Aging is characterized by the decline of physiological integrity, which culminates in functional defects and increased risk for age-associated diseases. Cell autonomous deficits include disturbances in cellular proteostasis, organellar homeostasis, and genome integrity, which in turn can elicit multiple adaptive signaling pathways and cellular stress responses. Work of CECAD PIs has begun to unravel the underlying cell autonomous mechanisms contributing to the decline of cellular functions during aging. The concerted analysis of key lifespan determinants by CECAD PIs has revealed a strong interdependence of different cell autonomous deficits that now need to be considered to provide an integrated and detailed overview on the decline of cellular activities during aging and their relationship to the onset and development of age-associated diseases. The key objectives of RA-1 are to investigate:
Figure 1: Purkinje nerve cells link the granular to the molecular layer of the cerebellar cortex. This brain region controls balance and muscle coordination.
Figure 2: View of the network of nerve cells in the brain.
Figure 3 and 6: Absence of mitochondrial fusion leads to mitochondrial fragmentation and respiratory incompetence. Fzo1 is essential for the presence of tubular mitochondria. Mitochondrial morphology of (a) wild-type and (b) Δfzo1 yeast cells expressing a mitochondrial-targeted GFP protein. Cellular (Nomarsky) and mitochondrial (GFP) morphology were visualized by fluorescence microscopy.
Figure 4: An example of a model organism used for research: the threadworm C. elegans.
Figure 5: Mitochondria are dynamic parts of the cell.