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. 2024 Feb 15;43(6):956–992. doi: 10.1038/s44318-024-00049-w

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© The Author(s) 2024

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. Creative Commons Public Domain Dedication waiver http://creativecommons.org/publicdomain/zero/1.0/ applies to the data associated with this article, unless otherwise stated in a credit line to the data, but does not extend to the graphical or creative elements of illustrations, charts, or figures. This waiver removes legal barriers to the re-use and mining of research data. According to standard scholarly practice, it is recommended to provide appropriate citation and attribution whenever technically possible.

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Figure EV5 — (A) In wild-type animals (top row), axons of the nerve ring (dashed red box) are located between the two pharyngeal bulbs. In GLR-ablated animals (bottom row) the nerve ring is anteriorly displaced, located on top of the anterior pharynx bulb. As evidenced in the images on the right, not only the axonal projections, but also neuronal cell bodies (panneuronal nuclear gfp) are anteriorly displaced. Panneuronal gfp = unc-119prom::gfp, panneuronal nuclear gfp = rab-3prom1::nls::yfp. (B) cwn-2(ok895), cam-1(gm122), sax-3(ky123) mutants with anteriorly displaced nerve rings exhibit locomotion defects to the same direction, although of different magnitude as the GLR glia-ablated animals. (C) Auxin (K-NAA) dependent LET-381::AID knockdown results in similar defects in the same locomotion parameters as the let-381(ns1026) autoregulatory mutation. Genotypes are: wild-type N2 (black), let-381(ns995) control (gray), LET-381::AID knockdown [let-381(ns995);nsIs879 (nep-2prom7::TIR1)] exposed to K-NAA auxin (dark blue), LET-381::AID control [let-381(ns995) ; nsIs879 (nep-2prom7::TIR1)] not exposed to K-NAA auxin (light blue) and let-381(ns1026) autoregulatory mutation (red). Data information: in (B) wild type n = 29 movies, GLR ablation n = 23 movies, cwn-2(ok895) n = 2 movies, cam-1(gm122) n = 4 movies, sax-3(ky123) n = 2 movies. Bar height indicates average (center of error bars) and error bars show standard deviation in (B). Unpaired t test used for statistical analysis in (C); controls (gray and light blue) were compared to wild type (black). LET-38::AID knockdown (dark blue) was compared to its control group (light blue) and let-381(ns1026) was compared to its control (gray). No statistically significant differences were observed between the LET-381::AID knockdown and let-381(ns1026) as indicated by the red line on the top of the three upper diagrams. Anterior is left, dorsal is up and scale bars are 10 μm for all animal images.