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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Actin depolymerization is sufficient to induce programmed cell death in self-incompatible pollen.

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.[1]

References

  1. Actin depolymerization is sufficient to induce programmed cell death in self-incompatible pollen. Thomas, S.G., Huang, S., Li, S., Staiger, C.J., Franklin-Tong, V.E. J. Cell Biol. (2006) [Pubmed]
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