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Fig. 11. Model linking Ras/cAMP signalling to actin remodelling, ROS release and apoptosis. In response to environmental stresses such as nutrient depletion or heat shock, the actin cytoskeleton undergoes remodelling as part of the survival response. Evidence suggests that the Ras/cAMP pathway is important in this remodelling. Also important are the actin-regulatory activities of Sla1p, which is targeted to the cortex by both End3p and Rsp5p activities. Inappropriate activation of the Ras/cAMP pathway or reduced actin dynamics as a result of a loss of Sla1p function lead to high levels of ROS accumulation. The exposure to high levels of oxidative stress lead to a reduced lifespan and an increased likelihood of apoptosis. We suggest that there is a cross-talk mechanism between the actin cytoskeleton and Ras/cAMP signalling machinery that regulates this pathway. This model provides a mechanism by which a colony of unicellular organisms can filter out older or genetically unfit individuals in response to environmental change.
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