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RNA seq of Saccharomyces cerevisiae expressing pathways designed to increase ATP or GTP consumption

ABSTRACT: RNA seq of Saccharomyces cerevisiae expressing pathways designed to increase ATP or GTP consumption

PROVIDER: PRJEB16729 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR1701930.fastq.gz	Fastqsanger.gz
	ERR1701940.fastq.gz	Fastqsanger.gz
	ERR1701950.fastq.gz	Fastqsanger.gz
	ERR1701960.fastq.gz	Fastqsanger.gz
	ERR1701970.fastq.gz	Fastqsanger.gz

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RNA seq of Saccharomyces cerevisiae expressing pathways designed to increase ATP or GTP consumption

Project description:Many studies in yeast have observed correlations between changes in phosphorylated adenosine and guanosine nucleotide concentrations, and changes in cell physiology or gene expression. Evidence for a causal relationship is however sparse. To investigate this further under controlled conditions, we have developed strains of S. cerevisiae containing inducible pathways which increase use of ATP or GTP. Analysis of the transcriptional response following induction of these strains during continuous culture in chemostats allowed the effects of specifically increasing the demand for each purine nucleotide triphosphate to be determined independently of growth rate and nutritional changes.

2018-08-23 | E-MTAB-5174 | biostudies-arrayexpress

E-MTAB-5174

Project description:RNA seq of Saccharomyces cerevisiae expressing pathways designed to increase ATP or GTP consumption

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Mitochondria inside acute myeloid leukemia cells hydrolyze ATP to resist chemotherapy

Project description:Despite early optimism, therapeutics targeting oxidative phosphorylation (OxPhos) have faced clinical setbacks, primarily stemming from their inability to distinguish healthy from cancerous mitochondria. Herein, we describe an actionable bioenergetic mechanism unique to cancerous mitochondria inside acute myeloid leukemia (AML) cells. Unlike healthy cells which couple respiration to the synthesis of ATP, AML mitochondria were discovered to support inner membrane polarization by consuming ATP. Because matrix ATP consumption allows cells to survive bioenergetic stress, we hypothesized that AML cells may resist cell death induced by OxPhos damaging chemotherapy by reversing the ATP synthase reaction. In support of our hypothesis, targeted inhibition of BCL-2 with venetoclax abolished OxPhos flux without impacting mitochondrial membrane potential. In surviving AML cells, sustained polarization of the mitochondrial inner membrane was dependent on matrix ATP consumption. Mitochondrial ATP consumption was further enhanced in AML cells made refractory venetoclax, consequential to downregulations in both the proton-pumping respiratory complexes, as well the endogenous F1-ATPase inhibitor ATP5IF1. In treatment-naive AML, ATP5IF1 knockdown was sufficient to drive venetoclax resistance, while ATP5IF1 overexpression impaired F1-ATPase activity and heightened sensitivity to venetoclax. Collectively, our data identify matrix ATP consumption as cancer-cell intrinsic bioenergetic vulnerability actionable in the context of mitochondrial damaging chemotherapy.

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