In the current issue of the the Journal of Cell Biology Rabl, Soubannier et al. report on their quest of slow-growing baker`s yeast mutants harbouring 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 hypothesise, 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."