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Methionine starvation caused reprogrammed metabolism in Streptococcus pneumoniae

ABSTRACT: Methionine starvation caused reprogrammed metabolism in Streptococcus pneumoniae

PROVIDER: PRJNA763168 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15887655_1.fastq.gz	Fastqsanger.gz
	SRR15887655_2.fastq.gz	Fastqsanger.gz
	SRR15887657_1.fastq.gz	Fastqsanger.gz
	SRR15887657_2.fastq.gz	Fastqsanger.gz
	SRR15887659_1.fastq.gz	Fastqsanger.gz

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Methionine starvation caused reprogrammed metabolism in Streptococcus pneumoniae

Project description:In our study, deletion of methionine synthesis gene metE (SPD_0510) impaired the growth of Streptococcus pneumoniae strain D39 significantly when bacteria were cultured in chemically defined medium with a low concentration of methionine. Bacteria undergo methionine starvation in this condition. We aimed to know how S. pneumoniae responses to methionine starvation, particularly at the transcriptional level. RNA-seq results show that 804 genes (41.2 % of whole genome) were differentially expressed under methionine starvation. Among them, 258 genes (32.1 %) are related to cell metabolism, with 75 genes involved in sugar and carbon metabolism, 88 genes for synthesis of metabolic products and 95 genes for uptake of amino acids and sugars. Combined with other experiments data, this showed the reprogrammed metabolism in S. pneumoniae under methionine starvation.

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Methionine starvation of M. tuberculosis H37Rv ΔmetA

Project description:Time-course transcriptional profiling of the methionine auxotroph M. tuberculosis H37Rv ΔmetA during methionine starvation

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Dietary methionine starvation impairs acute myeloid leukemia progression

Project description:Targeting altered tumor cell metabolism might provide an attractive opportunity for patients with acute myeloid leukemia (AML). An amino acid dropout screen on primary leukemic stem cells and progenitor populations revealed a number of amino acid dependencies, of which methionine was one of the strongest. By using various metabolite rescue experiments, NMR-based metabolite quantifications and 13C-tracing, polysomal profiling, and ChIP-seq, we identified that methionine is used predominantly for protein translation and to provide methyl groups to histones via S-adenosylmethionine for epigenetic marking. H3K36me3 was consistently the most heavily impacted mark following loss of methionine. Methionine depletion also reduced total RNA levels, enhanced apoptosis and induced a cell cycle block. ROS levels were not increased following methionine depletion and replacement of methionine with glutathione or N-acetylcysteine could not rescue phenotypes, excluding a role for methionine in controlling redox balance control in AML. Although considered to be an essential amino acid, methionine can be recycled from homocysteine. We uncovered that this is primarily performed by the enzyme methionine synthase and only when methionine availability becomes limiting. In vivo, dietary methionine starvation was not only tolerated by mice, but also significantly delayed both cell line and patient-derived AML progression. Finally, we show that inhibition of the H3K36-specific methyltransferase SETD2 phenocopies much of the cytotoxic effects of methionine depletion, providing a more targeted therapeutic approach. In conclusion, we show that methionine depletion is a vulnerability in AML that can be exploited therapeutically, and we provide mechanistic insight into how cells metabolize and recycle methionine.

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Dietary methionine starvation impairs acute myeloid leukemia progression

Project description:Dietary methionine starvation impairs acute myeloid leukemia progression

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Transcriptional adaptation during starvation of Mycobacterium tuberculosis H37Rv ∆thrA

Project description:Time-course transcriptional profiling of the methionine auxotroph M. tuberculosis H37Rv ΔthrA during methionine starvation

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SIRT1 regulates methionine metabolism and pluripotency of mouse embrynoic stem cells (mESCs)

Project description:The goal of this project is to understand the role of SIRT1, the most conserved mammalian NAD+-dependent protein deacetylase, in methionine metabolism and pluripotency of mESCs. Our recent studies indicate that SIRT1 deficient mESCs are hypersensitive to methionine restriction-induced differentiation and apoptosis, primarily due to a reduced conversion of methionine to S-adenosylmethionine. This reduction leads to marked decrease in methylation levels of histones in SIRT1 deficient mESCs. To understand the impact of histone methylation alterations on stem cell functions in SIRT1 KO mESCs, we examined the transcriptomes of SIRT1 WT and KO mESCs cultured in either complete M10 medium (com) or methionine restricted medium containing 6 uM methionine (6met) for 6, 24, and 72 hours by microarray analysis.

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Project description:Limitation of essential amino acids, such as tyrosine or methionine/cysteine, causes upregulation of exogenous integrated transgene expression in mammalian cells. This phenomenon is mediated by histone acetylation and chromatin remodelling, since histone deacetylase (HDAC) inhibitors reproduce starvation-induced transgene upregulation and chromatin immunoprecipitation analysis of amino acid-deprived cells reveals significant changes in total core histones detectable at the CMV promoter. Expression profiling of HeLa cells starved for 5 days in medium without tyrosine or methionine/cysteine provides important information on the cellular response to amino acid deprivation and suggests the involvement of HDAC4 (class II HDAC) in transgene derepression during amino acid starvation. Total RNA obtained from HeLa and HeLaOA1myc cells (HeLa cells with a human ocular albinism type 1 (OA1)+myc tag transgene) subjected to 5 days of tyrosine or methionine/cysteine starvation compared to control cells. Twelve samples are analyzed: HeLa and HeLaOA1myc grown for 5 days in RPMI deprived of tyrosine (Y) vs. complete RPMI; technical duplicates of HeLa and HeLaOA1myc grown for 5 days in DMEM deprived of methionine/cysteine (MC) vs. complete DMEM.

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Project description:Hepatocellular carcinoma (HCC) represents the third leading cause of cancer-related death worldwide and has been increasing in recent years in developed nations1,2. The MYC oncogene or its paralogs are frequently amplified or overexpressed in particularly aggressive subtypes of cancer associated with stem cell-like features and worse clinical outcomes3,4, including in liver cancer5. Unfortunately, selective inhibitors that target MYC or its transcriptional program are not yet clinically available for therapy of HCC. Here, we identified methionine metabolism as a selective vulnerability for MYC but not RAS-driven liver cancers. MYC-driven liver cancer cells are methionine dependent and S-adenosylmethionine (SAM), the predominant methyl donor, partially rescues methionine depletion. A low methionine diet, or the methylation inhibitor 5-azacytidine limited MYC-driven tumor formation, but RAS-driven liver cancer was resistant to a low methionine diet. Metabolic tracing of methionine catabolism in MYC high cells identified increased m5C methylation of genomic DNA or ribosomal RNA. We identified NOP2, an rRNA m5C-methyltransferase as a MYC target gene. Knockdown of NOP2 selectively inhibited MYC liver cancer cell proliferation and in vivo tumorigenesis. Thus, methionine catabolism is critical for MYC-driven liver tumorigenesis and NOP2 may serve as a new therapeutic target in liver cancer.

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