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. 2018 Oct 1;32(19-20):1285–1296. doi: 10.1101/gad.316547.118

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© 2018 Priesnitz and Becker; Published by Cold Spring Harbor Laboratory Press

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

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Figure 6. — Defects in mitochondrial protein import induce the UPR^mt. In C. elegans, the transcription factor ATFS-1 contains a mitochondrial (MTS) and a nuclear (NLS) targeting signal. The TOM and TIM23 complexes transport ATFS-1 into the matrix of intact mitochondria, where it is degraded by the LON protease. In damaged mitochondria, the membrane potential (Δψ) is diminished, and the import of ATFS-1 into mitochondria is impaired. Instead, a fraction of ATFS-1 relocalizes to the nucleus. Together with the transcription factors DVE-1 and UBL-5, it induces the transcription of genes involved in the UPR^mt. In addition, uncharacterized fractions of ATFS-1 silence the expression of nuclear and mitochondrial OXPHOS genes.