The victorin-induced mitochondrial permeability transition precedes cell shrinkage and biochemical markers of cell death, and shrinkage occurs without loss of membrane integrity


  • Marc J. Curtis,

    1. Department of Zoology, Oregon State University, 3029 Cordley Hall, Corvallis, OR 97331, USA, and
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  • Thomas J. Wolpert

    Corresponding author
    1. Department of Botany and Plant Pathology, Oregon State University, 2064 Cordley Hall, Corvallis, OR 97331, USA
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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 (Δψm), indicative of a mitochondrial permeability transition (MPT), on a per cell basis, did not occur simultaneously in the entire mitochondrial population. The loss of Δψm 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 Δψm. Results suggest that the victorin-induced collapse in Δψm 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.