Mitochondrial involvement in tracheary element programmed cell death

X. H. Yu, T. D. Perdue, Y. M. Heimer, A. M. Jones

    Research output: Contribution to journalArticlepeer-review

    98 Scopus citations

    Abstract

    The mitochondria pathway is regarded as a central component of some types of programmed cell death (PCD) in animal cells where specific signals cause the release of cytochrome c from mitochondria to trigger a proteolytic cascade involving caspases. However, plant cells lack canonical caspases, therefore a role for the mitochondria in programmed cell death in plant cells is not obvious. Using plant cells which terminally differentiate, we provide evidence supporting the involvement of mitochondria in PCD, however the release of cytochrome c is insufficient to trigger the PCD. Prior to execution of cellular autolysis initiated by the rupture of the large central vacuole to release sequestered hydrolases, mitochondria adopt a definable morphology, the inner membrane depolarizes prior to death, and cytochrome c is released from mitochondria. However, PCD can be blocked despite translocation of cytochrome c. These results suggest a role for the mitochondria in this PCD but do not support the current animal model for a causative role of cytochrome c in triggering PCD.

    Original languageEnglish
    Pages (from-to)189-198
    Number of pages10
    JournalCell Death and Differentiation
    Volume9
    Issue number2
    DOIs
    StatePublished - 1 Jan 2002

    Keywords

    • Betulinic acid
    • Cytochrome c
    • Mitochondria
    • Plant
    • Programmed cell death
    • Tracheary element

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