Figure 6.

Genetic interaction between kinesin-mediated intracellular trafficking and cellular proteolytic pathways mediating necrotic cell death. Dysfunction of either kinesin 1 heavy chain (UNC-116) or the monomeric kinesin UNC-104 does not significantly enhance suppression of neurodegeneration in aspartyl protease-deficient mutant animals (A, B), in animals with compromised lysosomal acidification (C, D), or in calpain protease-deficient mutants animals (E, F). Error bars denote s.e.m. values (n>250 for all populations examined; P>0.5, compared with single mutant control animals, unpaired t-test).