Figure 4: Local regulation of glycolysis in neurons upon disruptions of mitochondria localization.

(A) HYlight responses in a mutant of mitochondrial complex III, isp-1(qm150), and wild-type animals, upon transient hypoxia in the AIY interneuron. Glycolysis is elevated in isp-1 mutant animals prior to hypoxia treatment, and show reduced glycolytic response to hypoxia compared to wild-type worms. The shaded region per each graphed line represents standard deviation of the mean of 11 animals; hypoxia treatment is highlighted in grey. (B) Localization of synaptic vesicles (first column) and mitochondria (second column) in the AIY interneurons of wild type (first row) and ric-7(n2657) mutants (second row). AIY has distinct synaptic regions in the neurite(21, 41), labeled as Zone 2 (inset) and Zone 3, near which mitochondria localize in wild-type animals. In a mutant of the kinesin adapter protein ric-7, mitochondria are incapable of localizing to synapses and are only found within the cell body, consistent with prior work(30, 31). Scale bar, 10 μm. (C) HYlight responses in wild-type (top) and ric-7(n2657) mutant animals (bottom) in the AIY interneurons under normoxic conditions. In ric-7 mutants, Zone 2 of the neurite (inset) has a distinctly higher ratio compared to the cell soma, whereas these two regions are similar in wild-type worms. (D) Quantification of the HYlight ratio in different subcellular regions of AIY interneurons of wild-type and ric-7(n2657) mutant animals. P-values shown are 0.5568 (WT soma vs. neurite), 0.5835 (WT soma vs. ric-7 soma), and 0.0002 (ric-7 soma vs. neurite) as calculated by ANOVA with Tukey post-hoc test for 17 animals. (E) Subcellular responses to transient hypoxia in AIY interneurons in ric-7(n2657) mutant animals. The synaptic regions of AIY have elevated glycolysis prior to hypoxic treatment and do not respond upon treatment; the cell soma responds to hypoxia. Shading on each graphed line represents standard deviation of the mean for 13 animals; hypoxia treatment in grey box.