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Fig. 3 | BMC Biology

Fig. 3

From: The different axes of the mammalian mitochondrial unfolded protein response

Fig. 3

Integration of mitochondrial misfolding stress and different UPRmt axes. Cells contain numerous mitochondria with a certain, low percentage stressed upon basal conditions, due to aging and metabolic damage. Dealing with these refined incidents of mitochondrial proteostasis defects, which are not due to significant environmental perturbation, requires spatially defined responses. The UPRmt translational response acts via local, posttranslational regulation of MRPP3 levels and can decrease translation, and thus folding load, in an individual mitochondrion. Thus, it acts locally as a first response to mitochondrial protein misfolding in few damaged mitochondria without causing global effects. The transcriptional UPRmt effects occur cell-wide and likely require passing a certain threshold of mitochondrial proteostasis defects. This suggests a model in which mitochondrion-specific UPRmt effects (i.e., the UPRmt translation axis) are activated upon cellular conditions with a certain low percentage of mitochondria suffering from protein misfolding and activation of the cell-wide UPRmt axes upon proteostasis defects in a large percentage of mitochondria

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