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• W2168847792 abstract "Peroxisome biogenesis disorders lead to a myriad of clinical manifestations, among which is the dysfunction of the mitochondria. Mitochondria dysfunction is typically sensed by the UPR^mt, a broad protective transcriptional response governed by the transcription factor ATFS-1. Here, we investigated the role of the UPR^mt during peroxisomal stress. We show that mutations or knockdown of peroxins, the genes required for peroxisome assembly, lead to mitochondria dysfunction and the induction of the UPR^mt in <i>C.elegans</i>. The UPR^mt induced the transcription of the mitochondrial outer membrane translocase <i>mspn-1</i> (ATAD-1), that in turn alleviated mitochondrial stress most likely by extracting mislocalized proteins. Importantly, ATFS-1 regulated the transcription of peroxins and the peroxisomal transporter <i>pmp-4</i>. A <i>prx-5</i> loss of function strain induced a retrograde response that resulted in the transcriptional induction of peroxins, peroxisomal transporters, chaperons and proteases. And was dependent on ATFS-1 and on the peroxisome proliferator activator receptor alpha, NHR-49. Knockout of <i>atfs-1</i> during peroxisomal stress resulted in severe developmental delays, import defects to peroxisomes and the appearance of large peroxisomal structures. We propose that ATFS-1 regulates the biogenesis of peroxisomes and protects the organism by alleviating the stress of both peroxisomes and mitochondria during peroxisomal stress." @default.
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• W2168847792 date "2007-12-13" @default.
• W2168847792 modified "2023-10-15" @default.
• W2168847792 title "Elevated expression and polymorphisms of SOCS3 influence patient response to antiviral therapy in chronic hepatitis C" @default.
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• W2168847792 doi "https://doi.org/10.1136/gut.2007.129478" @default.
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