The UBR-1 ubiquitin ligase regulates glutamate metabolism to generate coordinated motor pattern in Caenorhabditis elegans
Fig 7
The loss of UBR-1 affects glutamate receptor expression in premotor interneurons AVA and AVE.
A) Representative confocal images of AVA, AVE, and RIM neurons visualized with the Pnmr-1-RFP reporter in wildtype, ubr-1, and ubr-1; got-1 adult animals, as well as in ubr-1 mutants with restored expression of UBR-1 in neurons including AVE and RIM. Note the prominent reduction of fluorescent intensity in AVA in ubr-1 mutants. B-D) Quantification of the fluorescent intensity in AVA, AVE and RIM (B), and relative fluorescent intensity between AVA and RIM (C) and between AVE and RIM (D), in animals with the respective genotypes denoted in A. N: more than 10 animals of each strain. * P<0.05, ** P< 0.01by the two-way ANOVA test. E) Representative confocal images of the GLR-1::GFP signals along the AVA and AVE neurites in the ventral nerve cords of animals with the same genotypes as denoted in panel A. ubr-1 mutants exhibited a marked decrease in fluorescent intensity. F) Quantification of the total GLR-1::GFP intensity along the AVA and AVE ventral cord neurites. N = 10–15, *P<0.05, **P<0.01, ***P<0.001 by the Kruskal-Wallis test. Data are represented as mean ± SEM. Scale bar, 5 μm.