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. 2024 Dec 13;20(12):e1011496. doi: 10.1371/journal.pgen.1011496

Fig 5. Impairing PAT-3/UNC-112/TLN-1 adhesome axis with a CRISPR-based, cell-specific protein degradation system results in premature axon termination.

Fig 5

A) Illustration of CRISPR-based cell-specific protein degradation system used to impair adhesome components in C. elegans mechanosensory neurons (mecDEG). Adapted from Wang et al. 2017. B) Schematic of mechanosensory neurons with imaged regions highlighted (light gray boxes). C) Representative images of PLM axons for indicated genotypes visualized using Pmec-7::mRFP (jsIs973). Premature axon termination defects (arrows) occur when mecDEG targets GFP that is CRISPR engineered onto adhesome components (PAT-3::GFP, UNC-112::GFP and GFP::TLN-1). Vulva (asterisks) used as anatomical reference point for premature termination. D) Quantitation of premature axon termination defects in PLM neurons for indicated genotypes. Note premature axon termination occurs with mecDEG targeting of adhesome components and in tln-1(ok1648) hypomorphic mutants. Means (bars) are shown for 5 or more counts (black dots) with 20 or more animals/count for each genotype. Error bars indicate SEM. Significance assessed using Student’s t-test with Bonferroni correction for multiple comparisons. ***p<0.001. Scale bar 10μm.