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Genome-wide essential gene identification for Shiga toxin-induced cell death using CRISPR/CAS9 screening system with Vero cells

ABSTRACT: Genome-wide essential gene identification for Shiga toxin-induced cell death using CRISPR/CAS9 screening system with Vero cells

PROVIDER: PRJNA716329 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14037533.fastq.gz	Fastqsanger.gz
	SRR14037534.fastq.gz	Fastqsanger.gz
	SRR14037535.fastq.gz	Fastqsanger.gz
	SRR14037536.fastq.gz	Fastqsanger.gz
	SRR14037537.fastq.gz	Fastqsanger.gz

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Genome-wide essential gene identification for Shiga toxin-induced cell death using CRISPR/CAS9 screening system with Vero cells

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Genome-wide essential gene identification for Shiga toxin-induced cell death using CRISPR/CAS9 screening system

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2011-10-10 | E-GEOD-32710 | biostudies-arrayexpress

Functional Dissection of the Retrograde Shiga Toxin Trafficking Inhibitor Retro-2

Project description:The retrograde transport inhibitor Retro-2 has a protective effect on cells and in mice against Shiga-like toxins and ricin. Retro-2 causes toxin accumulation in early endosomes, and the relocalization of the Golgi SNARE protein syntaxin-5 to the endoplasmic reticulum. The molecular mechanisms by which this is achieved remain unknown. Here, we show that Retro-2 targets the endoplasmic reticulum exit site component Sec16A, affecting anterograde transport of syntaxin-5 from the endoplasmic reticulum to the Golgi. The formation of canonical SNARE complexes involving syntaxin-5 is not affected in Retro-2-treated cells. In contrast, the interaction of syntaxin-5 with a newly discovered binding partner, the retrograde trafficking chaperone GPP130, is abolished, and we show that GPP130 must indeed bind to syntaxin-5 to drive Shiga toxin transport from endosomes to the Golgi. We thereby identify Sec16A as a druggable target, and provide evidence for a non-SNARE function for syntaxin-5 in interaction with the retrograde cycling protein GPP130. a) Clickable Retro-2 pulldown. To identify protein target of Retro-2.1, providing the first steps to explain effects of Retro-2 on inhibition of STxB retrograde trafficking from endosomes to Golgi. b) GFP-STX5 pulldown. To find interactors of STX5, to build a hypothesis to explain the affect of Retro-2-inhibited anterograde trafficking of STX5 to Golgi, which in turn inhibits STxB retrograde transport from endosomes to Golgi. c) GFP-Sec16A pulldown. The aim of this proteomics assay is to show the effects of Retro-2 on the Sec16A interactome. Results show the differential effects of Retro-2 treatment on the Sec16A interactome, giving insight into the mechanism by which Retro-2, via Sec16A, specifically affects the anterograde trafficking of Syntaxin-5.

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