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Molecular Plant Advance Access originally published online on October 17, 2008
Molecular Plant 2008 1(6):879-887; doi:10.1093/mp/ssn053
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© The Author 2008. Published by the Molecular Plant Shanghai Editorial Office in association with Oxford University Press on behalf of CSPP and IPPE, SIBS, CAS.

Initiation of Programmed Cell Death in Self-Incompatibility: Role for Cytoskeleton Modifications and Several Caspase-Like Activities

Maurice Boscha,b, Natalie S. Poultera, Sabina Vatoveca and Vernonica E. Franklin-Tonga,1

a School of Biosciences, University of Birmingham, Edgbaston, Birmingham. B15 2TT, UK
b Present address: Institute of Biological, Environmental and Rural Sciences (IBERS), Aberystwyth University, Plas Gogerddan, Aberystwyth SY23 3EB, UK

1 To whom correspondence should be addressed. Email V.E.Franklin-Tong{at}bham.ac.uk, fax +44 121 414 5925, tel. +44 121 414 3702.

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-induced 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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