Supplementary video 5.2: Mitochondria in the tail of a <i>degron::unc-116;somatic tir1</i> worm treated with 1 mM K-NAA for 24 h

<p dir="ltr">The data relates to the PhD thesis titled: Investigating kinesin-1 cargo dynamics and systemic effects of kinesin-1 loss in Caenorhabditis elegans.</p><p dir="ltr">The motor protein kinesin-1 is responsible for transporting cellular cargoes such as organelles, proteins and RNA to their correct locations within cells. The kinesin-1 homolog in the model organism <i>C. elegans </i>is known as UNC-116. </p><p dir="ltr">The generated <i>C. elegans</i> strain <i>degron::unc-116;somatic tir1</i> is tagged with an AID* degron tag at the endogenous <i>unc-116</i> gene. The strain also expresses the F-box protein TIR1. In the presence of auxin or synthetic auxin (K-NAA), the UNC-116 protein is conditionally degraded. Mitochondria is a known cargo of kinesin-1/UNC-116. Thus, the disruption of mitochondrial movement upon K-NAA treatment can both confirm that the degron system is working and provide insights into the role of kinesin-1/UNC-116 in mitochondrial movement.</p><p dir="ltr">The video shows mitochondria in a section of the tail of a <i>degron::unc-116;somatic tir1</i> worm treated with 1 mM K-NAA for 24 h. Mitochondria are visualised with Mitotracker. When compared to supplementary video 5.1, it becomes clear that K-NAA treatment leads to disrupted mitochondrial movement. The images are captured using a 3i Lattice Light Sheet microscope. </p>