TY  - JOUR
A1  - Knuppertz, Laura
A1  - Osiewacz, Heinz D.
T1  - Autophagy compensates impaired energy metabolism in CLPXP‐deficient Podospora anserina strains and extends healthspan
T2  - Aging cell
N2  - 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.
KW  - aging
KW  - autophagy
KW  - CLPXP protease
KW  - energy metabolism
KW  - mitochondria
KW  - Podospora anserina
Y1  - 2017
UR  - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/45224
UR  - https://nbn-resolving.org/urn:nbn:de:hebis:30:3-452246
SN  - 1474-9728
SN  - 1474-9718
N1  - © 2017 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
VL  - 16
IS  - 4
SP  - 704
EP  - 715
PB  - Wiley-Blackwell
CY  - Oxford [u. a.]
ER  -