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The victorin‐induced mitochondrial permeability transition precedes cell shrinkage and biochemical markers of cell death, and shrinkage occurs without loss of membrane integrity
Author(s) -
Curtis Marc J.,
Wolpert Thomas J.
Publication year - 2004
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/j.1365-313x.2004.02040.x
Subject(s) - biology , programmed cell death , microbiology and biotechnology , mitochondrion , population , mitochondrial permeability transition pore , cell , vacuole , cell membrane , biochemistry , apoptosis , cytoplasm , demography , sociology
Summary In this study, we determined the timing of events associated with cell death induced by the host‐selective toxin, victorin. We show that the victorin‐induced collapse in mitochondrial transmembrane potential (Δ ψ m ), indicative of a mitochondrial permeability transition (MPT), on a per cell basis, did not occur simultaneously in the entire mitochondrial population. The loss of Δ ψ m in a predominant population of mitochondria preceded cell shrinkage by 20–35 min. Rubisco cleavage, DNA laddering, and victorin binding to the P protein occurred concomitantly with cell shrinkage. During and following cell shrinkage, tonoplast rupture did not occur, and membranes, including the plasma membrane and tonoplast, retained integrity. Ethylene signaling was implicated upstream of a victorin‐induced loss in mitochondrial motility and the collapse in Δ ψ m . Results suggest that the victorin‐induced collapse in Δ ψ m is a consequence of an MPT and that the timing of the victorin‐induced MPT is poised to influence the cell death response. The retention of plasma membrane and tonoplast integrity during cell shrinkage supports the interpretation that victorin induces an apoptotic‐like cell death response.