Link to bioRxiv paper:
http://biorxiv.org/cgi/content/short/2022.10.24.513548v1?rss=1

Authors: Nguyen, T. T., Voeltz, G. K.

Abstract:
Mitochondria are dynamic organelles that undergo cycles of fission and fusion at a unified platform defined by endoplasmic reticulum (ER)-mitochondria membrane contact sites (MCSs). These MCSs or nodes co-localize fission and fusion machinery. We set out to identify how ER-associated mitochondrial nodes can regulate both fission and fusion machinery assembly. We have used a promiscuous biotin ligase linked to the fusion machinery, Mfn1, and proteomics to identify an ER membrane protein, Aphyd, as a major regulator of node formation. In the absence of Aphyd, fission and fusion machineries fail to recruit to ER-associated mitochondrial nodes and fission and fusion rates are significantly reduced. Aphyd contains an acyltransferase motif and an /{beta} hydrolase domain and point mutations in critical residues of these regions fail to rescue the formation of ER-associated mitochondrial hot spots. These data suggest a mechanism whereby Aphyd functions by altering phospholipid composition at ER mitochondria MCSs. Our data present the first example of an ER membrane protein that regulates the recruitment of both fission and fusion machineries to mitochondria.

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