiescence and death associated with aberrant tRNA biogenesis (CHX experiments)

Project description:This RNA-Seq analysis compares gene expression of fission yeast cells (Schizosaccharomyces pombe) at various times after phosphate starvation (2, 4, and 8 HR) either with 100 µg/ml cycloheximide or without drug contrasting to the cells grown in phosphate replete conditions (0HR) in the absence of the drug.

2023-01-19 | GSE217952 | GEO

Cellular responses to long-term phosphate starvation of fission yeast: Maf1 determines fate choice between quiescence and death associated with aberrant tRNA biogenesis

Project description:Cellular responses to long-term phosphate starvation of fission yeast: Maf1 determines fate choice between quiescence and death associated with aberrant tRNA biogenesis

| PRJNA880878 | ENA

Cellular responses to long-term phosphate starvation of fission yeast: Maf1 determines fate choice between quiescence and death associated with aberrant tRNA biogenesis

Project description:Cellular responses to long-term phosphate starvation of fission yeast: Maf1 determines fate choice between quiescence and death associated with aberrant tRNA biogenesis

| PRJNA901453 | ENA

Effects of cycloheximide (CHX) on ribosome profiling experiments in Schizosaccharomyces pombe

Project description:CHX is an inhibitor of translation elongation often used in ribosome profiling experiments. There is evidence that CHX treatment of cells may cause artefacts in the distribution of ribosomes on mRNAs. We investigate this possibility in S. pombe by performing ribosome profiling in the presence and absence of this drug.

2017-09-05 | E-MTAB-5794 | biostudies-arrayexpress

ChIP-seq experiments for “Chronic repression by MAF1 supports futile RNA cycling as a mechanism for obesity resistance”

Project description:To characterize the PolIII transcription changes in Maf1-/- samples, we perfomeded ChIP-seq on WT and Maf1-/- Mouse liver samples. Mice were either fasted during eight hours or fasted for four hours and then refed.

2019-11-04 | GSE104531 | GEO

RNA-seq total KO experiments for "Chronic repression by MAF1 supports futile RNA cycling as a mechanism for obesity resistance"

Project description:To examine the effect of MAF1 on the RNA polymerase II transcriptome, RNA-seq was performed on samples of liver from overnight fasted and four hour refed wild-type and whole-body Maf1-/- mice.

2019-11-04 | GSE104496 | GEO

Ribosome-profiling experiments for “Chronic repression by MAF1 supports futile RNA cycling as a mechanism for obesity resistance”

Project description:To characterize the translation defects in Maf1-/- samples, we used ribosome profiling on three WT and three Maf1-/- fed livers. Each sample was spiked with a fixed amount of Drosophila S2 Schneider cell material as an internal control for sample-to-sample normalization, and to allow detection of global changes in translation.

2019-11-04 | GSE104503 | GEO

MAF1 Represses CDKN1A through a Pol III-Dependent Mechanism

Project description:MAF1 represses Pol III-mediated transcription by interfering with TFIIIB and Pol III. Herein, we found that MAF1 knockdown induced CDKN1A transcription and chromatin looping concurrently with Pol III recruitment. Simultaneous knockdown of MAF1 with Pol III or BRF1 (subunit of TFIIIB) diminished the activation and looping effect, which indicates that recruiting Pol III was required for activation of Pol II-mediated transcription and chromatin looping. ChIP analysis after MAF1 knockdown indicated enhanced binding of Pol III and BRF1, as well as of CFP1, p300, and PCAF, which are factors that mediate active histone marks, along with the binding of TBP and POLR2E to the CDKN1A promoter. Simultaneous knockdown with Pol III abolished these regulatory events. Similar results were obtained for GDF15. Our results reveal a novel mechanism by which MAF1 and Pol III regulate the activity of a protein-coding gene transcribed by Pol II. Knockdown assay was performed using siRNA obtained from MISSION®RNA (Sigma). Inhibition of expression of Pol III (SASI_Hs01_00046568) and MAF1 (SASI_Hs01_00135954) was achieved by transfection with LipofectamineTM RNAiMax (Invitrogen) according to the manufacturer’s protocol. MISSION® siRNA Universal Negative Control (Sigma) was used as knockdown control. Cells were transfected in serum-free medium. After 8 h, the siRNA containing medium was replaced with complete medium.

2015-06-10 | E-GEOD-42239 | biostudies-arrayexpress

MAF1 Represses CDKN1A through a Pol III-Dependent Mechanism

2015-06-10 | GSE42239 | GEO