Pollen PCD, as seen by DNA fragmentation (green), is induced by actin filament destabilization.

Actin depolymerization is a death trigger for poppy pollen, according to Thomas et al. (page 221), that prevents self-fertilization.

Some plants prefer not to be fertilized by pollen grains that are genetically similar to themselves. These plants express self-incompatibility (S) proteins. A match between the pistil's S-proteins and the pollen's S-allele triggers a rapid calcium influx, actin filament destruction, and pollen cell death.

Several years ago, the researchers noticed that the amount of actin depolymerization far exceeded that required to inhibit pollen tube growth. The persistent actin destabilization also resembled that associated with animal cells about to undergo programmed cell death (PCD).

The authors now find that blocking actin depolymerization prevents pollen cell death in self-incompatible plants. Inducing actin depolymerization, on the other hand, activated pollen cell death. The dying cells showed the same pattern of DNA fragmentation and caspase-like activity as did pollen killed by self-incompatibility.

Changes in actin dynamics have been linked to PCD in animal and yeast cells, and a variety of noxious external stimuli triggers actin rearrangement in plants. Actin may thus serve as a sensor for extreme environmental stress to initiate PCD or other changes in cell behavior. As even a short exposure to depolymerizing drugs killed pollen cells, a brief change in actin dynamics seems to be all that is needed to kick off signaling cascades.