Aim24 and MICOS modulate respiratory function, tafazzin-related cardiolipin modification and mitochondrial architecture

Max Emanuel Harner; Ann Katrin Unger; Toshiaki Izawa; Dirk M. Walther; Cagakan Özbalci; Stefan Geimer; Fulvio Reggiori; Britta Brügger; Matthias Mann; Benedikt Westermann; Walter Neupert

doi:10.7554/eLife.01684

Aim24 and MICOS modulate respiratory function, tafazzin-related cardiolipin modification and mitochondrial architecture

Max Emanuel Harner, Ann Katrin Unger, Toshiaki Izawa, Dirk M. Walther, Cagakan Özbalci, Stefan Geimer, Fulvio Reggiori, Britta Brügger, Matthias Mann, Benedikt Westermann, Walter Neupert

Research output: Contribution to journal › Article › peer-review

52 Citations (Scopus)

Abstract

Structure and function of mitochondria are intimately linked. In a search for components that participate in building the elaborate architecture of this complex organelle we have identified Aim24, an inner membrane protein. Aim24 interacts with the MICOS complex that is required for the formation of crista junctions and contact sites between inner and outer membranes. Aim24 is necessary for the integrity of the MICOS complex, for normal respiratory growth and mitochondrial ultrastructure. Modification of MICOS subunits Mic12 or Mic26 by His-tags in the absence of Aim24 leads to complete loss of cristae and respiratory complexes. In addition, the level of tafazzin, a cardiolipin transacylase, is drastically reduced and the composition of cardiolipin is modified like in mutants lacking tafazzin. In conclusion, Aim24 by interacting with the MICOS complex plays a key role in mitochondrial architecture, composition and function.

Original language	English
Article number	e01684
Journal	eLife
Volume	2014
Issue number	3
DOIs	https://doi.org/10.7554/eLife.01684
Publication status	Published - 2014 Apr 8
Externally published	Yes

ASJC Scopus subject areas

Neuroscience(all)
Immunology and Microbiology(all)
Biochemistry, Genetics and Molecular Biology(all)

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10.7554/eLife.01684

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Aim24 and MICOS modulate respiratory function, tafazzin-related cardiolipin modification and mitochondrial architecture. / Harner, Max Emanuel; Unger, Ann Katrin; Izawa, Toshiaki; Walther, Dirk M.; Özbalci, Cagakan; Geimer, Stefan; Reggiori, Fulvio; Brügger, Britta; Mann, Matthias; Westermann, Benedikt; Neupert, Walter.

In: eLife, Vol. 2014, No. 3, e01684, 08.04.2014.

Research output: Contribution to journal › Article › peer-review

Harner, Max Emanuel ; Unger, Ann Katrin ; Izawa, Toshiaki ; Walther, Dirk M. ; Özbalci, Cagakan ; Geimer, Stefan ; Reggiori, Fulvio ; Brügger, Britta ; Mann, Matthias ; Westermann, Benedikt ; Neupert, Walter. / Aim24 and MICOS modulate respiratory function, tafazzin-related cardiolipin modification and mitochondrial architecture. In: eLife. 2014 ; Vol. 2014, No. 3.

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abstract = "Structure and function of mitochondria are intimately linked. In a search for components that participate in building the elaborate architecture of this complex organelle we have identified Aim24, an inner membrane protein. Aim24 interacts with the MICOS complex that is required for the formation of crista junctions and contact sites between inner and outer membranes. Aim24 is necessary for the integrity of the MICOS complex, for normal respiratory growth and mitochondrial ultrastructure. Modification of MICOS subunits Mic12 or Mic26 by His-tags in the absence of Aim24 leads to complete loss of cristae and respiratory complexes. In addition, the level of tafazzin, a cardiolipin transacylase, is drastically reduced and the composition of cardiolipin is modified like in mutants lacking tafazzin. In conclusion, Aim24 by interacting with the MICOS complex plays a key role in mitochondrial architecture, composition and function.",

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AU - Özbalci, Cagakan

AU - Geimer, Stefan

AU - Reggiori, Fulvio

AU - Brügger, Britta

AU - Mann, Matthias

AU - Westermann, Benedikt

AU - Neupert, Walter

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AB - Structure and function of mitochondria are intimately linked. In a search for components that participate in building the elaborate architecture of this complex organelle we have identified Aim24, an inner membrane protein. Aim24 interacts with the MICOS complex that is required for the formation of crista junctions and contact sites between inner and outer membranes. Aim24 is necessary for the integrity of the MICOS complex, for normal respiratory growth and mitochondrial ultrastructure. Modification of MICOS subunits Mic12 or Mic26 by His-tags in the absence of Aim24 leads to complete loss of cristae and respiratory complexes. In addition, the level of tafazzin, a cardiolipin transacylase, is drastically reduced and the composition of cardiolipin is modified like in mutants lacking tafazzin. In conclusion, Aim24 by interacting with the MICOS complex plays a key role in mitochondrial architecture, composition and function.

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Aim24 and MICOS modulate respiratory function, tafazzin-related cardiolipin modification and mitochondrial architecture

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