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. 2012 Apr 27;21(15):3356–3365. doi: 10.1093/hmg/dds167

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© The Author 2012. Published by Oxford University Press

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 3. — Rtnl1 interacts with the Acyl-CoA synthetase Acsl. Confocal sections showing overlapping localization of Rtnl1::YFP and Acsl in axons (linear staining indicated with arrowheads; A) and epidermal cells (B). (C) Protein lysates from OregonR (control) and Rtnl1::YFP flies were immunoprecipitated with Strep-Tactin Sepharose. Whole lysate (In), unbound (UB) and bound (Out) fractions were analysed by western blot. Loss of Rtnl1 reduces endogenous Acsl protein levels relative to controls in immunoblots of adult lysates (D) and single-confocal sections of larval epidermal cells (E). (F) Anti-Acsl staining of OK6GAL4;UAS-Acsl::myc motor neurons labels structures running along axons (arrowheads). Acsl staining is significantly lowered in posterior but not anterior segments of long motor axons upon knockdown of Rtnl1 (F). Graphs represent Acsl expression levels (ns, not significant, P > 0.2; **P < 0.01; n = 6–8 lysates in D, n = 14–16 larvae in E and F).