Evidence map›Paper›PMID 31108395›Full record

ArticleiScience2019

A CRISPR Screen Using Subtilase Cytotoxin Identifies SLC39A9 as a Glycan-Regulating Factor.

Toshiyuki Yamaji, Hisatoshi Hanamatsu, Tsuyoshi Sekizuka, Makoto Kuroda, Norimasa Iwasaki, Makoto Ohnishi, Jun-Ichi Furukawa, Kinnosuke Yahiro, Kentaro Hanada

Open access · goldAbstract read
In one paragraph

Article in iScience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
5.3field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

36 citing papers in PubMed, 50 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 1 country.

Toshiyuki YamajiDepartment of Biochemistry and Cell Biology, National Institute of Infectious Diseases, Shinjuku-ku, Tokyo 162-8640, Japan. Electronic address: tyamaji@nih.go.jp.
Hisatoshi HanamatsuDepartment of Advanced Clinical Glycobiology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Sapporo 001-0021, Japan; Department of Gastroenterology and Hepatology, Graduate School of Medicine, Hokkaido University, Sapporo 060-8638, Japan.
Tsuyoshi SekizukaPathogen Genomics Center, National Institute of Infectious Diseases, Shinjuku-ku, Tokyo 162-8640, Japan.
Makoto KurodaPathogen Genomics Center, National Institute of Infectious Diseases, Shinjuku-ku, Tokyo 162-8640, Japan.
Norimasa IwasakiDepartment of Advanced Clinical Glycobiology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Sapporo 001-0021, Japan; Department of Orthopaedic Surgery, Graduate School of Medicine, Hokkaido University, Sapporo 060-8638, Japan.
Makoto OhnishiDepartment of Bacteriology I, National Institute of Infectious Diseases, Shinjuku-ku, Tokyo 162-8640, Japan.
Jun-Ichi FurukawaDepartment of Advanced Clinical Glycobiology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Sapporo 001-0021, Japan.
Kinnosuke YahiroDepartment of Molecular Infectiology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan. Electronic address: yahirok@faculty.chiba-u.jp.
Kentaro HanadaDepartment of Biochemistry and Cell Biology, National Institute of Infectious Diseases, Shinjuku-ku, Tokyo 162-8640, Japan.
National Institute of Infectious Diseases · JPHokkaido University · JPChiba University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Subtilase cytotoxin (SubAB) is a virulence factor produced by locus of enterocyte effacement-negative Shiga-toxigenic Escherichia coli strains. The toxin recognizes sialoglycans for entry and cleaves an endoplasmic reticulum chaperon, binding immunoglobulin protein, to cause cell death. However, no systematic screening has yet been performed to identify critical host factors. Here, we performed a genome-wide CRISPR/Cas9 knockout screen for SubAB-induced cell death and identified various sialoglycan-related and membrane-trafficking genes. Analysis of glycan-deficient cells demonstrated that not only N-glycans but also O-glycans serve as SubAB receptors. In addition, SLC39A9, which is a predicted zinc transporter, as well as KDELRs and JTB, were required for SubAB to induce maximal cell death. Disruption of the SLC39A9 gene markedly reduced both complex-type N-glycans and core 1 O-glycans, and the O-glycan reduction was attributed to the reduction of core 1 synthase (C1GalT1). These results provide insights into the post-transcriptional regulation of glycosyltransferases by SLC39A9, as well as sialoglycan species as SubAB receptors.

Indexed as

BiochemistryBiological SciencesCell BiologyMicrobiologyMolecular Biology

Identifiers

PMID31108395
PMCPMC6526310
OpenAlexW2944703732

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.