Affirmative action groups would be proud of Mfn proteins. These fusion proteins work better with diverse partners, say Detmer and Chan (page 405). The results might help explain why only certain neurons are susceptible in Charcot-Marie-Tooth disease 2A (CMT2A).
CMT2A is a neurodegenerative disease caused by dominant mutations in the mammalian mitofusin Mfn2. Along with Mfn1, Mfn2 forms oligomers that tether the outer membranes of mitochondria before they fuse. The loss of either Mfn1 or Mfn2 causes some mitochondrial fragmentation by impairing fusion.
The authors now show that, alone, many Mfn2 mutants associated with CMT2A cannot fuse mitochondria. The mutants formed complexes with either Mfn1 or wild-type Mfn2, but only complexes that included Mfn1 fused mitochondria. Mitochondria with only Mfn1 fused with mitochondria with only mutant Mfn2, suggesting that the heterooligomers do not need to form on the same organelle.
The group suggests that...
