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. 2022 Apr 14;18(4):e1010152. doi: 10.1371/journal.pgen.1010152

Fig 4. Transgenic rescue and overexpression studies indicate CDK-5 functions cell-autonomously to regulate axon termination.

Fig 4

A) Schematic of transgenic workflow for evaluating CDK-5 rescue, cell-autonomous function and overexpression. B) Quantitation of axon termination defects in ALM neurons indicates transgenic CDK-5 expressed using native promoter (Pcdk-5) or promoter for mechanosensory neurons (Pmec) rescues reduced axon termination defects in cdk-5; rpm-1 double mutants. C) Representative images of axon termination in ALM neurons of transgenic animals overexpressing indicated constructs. Axon termination is impaired with overexpression of both CDK-5 and CDKA-1(p35). D) Quantitation of ALM axon termination defects caused by transgenic overexpression of indicated constructs. For all experiments, means (bars) are shown from data collected from 3 or more independent transgenic lines (two counts/line, black dots) for each genotype. Error bars indicate SEM. Significance assessed using Student’s t-test with Bonferroni correction. *** p<0.001. Scale bars 20 μm.