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Rackles, E.* ; Witting, M. ; Forné, I.* ; Zhang, X.* ; Zacherl, J.* ; Schrott, S.* ; Fischer, C.* ; Ewbank, J.J.* ; Osman, C.* ; Imhof, A.* ; Rolland, S.G.*

Reduced peroxisomal import triggers peroxisomal retrograde signaling.

Cell Rep. 34:108653 (2021)
Verlagsversion Forschungsdaten DOI
Open Access Gold
Creative Commons Lizenzvertrag
Maintaining organelle function in the face of stress is known to involve organelle-specific retrograde signaling. Using Caenorhabditis elegans, we present evidence of the existence of such retrograde signaling for peroxisomes, which we define as the peroxisomal retrograde signaling (PRS). Specifically, we show that peroxisomal import stress caused by knockdown of the peroxisomal matrix import receptor prx-5/PEX5 triggers NHR-49/peroxisome proliferator activated receptor alpha (PPARα)- and MDT-15/MED15-dependent upregulation of the peroxisomal Lon protease lonp-2/LONP2 and the peroxisomal catalase ctl-2/CAT. Using proteomic and transcriptomic analyses, we show that proteins involved in peroxisomal lipid metabolism and immunity are also upregulated upon prx-5(RNAi). While the PRS can be triggered by perturbation of peroxisomal β-oxidation, we also observed hallmarks of PRS activation upon infection with Pseudomonas aeruginosa. We propose that the PRS, in addition to a role in lipid metabolism homeostasis, may act as a surveillance mechanism to protect against pathogens.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter C. Elegans Immunity ; C. elegans ; Mdt-15 ; Nhr-49 ; Peroxisomal Lon Protease ; Peroxisomal Catalase ; Peroxisomal Retrograde Signaling ; Peroxisomal β-oxidation; Caenorhabditis-elegans; Gene-expression; C-elegans; Protein Import; Beta-oxidation; Responses; Biogenesis; Disorders; Infection; Bacterial
ISSN (print) / ISBN 2211-1247
e-ISSN 2211-1247
Zeitschrift Cell Reports
Quellenangaben Band: 34, Heft: 3, Seiten: , Artikelnummer: 108653 Supplement: ,
Verlag Cell Press
Verlagsort 50 Hampshire St, Floor 5, Cambridge, Ma 02139 Usa
Begutachtungsstatus Peer reviewed
Förderungen European Research Council
Deutsche Forschungsgemeinschaft
Institute for Basic Science
Agence Nationale de la Recherche
ChineseScholarship Council
National Institutes of Health National Center for Research Resources