Abstract
PERK protein, that is canonically associated with the response to endoplasmic reticulum stress, may be acquiring a new role as a regulator of the growth of mitochondrial cristae. This role is pertinent not only to the recruitment of brown adipose tissue thermogenic capacity but probably also to directing cristae formation in highly metabolically active organs such as the heart.
Highlights
The multitude of respiratory complexes synthesized must be highly organized within the mitochondria
This is because the PERK pathway is one of the pathways that are activated as part of the endoplasmic reticulum (ER) stress response
OGlcNAcetylation activates TOMM70, and more MIC19 is transported into the intermembrane space, leading to more mitochondrial contact site and cristae organizing system (MICOS) complex activity, and to mitochondrial cristae formation
Summary
The multitude of respiratory complexes synthesized must be highly organized within the mitochondria. This is because the PERK pathway is one of the pathways that are activated as part of the ER stress response. PERK, as one of three canonical pathways, is activated, autophosphorylates, and phosphorylates the initiation factor eIF2α.
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