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Fission inhibition fails to save cells
One of the ongoing topics for discussion in cell biology concerns the comparison of programmed cell death (PCD) in plants with that in animals. Some authors are firmly of the opinion that many aspects of plant PCD resemble closely apoptosis in animals, while others have been more cautious. Proponents of both sides of the debate are able to point to evidence that supports their view. Thus, for example, it has previously been shown that expression in plants of the mammalian apoptosis regulator BAX induces PCD in those plants, even though plants do not apparently possess a BAX homologue. However, Yoshinaga et al. (Tokyo and Iwate, Japan, pp. 1145–1149) now present evidence that supports the more cautious view. Various aspects of mitochondrial physiology are intimately involved in animal cell apoptosis, including fission and/or fragmentation of the organelle, loss of membrane integrity and efflux of cytochrome c. Inhibition of mitochondrial fission by various means (including down-regulation of proteins promoting mitochondrial fission and over-expression of proteins promoting mitochondrial elongation) actually inhibits apoptosis. Previous observations had indicated that mitochondrial fission and fragmentation occur in PCD induced by BAX or by reactive oxygen species (ROS) in Arabidopsis thaliana, suggesting another similarity with animal apoptosis. To test this idea further, the authors inhibited mitochondrial fission by the over-expression of DRP3B (K56A), a dominant-negative mutant form of the gene DRP3B, which in its wild-type state promotes mitochondrial fission. The expression of the dominant-negative mutant gene led to mitochondrial morphology similar to a string of sausages, indicating an inhibition of mitochondrial fission. However, PCD, whether induced by BAX or by ROS or by other factors, was not inhibited. In plants then, mitochondrial fission is probably a consequence of PCD and not part of the causative cascade.
Professor J. A. Bryant
University of Exeter, UK
j.a.bryant{at}exeter.ac.uk
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