共 67 条
Initiation of Programmed Cell Death in Self-incompatibility: Role for Cytoskeleton Modifications and Several Caspase-Like Activities
被引:32
作者:

Bosch, Maurice
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机构:
Univ Birmingham, Sch Biosci, Birmingham B15 2TT, W Midlands, England Univ Birmingham, Sch Biosci, Birmingham B15 2TT, W Midlands, England

Poulter, Natalie S.
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Univ Birmingham, Sch Biosci, Birmingham B15 2TT, W Midlands, England Univ Birmingham, Sch Biosci, Birmingham B15 2TT, W Midlands, England

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Franklin-Tong, Vernonica E.
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Univ Birmingham, Sch Biosci, Birmingham B15 2TT, W Midlands, England Univ Birmingham, Sch Biosci, Birmingham B15 2TT, W Midlands, England
机构:
[1] Univ Birmingham, Sch Biosci, Birmingham B15 2TT, W Midlands, England
基金:
英国惠康基金;
英国生物技术与生命科学研究理事会;
关键词:
D O I:
10.1093/mp/ssn053
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
Programmed cell death (PCD) is an important and universal process regulating precise death of unwanted cells in eukaryotes. in plants, the existence of PCD has been firmly established for about a decade, and many components shown to be involved in apoptosis/PCD in mammalian systems are found in plant cells undergoing PCD. Here, we review work from our lab demonstrating the involvement of PCD in the self-incompatibility response in Papaver rhoeas pollen. This utilization of PCD as a consequence of a specific pollen-pistil interaction provides a very neat way to destroy unwanted 'self', but not 'non-self' pollen. We discuss recent data providing evidence for SI-incluced activation of several caspase-like activities and suggest that an acidification of the cytosol may be a key turning point in the activation of caspase-like proteases executing PCD. We also review data showing the involvement of the actin and microtubule cytoskeletons as well as that of a MAPK in signalling to caspase-mediated PCD. Potential links between these various components in signalling to PCD are discussed. Together, this begins to build a picture of PCD in a single cell system, triggered by a receptor-ligand interaction.
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页码:879 / 887
页数:9
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