Localization of mitochondria along axons and at synapses in <i>C. elegans</i> touch receptor neurons is necessary for touch habituation.

Neuronal mitochondria are important for neuronal survival and function. Mitochondria buffer calcium, produce ATP, and contribute to reactive oxygen species (ROS) homeostasis, processes that help in neuronal outgrowth and synaptic transmission. <i>Caenorhabditis elegans</i> touch receptor neurons (TRNs) are essential for gentletouch perception and are also used as a model to study axon regeneration. We set up a localized touch habituation assay and investigated the role of the localization of mitochondria along axons and at synapses in the touch circuit for touch habituation behaviour. Mitochondrial transport mutant <i>ric-7</i> and the <i>metaxin-2;miro- 1</i> double mutant, which lack mitochondria in axons and at synapses, habituate faster to gentle touch compared with wild-type animals. The faster habituation phenotype is reversed upon restoration of mitochondria along axons and at synapses of only TRNs. Since mitochondria are shown to control actin dynamics, we asked two questions: (i) Can actin dynamics bypass the requirement of axonal mitochondria for touch habituation, and (ii) can upregulation of actin dynamics in injured axons occur independent of axonal mitochondria? Restoring axonal actin dynamics in the absence of axonal mitochondria did not restore defects in gentle-touch habituation of <i>ric-7</i> animals. Axotomized TRNs in <i>ric-7</i> animals show upregulation of axonal actin dynamics but do not show filopodial protrusions at the growth cone. Our study suggests that axonal mitochondria play key roles in habituation and axon regeneration independent of dynamic axonal actin.