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. 2018 Nov 19;9:4842. doi: 10.1038/s41467-018-07291-x

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© The Author(s) 2018

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/.

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Fig. 5 — The ectodomain of CED-1 can function from the muscle-type engulfing cell surface to promote axon regeneration. a The percentages of animals retaining axon debris 24 h after axotomy. Error bars represent SEP. ***p < 0.001 by Z-test for two proportions. b Average length of regenerating ALM axons. c Average length of regenerating ALM axons in ced-1 mutants expressing various transgenes 24 h after axotomy. Punc-54::ced-1 transgenes expressed either the full-length CED-1 protein (bar 3), the cytoplasmic domain-deleted CED-1 protein (bar 4), or the ectodomain only CED-1 protein (bar 5). In b and c, error bars indicate SEM; * and *** indicate p < 0.05 and p < 0.001, respectively; P values were calculated using a Student’s t-Test. d Representative images showing adhesion of regenerating ALM axons to muscles re-expressing either the wild-type CED-1 protein or the cytoplasmic domain-deleted CED-1 protein in ced-1 mutants. Regenerating ALM axon in ced-1 mutants alone did not adhere to body wall muscles. Images were taken in young adult stage 24 h after injury. Anterior is to the left; dorsal is up. Scale bar: 20 μm. Open red arrowheads mark axon contact regions. The axon and muscle tracing of each image was shown to the right. e The percentages of regenerating ALM axons adhered to muscles 24 h after injury. Error bars represent SEP. Asterisks represent P < 0.001 by Z-test for two proportions. f The CED-1 ectodomain-GFP fusion proteins were bound to the ALM process and soma. Single focal-plane images of the secretable CED-1 ectodomain-GFP fusion protein distribution in the extracellular environment (left), the ALM mCherry marker expression (middle), and the superimposed (right) were shown. Arrowheads indicate the enrichment of CED-1 ectodomain-GFP fusion proteins in the ALM axon and the cell body. Scale bar: 20 μm. g Model of distinct biochemical functions of CED-1. Injury signals released from damaged axons attract engulfing cells, which leads to removal of axon debris and promotion of axon regeneration. CED-1 functions in engulfing cells in both events through distinct biochemical pathways