MTCH2 is a mitochondrial outer membrane protein insertase

Alina Guna(Whitehead Institute for Biomedical Research), Taylor A. Stevens(California Institute of Technology), Alison J. Inglis(California Institute of Technology), Joseph M. Replogle(Howard Hughes Medical Institute), Theodore K. Esantsi(Howard Hughes Medical Institute), Gayathri Muthukumar(Whitehead Institute for Biomedical Research), Kelly Shaffer(California Institute of Technology), Maxine L. Wang(California Institute of Technology), Angela N. Pogson(Howard Hughes Medical Institute), Jeff Jones(California Institute of Technology), Brett Lomenick(California Institute of Technology), Tsui‐Fen Chou(California Institute of Technology), Jonathan S. Weissman(Howard Hughes Medical Institute), R.M. Voorhees(California Institute of Technology)
Science
October 20, 2022
Cited by 147Open Access
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Abstract

In the mitochondrial outer membrane, α-helical transmembrane proteins play critical roles in cytoplasmic-mitochondrial communication. Using genome-wide CRISPR screens, we identified mitochondrial carrier homolog 2 (MTCH2), and its paralog MTCH1, and showed that it is required for insertion of biophysically diverse tail-anchored (TA), signal-anchored, and multipass proteins, but not outer membrane β-barrel proteins. Purified MTCH2 was sufficient to mediate insertion into reconstituted proteoliposomes. Functional and mutational studies suggested that MTCH2 has evolved from a solute carrier transporter. MTCH2 uses membrane-embedded hydrophilic residues to function as a gatekeeper for the outer membrane, controlling mislocalization of TAs into the endoplasmic reticulum and modulating the sensitivity of leukemia cells to apoptosis. Our identification of MTCH2 as an insertase provides a mechanistic explanation for the diverse phenotypes and disease states associated with MTCH2 dysfunction.


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