Abstract
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-3-like 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. © The Rockefeller University Press.
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CITATION STYLE
Thomas, S. G., Huang, S., Li, S., Staiger, C. J., & Franklin-Tong, V. E. (2006). Actin depolymerization is sufficient to induce programmed cell death in self-incompatible pollen. Journal of Cell Biology, 174(2), 221–229. https://doi.org/10.1083/jcb.200604011
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