Knuppertz 2017 Aging Cell
Knuppertz L, Osiewacz HD (2017) Autophagy compensates impaired energy metabolism in CLPXP-deficient Podospora anserina strains and extends healthspan. Aging Cell 16:704-15. |
Knuppertz L, Osiewacz HD (2017) Aging Cell
Abstract: The degradation of nonfunctional mitochondrial proteins is of fundamental relevance for maintenance of cellular homeostasis. The heteromeric CLPXP protein complex in the mitochondrial matrix is part of this process. In the fungal aging model Podospora anserina, ablation of CLPXP leads to an increase in healthy lifespan. Here, we report that this counterintuitive increase depends on a functional autophagy machinery. In PaClpXP mutants, autophagy is involved in energy conservation and the compensation of impairments in respiration. Strikingly, despite the impact on mitochondrial function, it is not mitophagy but general autophagy that is constitutively induced and required for longevity. In contrast, in another long-lived mutant ablated for the mitochondrial PaIAP protease, autophagy is neither induced nor required for lifespan extension. Our data provide novel mechanistic insights into the capacity of different forms of autophagy to compensate impairments of specific components of the complex mitochondrial quality control network and about the biological role of mitochondrial CLPXP in the control of cellular energy metabolism. β’ Keywords: Podospora anserina, CLPXP protease, Aging, Autophagy, Energy metabolism, Mitochondria β’ Bioblast editor: Kandolf G β’ O2k-Network Lab: DE Frankfurt Osiewacz HD
Labels: MiParea: Respiration
Pathology: Aging;senescence
Organism: Fungi
Preparation: Isolated mitochondria
Coupling state: OXPHOS
Pathway: N, S, CIV, NS
HRR: Oxygraph-2k
Labels, 2018-02