Mitochondria

Regulation of cellular lifespan

We found that the cysteinyl-tRNA synthetase SYCO is expressed in the central cell, which is the precursor of the embryo nourishing tissue, but absent from the adjoining antipodal cells, which exhibit an extended lifespan in syco mutants. SYCO localizes to the mitochondria and ultrastructural analysis of mutant central cells revealed that the protein is necessary for mitochondrial cristae integrity. Furthermore, a dominant ATP/ADP translocator caused mitochondrial cristae degeneration and extended antipodal lifespan when expressed in the central cell of wild-type plants. Notably, this construct did not affect antipodal lifespan when expressed in antipodals. Our results thus identified an unexpected noncell autonomous role for mitochondria in the regulation of cellular lifespan and draw the attention away from the dying cell and toward adjacent nondying cells as a potential cause for Programmed Cell Death (PCD) (Kägi et al. 2010).

Mitochondria-associated diseases

In humans, mitochondria-associated diseases are among the most common inherited genetic disorders (3). Examples include diabetis, cancer, neurodegenerative and cardiovascular diseases (4-7). Recently, mitochondria have been implicated in the regulation of sleep (8), further emphasizing the great significance of these minute organelles.

Past research has mainly focused on mitochondria in their entity. However, several studies have reported on remarkable mitochondrial heterogeneity both, among and within cells. The biological significance of this differences is not well understood, which is to a large extend due to technical limitations associated with the analysis of mitochondria at the single cell or even single mitochondrion level.