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  MITRAC7 defines a checkpoint during cytochrome c oxidase assembly.

Dennerlein, S., Oeljeklaus, S., Jans, D. C., Hellwig, C., Bareth, B., Jakobs, S., et al. (2015). MITRAC7 defines a checkpoint during cytochrome c oxidase assembly. Cell Reports, 12(10), 1644-1655. doi:10.1016/j.celrep.2015.08.009.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-0028-466E-C Version Permalink: http://hdl.handle.net/11858/00-001M-0000-002A-0B80-3
Genre: Journal Article

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 Creators:
Dennerlein, S., Author
Oeljeklaus, S., Author
Jans, D. C.1, Author              
Hellwig, C., Author
Bareth, B., Author
Jakobs, S.1, Author              
Deckers, M., Author
Warscheid, B., Author
Rehling, P.2, Author              
Affiliations:
1Research Group of Mitochondrial Structure and Dynamics, MPI for biophysical chemistry, Max Planck Society, ou_578566              
2Max Planck Fellow Peter Rehling, ou_1298545              

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 Abstract: Cytochrome c oxidase, the terminal enzyme of the respiratory chain, is assembled from mitochondria- and nuclear-encoded subunits. The MITRAC complex represents the central assembly intermediate during this process as it receives imported subunits and regulates mitochondrial translation of COX1 mRNA. The molecular processes that promote and regulate the progression of assembly downstream of MITRAC are still unknown. Here, we identify MITRAC7 as a constituent of a late form of MITRAC and as a COX1-specific chaperone. MITRAC7 is required for cytochrome c oxidase biogenesis. Surprisingly, loss of MITRAC7 or an increase in its amount causes selective cytochrome c oxidase deficiency in human cells. We demonstrate that increased MITRAC7 levels stabilize and trap COX1 in MITRAC, blocking progression in the assembly process. In contrast, MITRAC7 deficiency leads to turnover of newly synthesized COX1. Accordingly, MITRAC7 affects the biogenesis pathway by stabilizing newly synthesized COX1 in assembly intermediates, concomitantly preventing turnover.

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Language(s): eng - English
 Dates: 2015-08-282015-09-08
 Publication Status: Published in print
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 Table of Contents: -
 Rev. Method: Peer
 Identifiers: DOI: 10.1016/j.celrep.2015.08.009
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Title: Cell Reports
Source Genre: Journal
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Pages: - Volume / Issue: 12 (10) Sequence Number: - Start / End Page: 1644 - 1655 Identifier: -