Nektarios Tavernarakis is the Director of the Institute of Molecular Biology and Biotechnology, at the Foundation for Research and Technology, and a Professor of Molecular Systems Biology at the Medical School of the University of Crete, in Heraklion, Greece. He is also heading the Neurogenetics and Ageing laboratory of the Institute. He earned his Ph.D. degree at the University of Crete, and trained as a postdoctoral researcher at Rutgers University in New Jersey, USA. His research focuses on studies of neuronal function and dysfunction. His main interests are the molecular mechanisms of necrotic cell death in neurodegeneration and senescent decline, the molecular mechanisms of sensory transduction and integration by the nervous system, the interplay between cellular metabolism and ageing, and the development of novel genetic tools for biomedical research. For his scientific accomplishments, Nektarios Tavernarakis has received several notable scientific prizes including a European Research Council (ERC) Advanced Investigator grant award, the European Molecular Biology Organization (EMBO) Young Investigator award, the Bodossaki Foundation Scientific Prize for Medicine and Biology, the Alexander von Humboldt Foundation, Friedrich Wilhelm Bessel research award, the Empeirikeion Foundation Academic Excellence Prize, the Research Excellence award of the Foundation for Research and Technology, and the BioMedicalResearchAwardoftheAcademyofAthens. Prof. Tavernarakis is also an elected member of EMBO and Academia Europaea.For more information, please visit: http://www.elegans.gr/
Mitochondria, the main energy hub of the cell, are highly dynamic organelles, playing essential roles in fundamental cellular processes. Mitochondrial function impinges on several signalling pathways modulating cellular metabolism, cell survival and healthspan. Maintenance of mitochondrial function and energy homeostasis requires both generation of newly synthesized and elimination of dysfunctional mitochondria. Impaired mitochondrial function and excessive mitochondrial content are major characteristics of ageing and several human pathophysiological conditions, highlighting the pivotal role of the coordination between mitochondrial biogenesis and mitophagy. However, the cellular and molecular underpinnings of mitochondrial mass homeostasis remain obscure. We found that DCT-1, the Caenorhabditis elegans homolog of mammalian BNIP3 and BNIP3L/NIX, is a key mediator of mitophagy promoting longevity under stress. DCT-1 acts downstream of the PINK-1-PDR-1/Parkin pathway and is ubiquitinated upon mitophagy-inducing conditions to mediate the removal of damaged mitochondria. Accumulation of damaged mitochondria triggers SKN-1 activation, which initiates a bipartite retrograde signaling pathway stimulating the coordinated induction of both mitochondrial biogenesis and mitophagy genes. Taken together, our results unravel a homeostatic feedback loop that allows cells to adjust their mitochondrial population in response to environmental and intracellular cues. Age-dependent decline of mitophagy both inhibits removal of dysfunctional or superfluous mitochondria and impairs mitochondrial biogenesis resulting in progressive mitochondrial accretion and consequently, deterioration of cell function.