(A) Panel showing AFD–NRE tagged puncta (blue arrows) within AMsh glial cell soma (magenta outline) in different genetic backgrounds, as noted. AFD cell body (red asterisk). Scale bar: 5 μm. (B) Quantification of puncta within AMsh cell soma in phagocytosis pathway mutants. Refer Figure 2D for data presentation details. Median puncta counts and N (number of animals): wild type (14 ± 1 puncta, n = 78 animals), pde-1(nj57) pde-5(nj49) double mutant animals (7.1 ± 1.4, n = 11 animals), tax-4(p678);cng-3(jh113) double mutants (23.8 ± 2.4 puncta, n = 17 animals), tax-2(p691) (28.1 ± 2 puncta, n = 37 animals), and ced-10(n3246); tax-2(p691) double mutants (1.8 ± 0.5 puncta, n = 25 animals). (C, D) Population counts of animals with AMsh glial puncta in genetic backgrounds indicated. Refer Figure 2C for data presentation details. (+) p<0.05 compared to wild type, (–) p≥0.05 compared to wild type. (C) Alleles used in this graph: pde-1(nj57), pde-5(nj49), tax-4(p678), cng-3(jh113), tax-2(p691), ced-10(n3246), and psr-1(tm469). (D) Alleles used in this graph: tax-2(p691), and psr-1(tm469). EV: empty vector control. (E) Percent wild type or ced-10(n3246) mutant animals with observable GFP+ puncta with or without histamine. N: number of animals. (F) Quantification of percent animals with puncta in AMsh glia (Y-axis) in transgenic strains carrying a histamine-gated chloride channel, with/out histamine activation as noted (X-axis). NRE: neuron-receptive ending.
Figure 6—source data 1. Glial phagocytic pathway tracks neuron activity to regulate AFD–NRE engulfment rate.