ChloroquineV1, Main, Exploration, bibRecord, 000D56

Subtilase cytotoxin produced by locus of enterocyte effacement-negative Shiga-toxigenic Escherichia coli induces stress granule formation.

Identifieur interne : 000D56 ( Main/Exploration ); précédent : 000D55; suivant : 000D57

Subtilase cytotoxin produced by locus of enterocyte effacement-negative Shiga-toxigenic Escherichia coli induces stress granule formation.

Auteurs : Hiroyasu Tsutsuki [Japon] ; Kinnosuke Yahiro [Japon] ; Kohei Ogura [Japon] ; Kimitoshi Ichimura [Japon] ; Sunao Iyoda [Japon] ; Makoto Ohnishi [Japon] ; Sayaka Nagasawa [Japon] ; Kazuko Seto [Japon] ; Joel Moss [États-Unis] ; Masatoshi Noda [Japon]

Source :

Cellular microbiology [ 1462-5822 ] ; 2016.

RBID : pubmed:26749168

Descripteurs français

English descriptors

KwdEn :
- Apoptosis Regulatory Proteins (metabolism), Caco-2 Cells (drug effects), Caco-2 Cells (metabolism), Caco-2 Cells (microbiology), Carrier Proteins (genetics), Carrier Proteins (metabolism), Chloroquine (pharmacology), Culture Media, Conditioned (pharmacology), Cytoplasmic Granules (metabolism), DNA Helicases, Escherichia coli Proteins (genetics), Escherichia coli Proteins (metabolism), Escherichia coli Proteins (pharmacology), Gene Knockout Techniques, HeLa Cells, Host-Pathogen Interactions, Humans, Poly-ADP-Ribose Binding Proteins, Protein Kinase C-delta (metabolism), RNA Helicases, RNA Recognition Motif Proteins, Shiga-Toxigenic Escherichia coli (metabolism), Shiga-Toxigenic Escherichia coli (pathogenicity), Signal Transduction (drug effects), Stress, Physiological (drug effects), Subtilisins (genetics), Subtilisins (metabolism), Subtilisins (pharmacology), eIF-2 Kinase (metabolism).
MESH :
- chemical , genetics : Carrier Proteins, Escherichia coli Proteins, Subtilisins.
- chemical , metabolism : Apoptosis Regulatory Proteins, Carrier Proteins, Escherichia coli Proteins, Protein Kinase C-delta, Subtilisins, eIF-2 Kinase.
- drug effects : Caco-2 Cells, Signal Transduction, Stress, Physiological.
- metabolism : Caco-2 Cells, Cytoplasmic Granules, Shiga-Toxigenic Escherichia coli.
- microbiology : Caco-2 Cells.
- pathogenicity : Shiga-Toxigenic Escherichia coli.
- chemical , pharmacology : Chloroquine, Culture Media, Conditioned, Escherichia coli Proteins, Subtilisins.
- chemical : DNA Helicases, Gene Knockout Techniques, HeLa Cells, Host-Pathogen Interactions, Humans, Poly-ADP-Ribose Binding Proteins, RNA Helicases, RNA Recognition Motif Proteins.

Abstract

Subtilase cytotoxin (SubAB) is mainly produced by locus of enterocyte effacement (LEE)-negative strains of Shiga-toxigenic Escherichia coli (STEC). SubAB cleaves an endoplasmic reticulum (ER) chaperone, BiP/Grp78, leading to induction of ER stress. This stress causes activation of ER stress sensor proteins and induction of caspase-dependent apoptosis. We found that SubAB induces stress granules (SG) in various cells. Aim of this study was to explore the mechanism by which SubAB induced SG formation. Here, we show that SubAB-induced SG formation is regulated by activation of double-stranded RNA-activated protein kinase (PKR)-like endoplasmic reticulum kinase (PERK). The culture supernatant of STEC O113:H21 dramatically induced SG in Caco2 cells, although subAB knockout STEC O113:H21 culture supernatant did not. Treatment with phorbol 12-myristate 13-acetate (PMA), a protein kinase C (PKC) activator, and lysosomal inhibitors, NH4 Cl and chloroquine, suppressed SubAB-induced SG formation, which was enhanced by PKC and PKD inhibitors. SubAB attenuated the level of PKD1 phosphorylation. Depletion of PKCδ and PKD1 by siRNA promoted SG formation in response to SubAB. Furthermore, death-associated protein 1 (DAP1) knockdown increased basal phospho-PKD1(S916) and suppressed SG formation by SubAB. However, SG formation by an ER stress inducer, Thapsigargin, was not inhibited in PMA-treated cells. Our findings show that SubAB-induced SG formation is regulated by the PERK/DAP1 signalling pathway, which may be modulated by PKCδ/PKD1, and different from the signal transduction pathway that results in Thapsigargin-induced SG formation.

DOI: 10.1111/cmi.12565
PubMed: 26749168

Affiliations:

Le document en format XML

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<term>Caco-2 Cells (drug effects)</term>
<term>Caco-2 Cells (metabolism)</term>
<term>Caco-2 Cells (microbiology)</term>
<term>Carrier Proteins (genetics)</term>
<term>Carrier Proteins (metabolism)</term>
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<term>Escherichia coli Proteins (genetics)</term>
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<term>Escherichia coli Proteins (pharmacology)</term>
<term>Gene Knockout Techniques</term>
<term>HeLa Cells</term>
<term>Host-Pathogen Interactions</term>
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<term>Poly-ADP-Ribose Binding Proteins</term>
<term>Protein Kinase C-delta (metabolism)</term>
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<term>Humans</term>
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<front><div type="abstract" xml:lang="en">Subtilase cytotoxin (SubAB) is mainly produced by locus of enterocyte effacement (LEE)-negative strains of Shiga-toxigenic Escherichia coli (STEC). SubAB cleaves an endoplasmic reticulum (ER) chaperone, BiP/Grp78, leading to induction of ER stress. This stress causes activation of ER stress sensor proteins and induction of caspase-dependent apoptosis. We found that SubAB induces stress granules (SG) in various cells. Aim of this study was to explore the mechanism by which SubAB induced SG formation. Here, we show that SubAB-induced SG formation is regulated by activation of double-stranded RNA-activated protein kinase (PKR)-like endoplasmic reticulum kinase (PERK). The culture supernatant of STEC O113:H21 dramatically induced SG in Caco2 cells, although subAB knockout STEC O113:H21 culture supernatant did not. Treatment with phorbol 12-myristate 13-acetate (PMA), a protein kinase C (PKC) activator, and lysosomal inhibitors, NH4 Cl and chloroquine, suppressed SubAB-induced SG formation, which was enhanced by PKC and PKD inhibitors. SubAB attenuated the level of PKD1 phosphorylation. Depletion of PKCδ and PKD1 by siRNA promoted SG formation in response to SubAB. Furthermore, death-associated protein 1 (DAP1) knockdown increased basal phospho-PKD1(S916) and suppressed SG formation by SubAB. However, SG formation by an ER stress inducer, Thapsigargin, was not inhibited in PMA-treated cells. Our findings show that SubAB-induced SG formation is regulated by the PERK/DAP1 signalling pathway, which may be modulated by PKCδ/PKD1, and different from the signal transduction pathway that results in Thapsigargin-induced SG formation.</div>
</front>
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<tree><country name="Japon"><noRegion><name sortKey="Tsutsuki, Hiroyasu" sort="Tsutsuki, Hiroyasu" uniqKey="Tsutsuki H" first="Hiroyasu" last="Tsutsuki">Hiroyasu Tsutsuki</name>
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<name sortKey="Ichimura, Kimitoshi" sort="Ichimura, Kimitoshi" uniqKey="Ichimura K" first="Kimitoshi" last="Ichimura">Kimitoshi Ichimura</name>
<name sortKey="Iyoda, Sunao" sort="Iyoda, Sunao" uniqKey="Iyoda S" first="Sunao" last="Iyoda">Sunao Iyoda</name>
<name sortKey="Nagasawa, Sayaka" sort="Nagasawa, Sayaka" uniqKey="Nagasawa S" first="Sayaka" last="Nagasawa">Sayaka Nagasawa</name>
<name sortKey="Noda, Masatoshi" sort="Noda, Masatoshi" uniqKey="Noda M" first="Masatoshi" last="Noda">Masatoshi Noda</name>
<name sortKey="Ogura, Kohei" sort="Ogura, Kohei" uniqKey="Ogura K" first="Kohei" last="Ogura">Kohei Ogura</name>
<name sortKey="Ohnishi, Makoto" sort="Ohnishi, Makoto" uniqKey="Ohnishi M" first="Makoto" last="Ohnishi">Makoto Ohnishi</name>
<name sortKey="Seto, Kazuko" sort="Seto, Kazuko" uniqKey="Seto K" first="Kazuko" last="Seto">Kazuko Seto</name>
<name sortKey="Yahiro, Kinnosuke" sort="Yahiro, Kinnosuke" uniqKey="Yahiro K" first="Kinnosuke" last="Yahiro">Kinnosuke Yahiro</name>
</country>
<country name="États-Unis"><region name="Maryland"><name sortKey="Moss, Joel" sort="Moss, Joel" uniqKey="Moss J" first="Joel" last="Moss">Joel Moss</name>
</region>
</country>
</tree>
</affiliations>
</record>

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   |wiki=    Sante
   |area=    ChloroquineV1
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   |clé=     pubmed:26749168
   |texte=   Subtilase cytotoxin produced by locus of enterocyte effacement-negative Shiga-toxigenic Escherichia coli induces stress granule formation.
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Serveur d'exploration Chloroquine

Subtilase cytotoxin produced by locus of enterocyte effacement-negative Shiga-toxigenic Escherichia coli induces stress granule formation.

Subtilase cytotoxin produced by locus of enterocyte effacement-negative Shiga-toxigenic Escherichia coli induces stress granule formation.

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	Serveur d'exploration Chloroquine
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