A designed point mutant in Fis1 disrupts dimerization and mitochondrial fission.

Mitochondrial and peroxisomal fission are essential processes with defects resulting in cardiomyopathy and neonatal lethality. Central to organelle fission is Fis1, a monomeric tetratricopeptide repeat (TPR)-like protein whose role in assembly of the fission machinery remains obscure. Two nonfunctional, Saccharomyces cerevisiae Fis1 mutants (L80P or E78D/I85T/Y88H) were previously identified in genetic screens.