Induction of apoptosis by the severe acute respiratory syndrome coronavirus 7a protein is dependent on its interaction with the Bcl-XL protein
Identifieur interne : 003D18 ( Main/Merge ); précédent : 003D17; suivant : 003D19Induction of apoptosis by the severe acute respiratory syndrome coronavirus 7a protein is dependent on its interaction with the Bcl-XL protein
Auteurs : Ying-Xim Tan [Singapour] ; Timothy H. P. Tan [Singapour] ; Marvin J.-R. Lee [Singapour] ; Puay-Yoke Tham [Singapour] ; Vithiagaran Gunalan [Singapour] ; Julian Druce [Australie] ; Chris Birch [Australie] ; Mike Catton [Australie] ; NAI YANG FU [Singapour] ; Victor C. Yu [Singapour] ; Yee-Joo Tan [Singapour]Source :
- Journal of virology [ 0022-538X ] ; 2007.
Descripteurs français
- Pascal (Inist)
English descriptors
Abstract
The severe acute respiratory syndrome coronavirus (SARS-CoV) 7a protein, which is not expressed by other known coronaviruses, can induce apoptosis in various cell lines. In this study, we show that the overexpression of Bcl-XL, a prosurvival member of the Bcl-2 family, blocks 7a-induced apoptosis, suggesting that the mechanism for apoptosis induction by 7a is at the level of or upstream from the Bcl-2 family. Coimmunoprecipitation experiments showed that 7a interacts with Bcl-XL and other prosurvival proteins (Bcl-2, Bcl-w, Mcl-1, and Al) but not with the proapoptotic proteins (Bax, Bak, Bad, and Bid). A good correlation between the abilities of 7a deletion mutants to induce apoptosis and to interact with Bcl-XL was observed, suggesting that 7a triggers apoptosis by interfering directly with the prosurvival function of Bcl-XL. Interestingly, amino acids 224 and 225 within the C-terminal transmembrane domain of Bcl-XL are essential for the interaction with the 7a protein, although the BH3 domain of Bcl-XL also contributes to this interaction. In addition, fractionation experiments showed that 7a colocalized with Bcl-XL at the endoplasmic reticulum as well as the mitochondria, suggesting that they may form complexes in different membranous compartments.
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Apoptosis</term>
<term>Cell death</term>
<term>Coronavirus</term>
<term>Protein</term>
<term>Severe acute respiratory syndrome</term>
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</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Coronavirus</term>
<term>Apoptose</term>
<term>Mort cellulaire</term>
<term>Protéine</term>
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<front><div type="abstract" xml:lang="en">The severe acute respiratory syndrome coronavirus (SARS-CoV) 7a protein, which is not expressed by other known coronaviruses, can induce apoptosis in various cell lines. In this study, we show that the overexpression of Bcl-X<sub>L</sub>
, a prosurvival member of the Bcl-2 family, blocks 7a-induced apoptosis, suggesting that the mechanism for apoptosis induction by 7a is at the level of or upstream from the Bcl-2 family. Coimmunoprecipitation experiments showed that 7a interacts with Bcl-X<sub>L</sub>
and other prosurvival proteins (Bcl-2, Bcl-w, Mcl-1, and Al) but not with the proapoptotic proteins (Bax, Bak, Bad, and Bid). A good correlation between the abilities of 7a deletion mutants to induce apoptosis and to interact with Bcl-X<sub>L</sub>
was observed, suggesting that 7a triggers apoptosis by interfering directly with the prosurvival function of Bcl-X<sub>L</sub>
. Interestingly, amino acids 224 and 225 within the C-terminal transmembrane domain of Bcl-X<sub>L</sub>
are essential for the interaction with the 7a protein, although the BH3 domain of Bcl-X<sub>L</sub>
also contributes to this interaction. In addition, fractionation experiments showed that 7a colocalized with Bcl-X<sub>L</sub>
at the endoplasmic reticulum as well as the mitochondria, suggesting that they may form complexes in different membranous compartments.</div>
</front>
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<tree><country name="Singapour"><noRegion><name sortKey="Tan, Ying Xim" sort="Tan, Ying Xim" uniqKey="Tan Y" first="Ying-Xim" last="Tan">Ying-Xim Tan</name>
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<name sortKey="Nai Yang Fu" sort="Nai Yang Fu" uniqKey="Nai Yang Fu" last="Nai Yang Fu">NAI YANG FU</name>
<name sortKey="Tan, Timothy H P" sort="Tan, Timothy H P" uniqKey="Tan T" first="Timothy H. P." last="Tan">Timothy H. P. Tan</name>
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<name sortKey="Tham, Puay Yoke" sort="Tham, Puay Yoke" uniqKey="Tham P" first="Puay-Yoke" last="Tham">Puay-Yoke Tham</name>
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