Published online 10 July 2006. doi:10.1083/jcb.200604011
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 174, Number 2, 221-229
Actin depolymerization is sufficient to induce programmed cell death in self-incompatible pollen
Steven G. Thomas1,
Shanjin Huang2,
Shutian Li1,
Christopher J. Staiger2,3, and
Vernonica E. Franklin-Tong1
1 School of Biosciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, England, UK
2 Department of Biological Sciences and 3 Bindley Bioscience Center, Purdue University, West Lafayette, IN 47907
Correspondence to Vernonica E. Franklin-Tong: v.e.franklin-tong{at}bham.ac.uk
Self-incompatibility (SI) prevents inbreeding through specific recognition and rejection of incompatible pollen. In incompatible Papaver rhoeas pollen, SI triggers a Ca2+ signaling cascade, resulting in the inhibition of tip growth, actin depolymerization, and programmed cell death (PCD). We investigated whether actin dynamics were implicated in regulating PCD. Using the actin-stabilizing and depolymerizing drugs jasplakinolide (Jasp) and latrunculin B, we demonstrate that changes in actin filament levels or dynamics play a functional role in initiating PCD in P. rhoeas pollen, triggering a caspase-3like activity. Significantly, SI-induced PCD in incompatible pollen was alleviated by pretreatment with Jasp. This represents the first account of a specific causal link between actin polymerization status and initiation of PCD in a plant cell and significantly advances our understanding of the mechanisms involved in SI.
S.G. Thomas and S. Huang contributed equally to this paper.
Abbreviations used in this paper: CD, cytochalasin D; F-actin, filamentous actin; G-actin, globular actin; GM, germination medium; Jasp, jasplakinolide; LatB, latrunculin B; PCD, programmed cell death; ROS, reactive oxygen species; SI, self-incompatibility.

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