Aging Research in Yeast

Volume 57 of the series Subcellular Biochemistry pp 331-352


Cellular Ageing and the Actin Cytoskeleton

  • David AmbergAffiliated withDepartment of Biochemistry and Molecular Biology, SUNY Upstate Medical University
  • , Jane E. LeadshamAffiliated withKent Fungal Group, School of Biosciences, University of Kent
  • , Vasillios KotiadisAffiliated withKent Fungal Group, School of Biosciences, University of Kent
  • , Campbell W. GourlayAffiliated withKent Fungal Group, School of Biosciences, University of Kent Email author 

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For some time the view that the actin cytoskeleton acts primarily as a scaffold, to be assembled in response to a signaling cascade as an end point in the pathway, has prevailed. However, it is now clear that the dynamic nature of the cytoskeleton is linked to downstream signaling events that further modulate cellular activity, and which can determine cell fate. Examples of this lie within the regulation of programmed cell death, the maintenance of homeostasis and the process of cellular ageing. In yeast the actin cytoskeleton has been shown to interact directly with signaling pathways known to be important in the regulation of both ageing and cell death. For example it has been discovered that the level of damage sustained by the actin cytoskeleton under conditions of oxidative stress is directly linked to apoptosis. Further evidence comes from the finding that actin based propulsion mechanisms are required for the inheritance of mitochondria and anti-ageing factors into newly formed cells. In addition to this actin is known to directly influence the formation of protein aggregations. In this chapter we will discuss these points and postulate as to their significance with respect to the maintenance of cellular homeostasis.


Actin Mitochondria Protein aggregation Oxidative stress ROS Cytoskeleton Ras/cAMP/PKA Autophagy Mitophagy