Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2017 Sep 6;7:10681. doi: 10.1038/s41598-017-11031-4

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

PMC Copyright notice

Two interface mutants affect CRMP2 functions in chick and c-elegans neurons. (A) Sequence alignment of the regions to be mutated. T246-N247, green; K483–R485–R487, blue. N247 hydrogen-bonds with S486 in the wild type CP525 structure. (B) Micrograph of DRG explants. Chick E7 DRG explants were infected with recombinant herpes-simplex virus harboring the indicted constructs (see Fig. S4 for infection efficiency). The neurites were visualized by α-tubulin immunostaining. Note that CRMP2-wild type (wt) enhances the neurite-outgrowth from the explant. This effect is canceled by the expression of RA mutant. Scale bar, 500 µm. (C) Scored graph. The covered area with the neurites was measured with ImageJ software. The relative area size of each sample was scored against the average of EGFP controls in the same experiment. Bar graph represents the mean ± s.e.m of 24 samples in each condition from 4 independent experiments. *P < 0.05; **P < 0.01, one-way ANOVA with post-hoc Tukey-Kramer test. (D–G) UNC-33 and UNC-33 mutants were expressed in unc-33(ky880): kyIs445 and the localization of mCherry::RAB-3 was observed in PVD neurons. (D) The localization of synaptic vesicles visualized by mCherry::RAB-3 in PVD neurons. wt, unc-33(ky880) and unc-33(ky880) expressing UNC-33 mutants were observed in the dendritic region and the axonal region. (E) Schema showing the localization of synaptic vesicles in wt and unc-33. (F) Dendritic mislocalization was statistically analyzed. The phenotype was sorted to either wt or unc-33 and counted. *P < 0.01, compared to wt, Chi-square test, n = 100 worms. (G) The axonal fluorescent intensity was measured in each strain. Mean ± S.D., *P < 0.01, compared to control, Dunnett test, n = 20 worms.