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Path-seq identifies essential mycolate remodeling program for mycobacterial adaptation in host cells [RNA-seq]

ABSTRACT: Path-seq identifies essential mycolate remodeling program for mycobacterial adaptation in host cells [RNA-seq]

PROVIDER: PRJNA476854 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7371350_1.fastq.gz	Fastqsanger.gz
	SRR7371350_2.fastq.gz	Fastqsanger.gz
	SRR7371351_1.fastq.gz	Fastqsanger.gz
	SRR7371351_2.fastq.gz	Fastqsanger.gz
	SRR7371352_1.fastq.gz	Fastqsanger.gz

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Path-seq identifies an essential mycolate remodeling program for mycobacterial host adaptation.

Project description:The success of Mycobacterium tuberculosis (MTB) stems from its ability to remain hidden from the immune system within macrophages. Here, we report a new technology (Path-seq) to sequence miniscule amounts of MTB transcripts within up to million-fold excess host RNA Using Path-seq and regulatory network analyses, we have discovered a novel transcriptional program for in vivo mycobacterial cell wall remodeling when the pathogen infects alveolar macrophages in mice. We have discovered that MadR transcriptionally modulates two mycolic acid desaturases desA1/desA2 to initially promote cell wall remodeling upon in vitro macrophage infection and, subsequently, reduces mycolate biosynthesis upon entering dormancy. We demonstrate that disrupting MadR program is lethal to diverse mycobacteria making this evolutionarily conserved regulator a prime antitubercular target for both early and late stages of infection.

| S-EPMC6398593 | biostudies-literature

Path-seq identifies an essential mycolate remodeling program for mycobacterial adaptation in host cells [ChIP-seq]

Project description:Path-seq identifies an essential mycolate remodeling program for mycobacterial adaptation in host cells [ChIP-seq]

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Path-seq identifies essential mycolate remodeling program for mycobacterial adaptation in host cells [RNA-seq]

Project description:Comparison of transcriptional differences (RNA-seq) between induced and uninduced overexpression of MSMEG_0916 in Mycobacterium smegmatis

2019-03-04 | GSE116027 | GEO

Path-seq identifies an essential mycolate remodeling program for mycobacterial adaptation in host cells [ChIP-seq]

Project description:Study of the DNA binding sites of the transcriptional regulator MSMEG_0916 through chromatin immunoprecipitation couple with deep sequenicng (ChIP-seq) and induced or uninduced overexpression of MSMEG_0916 in Mycobacterium smegmatis

2019-03-04 | GSE116084 | GEO

An essential mycolate remodeling program for mycobacterial adaptation in host cells

Project description:An essential mycolate remodeling program for mycobacterial adaptation in host cells

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An essential mycolate remodeling program for mycobacterial adaptation in host cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-03-05 | GSE116085 | GEO

Atlantic PATH microbiome

Project description:Microbiome sequencing of the Atlantic PATH cohort

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Mycobacterial communities in pulmonary NTM

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Sensing of mycobacterial arabinogalactan by galectin-9 exacerbates mycobacterial infection by inducing matrix metalloproteinases

Project description:Mycobacterial arabinogalactan (AG) is an essential cell wall component of Mycobacteria and a frequent structural and bio-synthetical target for anti-tuberculosis (TB) drug development. Yet, it is unclear whether mycobacterial AG is a pathogen-associated molecular pattern (PAMP) with an elusive pattern recognition receptor (PRR). Here, we report that mycobacterial AG is recognized by galectin-9 and exacerbates mycobacterial infection. Administration of AG-specific aptamers inhibited cellular infiltration caused by Mycobacterium tuberculosis (Mtb) or Mycobacterium bovis BCG, and moderately increased survival of Mtb-infected mice or Mycobacterium marinum-infected zebrafish. AG interacted with carbohydrate recognition domain (CRD) 2 of galectin-9 with high affinity, and galectin-9 associated with transforming growth factor β-activated kinase 1 (TAK1) via CRD2 to trigger subsequent activation of extracellular signal-regulated kinase (ERK) as well as induction of the expression of matrix metalloproteinases (MMPs). Moreover, deletion of galectin-9 or inhibition of MMPs blocked AG-induced pathological impairments in the lung, and the AG-galectin-9 axis aggravated the process of Mtb infection in mice. These results demonstrate that AG is an important virulence factor of mycobacteria and galectin-9 is a novel receptor for Mtb and other mycobacteria, paving the way for the development of novel effective TB immune modulators.

2021-02-17 | GSE166850 | GEO

Mycobacterial TDM Reprograms Macrophage Global Gene Expression

Project description:Effect of mycobacterial cell wall component TDM (trehalose dimycolate) of murine macrophage gene expression.

2013-03-09 | E-MEXP-3814 | biostudies-arrayexpress