Fig. 3: UNC-64 (Ser65) regulates glutamate release to direct navigation behaviors.
From: Molecular encoding and synaptic decoding of context during salt chemotaxis in C. elegans
a unc-64 phospho-deficient mutants (unc-64 Ser65Ala) tend to migrate toward lower NaCl concentrations. n = 6 independent experimental repeats(assays). b UNC-64 Ser65 functions in ASER. Migration bias in the unc-64(S65A) mutant was rescued by Si[H20p::frt::unc-64(wt)::frt], and the effect of this transgene is suppressed by FLP expression in ASER. n = 7 independent experimental repeats(assays). c The deficiency of either neuropeptide release (unc-31(e928)/CAPS deletion) or glutamate release (eat-4(ky5)/vGluT deletion) fails to suppress migration toward higher NaCl induced by ASERp::pkc-1(gf). The double mutants of these genes suppressed ASERp::pkc-1(gf). n = 6 independent experimental repeats(assays). d Conditional knockout of glutamatergic transmission in ASER suppresses chemotactic bias caused by unc-64(S65A). Genomic frt::eat-4::frt is excised by ASERp::FLP27. n = 6 independent experiments(assays). e An illustration of PKC-1 signaling. PKC-1 regulates both neuropeptidergic transmission and glutamatergic transmission to drive navigation behavior, and glutamatergic transmission is regulated via the phosphorylation of UNC-64 Ser65. f The locomotion rate (=body bends) of unc-64(S65A) mutants. As predicted from panel a, unc-64(S65A) mutants show a defect in locomotion. n = 18 (N2), 17 (unc-64(S65A)) animals. Error bars indicate SEM for all panels in Fig. 3. p values were calculated by the two-sided Welch’s test (single comparison) or Tukey’s test (multiple comparisons). Source data are provided as a Source Data file.
