David C. Logan

On the developmental dependence of leaf respiration: responses to short- and long-term changes in growth temperature.

Using measurements of leaf respiratory O(2) uptake (R), we investigated whether immature and mature Arabidopsis thaliana (ecotype Columbia) leaves differed in their response to temperature. Confocal microscopy (using plants with mitochondrially targeted green fluorescent protein [GFP]) was used to determine whether ontogenetic changes in R are associated with concomitant changes in mitochondrial morphology/abundance. Comparisons were made of warm-grown (25/20°C) leaves, warm-grown leaves shifted to cold (5°C) for 10 days, and cold-developed leaves. Short-term Q(10) values and the ability to cold-acclimate were determined. In warm-grown plants, rates of R per mass were highest in immature leaves, decreasing as leaves developed. Moreover, although mitochondrial size (5.6-6.5 μm(3)) remained constant during development, mitochondrial number per μm(3) declined from 0.01 to 0.003 as leaves expanded (i.e., mitochondrial density decreased). Immature and mature leaves did not differ in Q(10) values but did differ in their ability to cold-acclimate. Whereas mature leaves had clear evidence of cold acclimation (e.g., when measured at 25°C, R was highest in cold-developed leaves), young leaves had none. Collectively, the results highlight the changes in rates of R, mitochondrial density, and biomass allocation associated with leaf development and that changes in respiratory flux associated with acclimation only take place within mature tissues.

Mitochondria and cell death pathways in plants Actions speak louder than words

The mitochondrion has a central role during programmed cell death (PCD) in animals, acting as both a sensor of death signals, and as an initiator of the biochemical processes which lead to the controlled destruction of the cell. In contrast to our extensive knowledge of animal cell death, the part played by mitochondria in the death of plant cells has received relatively little attention. Using a combination of whole-organism and cell-based models, we recently demonstrated that changes in mitochondrial morphology are an early and crucial step in plant cell death. Here, we discuss these findings in the light of recent literature, and how they relate to our knowledge of plant cell death as a whole.

Mitochondrial Morphology, Dynamics and Inheritance

The first eukaryotes are thought to have arisen around 2 billion years ago through symbiosis of an archaebacterial host cell and a eubacterial symbiont (mitochondrial ancestor). The mitochondrion we know today is the result, therefore, of 2 billion years of evolution of this symbiosis. Like modern day bacteria, mitochondria cannot be created de novo but instead must arise from the fission (division) of a parental organelle. In addition to fission, mitochondria also fuse with one another and it is thought that a co-ordinated balance of these two processes controls mitochondrial shape, size and number. In the past five to seven years, molecular genetics coupled to state-of-the-art cell biology, in particular the use of mitochondrial-targeted GFP, has enabled identification of proteins controlling mitochondrial shape, size and number in yeast and mammalian cells. Whilst little is known about higher plant mitochondrial dynamics several genes involved in the control of plant mitochondrial dynamics have been identified recently.