A (skeptical) discussion is underway over at the sci.life-extension group on a recent paper that suggests the constant fusion of mitochondria is a challenge to mitochondrial theories of aging. You might want to start with a primer on mitochondrial fusion before going too much further:
Fusion of mitochondria serves to mix and unify mitochondrial compartments. This is of particular importance for the inheritance and maintenance of the mitochondrial genome
Ono et al. (2001) established two respiration-deficient HeLa cell lines, each carrying a pathogenic mutation in a different mitochondrial tRNA gene. Hybrids obtained by fusion of these cells showed restoration of normal respiratory activity within a few days.
These findings suggest that mitochondrial fusion counteracts the manifestation of [mitochondrial DNA (mtDNA)]-linked diseases. Moreover, it has physiological significance in individuals born with intact mitochondrial genomes. The highly oxidative metabolism of mitochondria increases the risk for mtDNA damage. Thus, lesions and point mutations of mtDNA accumulate during aging and result in the loss of bioenergetic function (Wallace, 1992; Nagley and Wei, 1998; Raha and Robinson, 2000). Fusion of mitochondria might contribute to the maintenance of respiratory activity by allowing trans-complementation of somatic mutations that accumulate in mitochondrial chromosomes over time (Ono et al., 2001), and thus mitochondrial fusion may be a crucial defence mechanism against cellular aging.
But back to the discussion - I'd agree that it doesn't look like a very defensible assertion, but as noted, the theory would have to explain how it all fits together.
In mammalian cells, there is an extensive and continuous exchange of mitochondrial DNA (mtDNA) and its products between mitochondria. This mitochondrial complementation prevents individuals from expression of respiration deficiency caused by mutant mtDNAs. Thus, the presence of mitochondrial complementation does not support the generally accepted mitochondrial theory of aging, which proposes that accumulation of somatic mutations in mtDNA is responsible for age-associated mitochondrial dysfunction. Moreover, the presence of mitochondrial complementation enables gene therapy for mitochondrial diseases using nuclear transplantation of zygotes.
I don't agree with their proposition. However the [mitochondrial / free radical theory of aging] needs to account for this. The results they are reporting obviously don't seem to be happening in vivo. It does perhaps offer the hope that mitochondria may be reparable.
Mitochondrial fusion has the look of a process that slows the rate at which accumulating damage impares efficiency. Without it, you'd keel over much more rapidly (leaving aside all the other reasons as to why the process is or might be necessary for life), but that doesn't challenge the basic concept of mitochondrial DNA damage as a root cause of aging.
I think that groups have already demonstrated that mitochondria can in principle be repaired, at least by outright replacement of their DNA via protofection.