Figure 2
From: LIN-32/Atonal Controls Oxygen Sensing Neuron Development in Caenorhabditis elegans
LIN-32 is required for URX specification and function. (A) Quantification of lin-32(tm1446)-induced URX defects in reporters for URX neuronal fate. Loss of lin-32 severely affects the expression of all URX reporters tested: flp-8, flp-19, gcy-36, gcy-35, egl-13 and unc-86. The black (wild type) and red (lin-32) bars represent the percentage of worms that show expression in either 1 or 2 URX neurons. 1-like and 2-like indicate that the neurons have a URX morphology but are mispositioned. N > 60. Statistical significance between wild-type and lin-32(tm1446) animals was evaluated using a t-test. ****P < 0.0001. (B) Micrographs of representative animals expressing fluorescent markers for the URX neurons (flp-8, flp-19, gcy-36, gcy-35, egl-13 and unc-86) in wild type and lin-32(tm1446) mutant animals. URX neuron positions are marked with red dashed circles. Anterior to the left. Ventral views except for unc-86::GFP which is a lateral view. Scale bar 20 μm. (C) lin-32 oxygen-sensing behavior analysis. Locomotion speed of wild type (left) and lin-32(tm1446) mutant animals (center) during O2 concentration shifts between 21% and 10%. The data represent averages of multiple assays. The right graph shows the quantification of changes in relative speed in response to changes in O2 concentration. lin-32(tm1446) mutants fail to respond to O2 upshifts (URX-mediated) but exhibit a similar response to wild type animals to O2 downshifts (BAG-mediated). Statistical significance between wild-type and lin-32(tm1446) animals was evaluated using one-way ANOVA analysis. ***P < 0.001; n.s., not significantly different from wild type controls. Assays were repeated at least four times using 80–120 animals per assay.
