FIGURE 1.

Miro is the nexus of mitochondrial function and transport. (a) Miro1 has been proposed to differentially regulate motor–microtubule interaction (Wang and Schwarz, 2009) or TRAK–motor interaction (Macaskill et al., 2009) in the presence of high intracellular Ca²⁺. Selective binding of miro1 to TRAK1 or TRAK2 may regulate interaction with kinesin or dynein to modulate directionality of mitochondrial movement (van Spronsen et al., 2013). (b) Phosphorylation of miro1 by PINK1 and subsequent ubiquination of miro by parkin have been found to play a critical role in the initial stages of mitophagy (Wang et al., 2011). (c) Miro has been found to play a role upstream of the mitochondrial calcium uniporter complex in controlling Ca²⁺ influx into the matrix. Mutations in the EF-hands of miro1 removes this function (Chang et al., 2011). Ca²⁺ influx through the mitochondrial calcium uniporter has also been shown to gate mitochondrial movement (Chang et al., 2011).