Having a swell time - mitochondrial morphology and plant cell death programmes

D. C. Logan

Research output: Contribution to journalArticlepeer-review

16 Citations (Scopus)

Abstract

Cell death is a vital process in multi-cellular eukaryotes. Rather than being a contradiction in terms, this statement highlights the importance of limited and localized cell killing to the health and normal development of complex organisms. The main focus of this article is the role of mitochondrial morphological changes during cell death programmes, and the conserved role of mitochondrial permeability transition (increased permeability of either the outer or inner membrane) as an early mechanistic event preceding cell death in both plant and non-plant eukaryotes. A second focus of this article is a review of the terminology and fundamental paradigms underpinning cell death research. Because of the importance of the process of cell death, there has been an enormous quantity of research performed to try to understand the underlying biological mechanisms. One result of such a large and varied research effort, and a result that is perhaps particularly evident to investigators coming into the field anew, is that some of the basic tenets of cell death research appear to have become confused. In this short article, I make an attempt to clarify the subject, focussing on the role of mitochondria, and the difficulties in comprehensibility arising from the sometimes-erroneous, or at least unnecessarily confusing use of specific terminology; there are several key terms in the cell death literature that appear interchangeable when they are not, or are interchanged when they should not be.

Original languageEnglish
Pages (from-to)215-224
Number of pages10
JournalJournal of Microscopy
Volume231
Issue number2
DOIs
Publication statusPublished - Aug 2008

Keywords

  • apoptosis
  • calcium
  • mitochondrial permeability transition
  • morphology
  • necrosis
  • programmed cell death
  • PERMEABILITY TRANSITION PORE
  • ADENINE-NUCLEOTIDE TRANSLOCASE
  • DEPENDENT ANION CHANNEL
  • CYCLOPHILIN-D
  • CYTOCHROME-C
  • CYCLOSPORINE-A
  • ENDOPLASMIC-RETICULUM
  • ARABIDOPSIS-THALIANA
  • CERAMIDE CHANNELS
  • INDUCED APOPTOSIS

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