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An ATP signalling pathway in plant cells: extracellular ATP triggers programmed cell death in Populus euphratica.

Identifieur interne : 002C08 ( Main/Exploration ); précédent : 002C07; suivant : 002C09

An ATP signalling pathway in plant cells: extracellular ATP triggers programmed cell death in Populus euphratica.

Auteurs : Jian Sun [République populaire de Chine] ; Chun-Lan Zhang ; Shu-Rong Deng ; Cun-Fu Lu ; Xin Shen ; Xiao-Yang Zhou ; Xiao-Jiang Zheng ; Zan-Min Hu ; Shao-Liang Chen

Source :

RBID : pubmed:22070751

Descripteurs français

English descriptors

Abstract

We elucidated the extracellular ATP (eATP) signalling cascade active in programmed cell death (PCD) using cell cultures of Populus euphratica. Millimolar amounts of eATP induced a dose- and time-dependent reduction in viability, and the agonist-treated cells displayed hallmark features of PCD. eATP caused an elevation of cytosolic Ca(2+) levels, resulting in Ca(2+) uptake by the mitochondria and subsequent H(2) O(2) accumulation. P. euphratica exhibited an increased mitochondrial transmembrane potential, and cytochrome c was released without opening of the permeability transition pore over the period of ATP stimulation. Moreover, the eATP-induced increase of intracellular ATP, essential for the activation of caspase-like proteases and subsequent PCD, was found to be related to increased mitochondrial transmembrane potential. NO is implicated as a downstream component of the cytosolic Ca(2+) concentration but plays a negligible role in eATP-stimulated cell death. We speculate that ATP binds purinoceptors in the plasma membrane, leading to the induction of downstream intermediate signals, as the proposed sequence of events in PCD signalling was terminated by the animal P2 receptor antagonist suramin.

DOI: 10.1111/j.1365-3040.2011.02461.x
PubMed: 22070751


Affiliations:


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Le document en format XML

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<div type="abstract" xml:lang="en">We elucidated the extracellular ATP (eATP) signalling cascade active in programmed cell death (PCD) using cell cultures of Populus euphratica. Millimolar amounts of eATP induced a dose- and time-dependent reduction in viability, and the agonist-treated cells displayed hallmark features of PCD. eATP caused an elevation of cytosolic Ca(2+) levels, resulting in Ca(2+) uptake by the mitochondria and subsequent H(2) O(2) accumulation. P. euphratica exhibited an increased mitochondrial transmembrane potential, and cytochrome c was released without opening of the permeability transition pore over the period of ATP stimulation. Moreover, the eATP-induced increase of intracellular ATP, essential for the activation of caspase-like proteases and subsequent PCD, was found to be related to increased mitochondrial transmembrane potential. NO is implicated as a downstream component of the cytosolic Ca(2+) concentration but plays a negligible role in eATP-stimulated cell death. We speculate that ATP binds purinoceptors in the plasma membrane, leading to the induction of downstream intermediate signals, as the proposed sequence of events in PCD signalling was terminated by the animal P2 receptor antagonist suramin.</div>
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<name sortKey="Hu, Zan Min" sort="Hu, Zan Min" uniqKey="Hu Z" first="Zan-Min" last="Hu">Zan-Min Hu</name>
<name sortKey="Lu, Cun Fu" sort="Lu, Cun Fu" uniqKey="Lu C" first="Cun-Fu" last="Lu">Cun-Fu Lu</name>
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<name sortKey="Zhang, Chun Lan" sort="Zhang, Chun Lan" uniqKey="Zhang C" first="Chun-Lan" last="Zhang">Chun-Lan Zhang</name>
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