The interplay between mitochondrial fusion and fission controls mitochondrial morphology and influences important mitochondrial properties. The key molecular factors involved in mitochondrial fusion–fission are known: mitofusin 1 and 2 (Mfn1 and Mfn2) together with Opa1 regulate fusion, whereas Fis1 and Drp1 are responsible for fission, and Miro-1 (also known as Rhot1) controls mitochondrial mobility. Nevertheless, it remains unclear how mitochondrial fusion and fission events sense each other and, together, control mitochondrial morphology. Here (p. 2187), Allen Kaasik and co-workers address these questions in living neurons by visualising a photoconvertable mitochondria-targeted fluorescent probe to examine the dynamics of mitochondrial morphology. They find that mitochondrial length influences the rate of mitochondrial fission, whereas mitochondrial motility affects its rate of fusion. The authors then extend their analysis to neuronal models of neurodegenerative disease and investigate mitochondrial dynamics in neurons that overexpress Tau or a mutant Huntingtin construct containing 120 polyglutamines. They show that the impaired mitochondrial fusion that has been described previously in these neurons can be rescued when they increase mitochondrial motility by overexpression of Miro-1. Taken together, these results provide insights into the crosstalk between mitochondrial fusion and fission, which might also help to further our understanding of the pathogenesis of neurodegenerative disease.