The mitochondrion - An organelle commonly involved in programmed cell death in Arabidopsis thaliana

Abstract

Plant cells undergoing programmed cell death (PCD) at late stages typically show chromatin condensation and endonucleolytic cleavage prior to obvious membrane or organelle ultrastructural changes. To investigate possible early PCD-associated events, we used microscopic observations and flow cytometry to quantitate mitochondrial membrane potential (ΔΨm) changes during PCD at the single cell and population levels using Arabidopsis protoplasts. A ΔΨm loss was commonly induced early during plant PCD and was important for PCD execution, as evidenced by the concomitant reduction of the change in ΔΨm and PCD by cyclosporin A, which inhibits mitochondrial permeability transition pores in animal cells. ΔΨm loss occurred prior to nuclear morphological changes and was only associated with mitochondrial cytochrome c release (an apoptotic trigger in animals) in response to one of three PCD elicitors. Three different stimuli in wild type implicated ΔΨm changes in PCD: ceramide, protoporphyrin IX, and the hypersensitive response elicitor AvrRptZ. Additionally, the behavior of the conditional ectopic cell death mutant accelerated cell death2 and 4CD2-overproducing plants also implicated ΔΨm alteration as key for PCD execution. Because ACD2 is largely a chloroplast component in mature plants, the observation that the cell death in acd2 mutants requires changes in mitochondrial functions implicates communication between chloroplasts and mitochondria in mediating PCD activation. We suggest that ΔΨm loss is a common early marker in plant PCD, similar to what has been documented in animals. However, unlike in animal cells, in plant cells, mitochondria! cytochrome c release is not an obligatory step in PCD control.