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Rv0500A is a transcription factor that links Mycobacterium tuberculosis environmental response with division and impacts host colonization

ABSTRACT: Rv0500A is a transcription factor that links Mycobacterium tuberculosis environmental response with division and impacts host colonization

PROVIDER: PRJNA800022 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17717763.fastq.gz	Fastqsanger.gz
	SRR17717764.fastq.gz	Fastqsanger.gz
	SRR17717765.fastq.gz	Fastqsanger.gz
	SRR17717766.fastq.gz	Fastqsanger.gz
	SRR17717767.fastq.gz	Fastqsanger.gz

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Rv0500A is a transcription factor that links Mycobacterium tuberculosis environmental response with division and impacts host colonization

Project description:The purpose of this study was to identify genes that are differentially expressed upon rv0500A deletion, to reveal the impact of Rv0500A on global transcription in different environmental conditions.

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Rv0500A is a transcription factor that links Mycobacterium tuberculosis environmental response and division

Project description:Rv0500A is a transcription factor that links Mycobacterium tuberculosis environmental response and division

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Transcriptomic analysis to study interactions between murine host and fungal commensal Candida albicans upon its gastrointestinal colonization

Project description:Candida albicans is a ubiquitous fungus in the human gut microbiome as well as a prevalent cause of opportunistic mucosal and systemic disease. There is currently little understanding, however, as to how crosstalk between C. albicans and the host regulates colonization of this key niche. Here, we performed expression profiling on ileal and colonic tissues in germ-free mice colonized with C. albicans to define the global response to this fungus. We reveal that Duox2 and Duoxa2, encoding dual NADPH oxidase activity, are upregulated in both the ileum and colon, and that induction requires the C. albicans yeast-hyphal transition and hyphal-specific toxin candidalysin. Hosts lacking the IL-17 receptor failed to upregulate Duox2/Duoxa2 in response to C. albicans, while addition of IL-17A to colonoids induced these genes together with the concomitant production of hydrogen peroxide. To directly define the role of Duox2/Duoxa2 in fungal colonization, antibiotic-treated mice lacking intestinal DUOX2 activity were evaluated for C. albicans colonization and host responses. Surprisingly, loss of DUOX2 function reduced fungal colonization at extended time points (>17 days colonization) and increased the proportion of hyphal cells in the gut. IL-17A levels were also elevated in C. albicans-colonized mice lacking functional DUOX2 highlighting cross-regulation between DUOX2 on this cytokine. Together, these experiments reveal novel links between fungal cells, candidalysin and the host IL-17-DUOX2 axis, and that a complex interplay between these factors regulates C. albicans filamentation and colonization in the gut.

2025-07-01 | GSE274260 | GEO

E. coli toxin YjjJ (HipH) is a Ser/Thr protein kinase that impacts cell division, carbon metabolism and ribosome assembly

Project description:Protein Ser/Thr kinases are post-translational regulators of key molecular processes in bacteria, such as cell division and antibiotic tolerance. Here we characterize the E. coli toxin YjjJ (HipH), a putative protein kinase annotated as a member of the family of HipA-like Ser/Thr kinases which are involved in antibiotic tolerance. Using SILAC-based phosphoproteomics we provide experimental evidence that YjjJ is a Ser/Thr protein kinase and its primary protein substrates are the ribosomal protein RpmE (L31) and the carbon storage regulator CsrA. YjjJ activity impacts ribosome assembly, cell division and central carbon metabolism but it does not increase antibiotic tolerance as does its homologue HipA. Intriguingly, overproduction of YjjJ and its kinase-deficient variant can activate HipA and other kinases, pointing to a crosstalk between Ser/Thr kinases in E. coli.

2022-11-28 | PXD033071 | Pride

Interspecies commensal interactions have nonlinear impacts on host immunity

Project description:The impacts of individual commensal microbes on immunity and disease can differ dramatically depending on the surrounding microbial context, yet the specific bacterial combinations that dictate divergent immunological outcomes in humans remain largely undefined. We isolated a novel Allobaculum strain from an inflammatory bowel disease (IBD) patient that elicited antigen-specific mucosal and systemic antibody responses at homeostasis and exacerbated colitis in gnotobiotic mice. Using human microbiota-associated mouse models, we uncovered an inverse correlation between Allobaculum and the taxonomically-divergent immunostimulatory species Akkermansia muciniphila, which was also reflected in human cohorts. Co-colonization with Allobaculum and A. muciniphila reprogrammed the immune responses evoked by each microbe on its own, ameliorated Allobaculum-induced colitis, and blunted A. muciniphila-induced T and B cell responses. These studies thus identify a reciprocal ‘epistatic’ interaction between unique immunostimulatory human gut bacteria and establish a generalizable framework to dissect the role of microbial context in strain-specific microbial effects on human disease.

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Project description:Manipulation of soil microbiome impacts arbuscular mycorrhiza colonization of plants: a study of the influences of the soil microbiome colonisation rates of arbuscular mycorrhiz colonization rates in sterilized and inoculated soils

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Rapid cell division of Staphylococcus aureus

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Anatomical Site-Specific Carbohydrate Availability Impacts Streptococcus pneumoniae Virulence and Fitness during Colonization and Disease

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Gut colonization by Proteobacteria alters host metabolism and modulates cocaine neurobehavioral responses

Project description:Gut-microbiota membership is associated with diverse neuropsychological-diseases, including substance use disorders (SUDs). Unravelling mechanistic interactions between gut microbes and the host during psychostimulant use remains challenging. Here we show that cocaine exposure increases intestinal levels of norepinephrine, sensed through the bacterial adrenergic receptor QseC, promoting intestinal colonization of g-Proteobacteria. Gut colonization by g-Proteobacteria depletes the neuroactive metabolite glycine (used as a nitrogen source) both in the gut and cerebrospinal fluid, enhancing host cocaine-induced behaviors. Glycine repletion reversed this response, and intestinal colonization by g-Proteobacteria unable to uptake glycine did not alter the host response to cocaine. Transcriptomic profiling indicates a role of g-Proteobacteria modulated glycine levels in cocaine induced transcriptional plasticity in the nucleus accumbens through the glutamatergic transmission. Altogether, we introduce a mechanism by which intestinal bacteria alter the host’s brain responses to cocaine that could be exploited to modulate reward-related brain circuits that contribute to SUDs.

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