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Role of nitric oxide in actin depolymerization and programmed cell death induced by fusicoccin in sycamore ( Acer pseudoplatanus ) cultured cells
Author(s) -
Malerba Massimo,
Contran Nicla,
Tonelli Mariagrazia,
Crosti Paolo,
Cerana Raffaella
Publication year - 2008
Publication title -
physiologia plantarum
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.351
H-Index - 146
eISSN - 1399-3054
pISSN - 0031-9317
DOI - 10.1111/j.1399-3054.2008.01085.x
Subject(s) - programmed cell death , microbiology and biotechnology , cytochrome c , biology , apoptosis , fragmentation (computing) , fusicoccin , cytoskeleton , nitric oxide , actin , cytoplasm , cell , biochemistry , mitochondrion , ecology , atpase , endocrinology , enzyme
Programmed cell death (PCD) plays a vital role in plant development and is involved in defence mechanisms against biotic and abiotic stresses. Different forms of PCD have been described in plants on the basis of the cell organelle first involved. In sycamore ( Acer pseudoplatanus L.) cultured cells, the phytotoxin fusicoccin (FC) induces cell death. However, only a fraction of the dead cells shows the typical hallmarks of animal apoptosis, including cell shrinkage, chromatin condensation, DNA fragmentation and release of cytochrome c from the mitochondrion. In this work, we show that the scavenging of nitric oxide (NO), produced in the presence of FC, by 2‐(4‐carboxyphenyl)‐4,4,5,5‐tetramethylimidazoline‐1‐oxyl‐3‐oxide (cPTIO) and rutin inhibits cell death without affecting DNA fragmentation and cytochrome c release. In addition, we show that FC induces a massive depolymerization of actin filaments that is prevented by the NO scavengers. Finally, the addition of actin‐depolymerizing drugs induces PCD in control cells and overcomes the inhibiting effect of cPTIO on FC‐induced cell death. Vice versa, the addition of actin‐stabilizing drugs to FC‐treated cells partially inhibits the phytotoxin‐induced PCD. These results suggest that besides an apoptotic‐like form of PCD involving the release of cytochrome c , FC induces at least another form of cell death, likely mediated by NO and independent of cytochrome c release, and they make it tempting to speculate that changes in actin cytoskeleton are involved in this form of PCD.