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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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The actin cytoskeleton, RAS-cAMP signaling and mitochondrial ROS in yeast apoptosis.

The release of reactive oxygen species (ROS) by mitochondria instigates the pathways of programmed cell death in eukaryotic cells. Gourlay and Ayscough present intriguing experimental evidence that mutations in the genes encoding the regulatory proteins End3p and Sla1p, which influence actin dynamics in budding yeast, lead to a loss of mitochondrial membrane potential, resulting in ROS production and apoptosis. This effect can be suppressed by downregulation of the RAS-cAMP signaling pathway, thus establishing the existence of a new and complex regulatory network.[1]

References

  1. The actin cytoskeleton, RAS-cAMP signaling and mitochondrial ROS in yeast apoptosis. Breitenbach, M., Laun, P., Gimona, M. Trends Cell Biol. (2005) [Pubmed]
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