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Anthrax anthrax

ABSTRACT: Anthrax anthrax overview

PROVIDER: PRJNA1084976 | ENA |

REPOSITORIES: ENA

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Dataset's files

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			Action	DRS
		Other
	ERR11814109_1.fastq.gz	Fastqsanger.gz
	ERR11814109_2.fastq.gz	Fastqsanger.gz
	ERR11809142.fastq.gz	Fastqsanger.gz

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Multiple stages of evolutionary change in anthrax toxin receptor expression in humans

Project description:The advent of animal husbandry and hunting increased human exposure to zoonotic pathogens. To understand how a zoonotic disease influenced human evolution, we studied changes in human expression of anthrax toxin receptor 2 (ANTXR2), which encodes a cell surface protein necessary for Bacillus anthracis virulence toxins to cause anthrax disease. In immune cells, ANTXR2 was 8-fold down-regulated in all available human samples compared to non-human primates, indicating regulatory changes early in the evolution of modern humans. We also observed multiple genetic signatures consistent with recent positive selection driving a European-specific decrease in ANTXR2 expression in several non-immune tissues affected by anthrax toxins. Our observations fit a model in which humans adapted to anthrax disease following early ecological changes associated with hunting and scavenging, as well as a second period of adaptation after the rise of modern agriculture.

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Project description:From article abstract: Inhalational anthrax is caused by spores of the bacterium Bacillus anthracis (B. anthracis), and is an extremely dangerous disease that can kill unvaccinated victims within 2 weeks. Modern antibiotic-based therapy can increase the survival rate to ~50%, but only if administered presymptomatically (within 24-48 h of exposure). To discover host signaling responses to presymptomatic anthrax, label-free quantitative phosphoproteomics via liquid chromatography coupled to mass spectrometry was used to compare spleens from uninfected and spore-challenged mice over a 72 h time-course. Late-stage (48-72 h post-challenge) Sterne strain (lethal) infections resulted in global alterations to the spleen phosphoproteome. In contrast, delta-Sterne strain (asymptomatic; missing the anthrax toxin) infections resulted in 188 (5.8%) significantly altered (q<0.05) phosphopeptides. Twenty-six highly tentative phosphorylation responses to early-stage (24 h post-challenge) anthrax were discovered (q<0.5), and ten of these originated from eight proteins that have known roles in the host immune response. These tentative early-anthrax host response signaling events within mouse spleens may translate into presymptomatic diagnostic biomarkers of human anthrax detectable within circulating immune cells, and could aid in the identification of pathogenic mechanisms and therapeutic targets. [Molecular & Cellular Proteomics 10: 10.1074/mcp.M110.000927, 1–11, 2011. The files in this dataset are exactly the same files that were originally uploaded to Proteome Commons Tranche as described in the article.]

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Project description:To promote infections, pathogens exploit host cell machineries including structural elements of the plasma membrane. Studying these interactions and identifying molecular players is an ideal way to gain insights into the fundamental biology of the host cell. Here, we used the anthrax toxin to screen a library of 1500 regulatory, cell surface, and membrane trafficking genes for their involvement in the intoxication process. We found that ER-Golgi localized proteins TMED2 and TMED10 are required for toxin oligomerization at the plasma-membrane of human cells, an essential step dependant on localization to cholesterol-rich lipid nanodomains. Biochemical, morphological and mechanistic analyses showed that TMED2 and TMED10 are essential components of a complex that operates the exchange of both cholesterol and ceramides at ER-Golgi membrane contact sites. Overall, this study of anthrax intoxication led to the discovery that lipid compositional remodelling at ER-Golgi interfaces fully controls the formation of functional membrane nanodomains at the cell surface.

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