How mitochondria get their membranes bent

Jun 24, 2009

Underneath their smooth surface mitochondria harbor an elaborately folded inner membrane. It holds a multitude of bottleneck like invaginations, which expand into elongated cavities. Now researchers have identified two proteins linked in an antagonistic manner that are relevant for governing inner membrane structure.

Mitochondria are the powerhouses of cells. Underneath their smooth surface they harbor an elaborately folded inner . It holds a multitude of bottleneck like invaginations, which expand into elongated cavities (cristae). The narrow shape of the entrance or pore to the cristae ('crista junction') allows separation of the intracristal space and storage of molecules. Cytochrome c, for example, an important signaling protein in (), is stored in this compartment. When apoptosis is triggered, the pores enlarge and cytochrome c is released into the cytosol.

Thus, understanding of how the pore diameter and the shape of the inner membrane are regulated on a molecular basis is of great relevance to a better understanding of mitochondrial function in general. Recently, in cooperation with other research teams, the group of Prof. Andreas Reichert, who has been appointed as professor for Mitochondrial Biology to the Goethe University within the Cluster of Excellence Macromolecular Complexes in 2007, has identified two proteins linked in an antagonistic manner that are relevant for governing inner membrane structure.

In the current issue of the the Rabl, Soubannier et al. report on their quest of slow-growing baker`s yeast mutants harboring deformed mitochondria. Thereby, they discovered the protein Fcj1 ("Formation of criasta junction protein 1"), which is embedded in the inner membrane and accumulates at crista junctions. Upon increased expression of Fcj1 the number of cristae junctions goes up. Without the protein, however, crista junctions are lacking and the inner cristae membrane forms internal parallel stacks of vesicles.

On the other hand, the researchers found that regular assemblies (supercomplexes) of the F1FO-ATPase, a protein complex required for supplying the cell's energy, accumulated at the cristae tips but were less abundant at crista junctions. In addition, Fcj1 and the F1FO-ATPase appear to have opposing functions. In fact, Fcj1 reduces the formation of F1FO-supercomplexes. "We hypothesize, Fcj1 makes sure that the membrane can adopt a negative curvature, while the F1FO-ATPase supercomplex induces positive bending", Andreas Reichert interprets the results. "This is highly exciting, as we have for the first time found out how mitochondrial ultrastructure is regulated and which components determine the structure of crista junctions at all."

More information: Rabl, R.*, Soubannier, V.*, Scholz, R., Vogel, F., Mendl, N., Vasiljev-Neumeyer, A., Körner, C., Jagasia, R., Keil, T., Baumeister, W., Cyrklaff, M., Neupert, W., and Reichert, A.S. (2009). Formation of cristae and crista junctions in mitochondria depends on antagonism between Fcj1 and Su e/g. J Cell Biol, 2009; ePub 15th June 2009.

Source: Goethe University Frankfurt

Explore further: Genomes of malaria-carrying mosquitoes sequenced

add to favorites email to friend print save as pdf

Related Stories

Key Event in Cell Death Occurs as Single, Quick Event

Aug 03, 2006

Scientists at St. Jude Children's Research Hospital have demonstrated that a key event during apoptosis (cell suicide) occurs as a single, quick event, rather than as a step-by-step process. Apoptosis eliminates extraneous ...

Immune cells kill foes by disrupting mitochondria 2 ways

May 15, 2008

When killer T cells of the immune system encounter virus-infected or cancer cells, they unload a lethal mix of toxic proteins that trigger the target cells to self-destruct. A new study shows T cells can initiate cellular ...

Nixing immaturity in red blood cells

May 04, 2008

A process of self-digestion called autophagy prompts the maturation of red blood cells. Without a protein called Nix, the cells would not effectively rid themselves of organelles called mitochondria and consequently become ...

Key step in the 'puncture' mechanism of cell death revealed

May 12, 2008

A team of medical researchers led by Dr Ruth Kluck at Melbourne’s Walter and Eliza Hall Institute (WEHI) has discovered a key step in the mechanism by which cells destroy themselves. In this process, called “apoptosis”, ...

New clues about mitochondrial 'growth spurts'

Mar 02, 2009

Mitochondria are restless, continually merging and splitting. But contrary to conventional wisdom, the size of these organelles depends on more than fusion and fission, as Berman et al. show. Mitochondrial ...

Recommended for you

Genomes of malaria-carrying mosquitoes sequenced

17 hours ago

Nora Besansky, O'Hara Professor of Biological Sciences at the University of Notre Dame and a member of the University's Eck Institute for Global Health, has led an international team of scientists in sequencing ...

How calcium regulates mitochondrial carrier proteins

Nov 26, 2014

Mitochondrial carriers are a family of proteins that play the key role of transporting a chemically diverse range of molecules across the inner mitochondrial membrane. Mitochondrial aspartate/glutamate carriers are part of ...

Team conducts unprecedented analysis of microbial ecosystem

Nov 26, 2014

An international team of scientists from the Translational Genomics Research Institute (TGen) and The Luxembourg Centre for Systems Biomedicine (LCSB) have completed a first-of-its-kind microbial analysis of a biological ...

Students create microbe to weaken superbug

Nov 25, 2014

A team of undergraduate students from the University of Waterloo have designed a synthetic organism that may one day help doctors treat MRSA, an antibiotic-resistant superbug.

User comments : 0

Please sign in to add a comment. Registration is free, and takes less than a minute. Read more

Click here to reset your password.
Sign in to get notified via email when new comments are made.