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Transcriptome analysis of methionine restriction and folate metabolism inhibitor SHIN1 treatment in P3HR-1 cells

ABSTRACT: Transcriptome analysis of methionine restriction and folate metabolism inhibitor SHIN1 treatment in P3HR-1 cells

PROVIDER: PRJNA789237 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17261400.fastq.gz	Fastqsanger.gz
	SRR17261401.fastq.gz	Fastqsanger.gz
	SRR17261402.fastq.gz	Fastqsanger.gz
	SRR17261403.fastq.gz	Fastqsanger.gz
	SRR17261404.fastq.gz	Fastqsanger.gz

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Transcriptome analysis of methionine restriction and folate metabolism inhibitor SHIN1 treatment in P3HR-1 cells

Project description:RNAseq was used to identify host and viral transcriptome changes in methionine restricted or SHIN1 treated P3HR-1 cells.

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Project description:Folate is important for fetal development and growth, yet its role in placentation is understudied. Here we report that disrupting folate metabolism by the hypomorphic Mtrr mutation in mice causes morphological and functional defects in their placentas that correspond with early- and late-onset fetal growth restriction. Remarkably, Mtrr heterozygous males initiate inheritance of similar placenta phenotypes and fetal growth defects in their wildtype grandprogeny. An integrated genome-wide approach shows placental transcriptional change and epigenetic instability is caused by an intrinsic or ancestral Mtrr mutation, affecting genes important for placenta development and function (e.g., pregnancy specific glycoprotein (Psg)/Ceacams). Crucially, we establish a functional association between mouse placenta transcript levels and fetal size and identify a human PSG gene variant linked to birthweight. This study provides molecular insight into how folate metabolism influences placental development and attributes a potential multigenerational epigenetic mechanism to unexplained cases of fetal growth defects.

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Data files for "A novel inhibitor of P. aeruginosa folate metabolism exploits metabolic differences for narrow-spectrum antibiotic targeting"

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Project description:The goals of this study were to compare the distribution of H3K4me3 before and after methionine restriction to understand how nutrient availability and alterations in methionine metabolism affect the epigenetic state and regulate gene transcription. To do this we performed ChIP-seq with an H3K4me3 antibody and RNA-seq using PolyA+ mRNA.

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Folate Pathway Disruption Leads to Critical Depletion of Methionine Derivatives in Mycobacterium tuberculosis

Project description:In this study, screening efforts identified novel antifolates with potent, targeted activity against whole cell Mycobacterium tuberculosis. Liquid chromatography-mass spectrometry analysis of antifolate-treated cultures revealed unique metabolic disruption, including decreased pools of methionine and S-adenosylmethionine. Transcriptomic analysis highlighted up-regulation genes involved in the biosynthesis and utilization of methionine. Supplementation with amino acids or methionine derivatives was sufficient to rescue cultures from MIC-level antifolate treatment. Instead of the “thymineless death” that characterizes folate pathway inhibition in a wide variety of organisms, these data suggest that M. tuberculosis is vulnerable to a critical disruption of the biosynthesis of methionine-derived compounds. These arrays look at the expression profile triggered by exposure to three different anti-folates (WR99210, dimethyl and diethyl methotrexate) in three biological replicates and in a matched set of untreated samples.

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Project description:Methionine, a sulfur-containing essential amino acid, is a key component of dietary proteins important for protein synthesis, sulfur metabolism, antioxidant defense, and signaling. However, the role of methionine in cancer progression remains inconclusive. On one hand, dietary methionine restriction is known to repress cancer growth and improve cancer therapy in xenografted tumors. On the other hand, methionine is also critical for T cell activation and differentiation, making it a potential tumor suppression nutrient by enhancing T cell-mediated anti-tumor immunity. Here we investigated the interaction between dietary methionine, immune cells, and cancer cells by allografting CT26.WT mouse colon carcinoma cells into immunocompetent Balb/c mice or immunodeficient NSG mice, then analyzed how dietary methionine contents affect their growth. Our results show that dietary methionine restriction suppresses tumor growth in immunodeficient NSG mice but promotes tumor progression in immunocompetentt Balb/c mice.

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Folate Pathway Disruption Leads to Critical Depletion of Methionine Derivatives in Mycobacterium tuberculosis

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