The plant response to attempted infection by microbial pathogens is often a
ccompanied by rapid cell death in and around the initial infection site, a
reaction known as the hypersensitive response. This response is associated
with restricted pathogen growth and represents a form of programmed cell de
ath (PCD). Recent pharmacological and molecular studies have provided funct
ional evidence for the conservation of some of the basic regulatory mechani
sms underlying the response to pathogens and the activation of PCD in anima
l and plant systems. In animals, the mitochondrion integrates diverse cellu
lar stress signals and initiates the death execution pathway, and studies i
ndicate a similar involvement for mitochondria in regulating PCD in plants.
But many of the cell-death regulators that have been characterized in huma
ns, worms and flies are absent from the Arabidopsis genome, indicating that
plants probably use other regulators to control this process.