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. 2019 Jul 5;10:2998. doi: 10.1038/s41467-019-10992-6

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© The Author(s) 2019

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. 6 — An Inc- and Cul3-interaction screen identifies peflin to be required postsynaptically for PHP expression. a Flow diagram and screening strategy of Inc- and Cul3-interacting genes identifies a mutation and RNAi line targeting Drosophila peflin (CG17765; pef). b Quantification of mEPSP and quantal content values in a subset of mutants screened normalized to baseline values (–PhTx) (n = 6–20; see Supplementary Table 1). c Schematic summarizing the role of mammalian Pef functioning as a co-adaptor for the Cul3-KLHL12 complex, which is regulated by Ca²⁺ signaling. This signaling activates Cul3^KLHL12 to mono-ubiquitinate substrates involved in membrane trafficking at the ER to modulate Collagen secretion. d Schematic and representative traces of wild type, peflin mutants (pef^C295), and Pef RNAi driven in the postsynaptic muscle (muscle > Pef RNAi: G14-Gal4/UAS-Pef RNAi) before and following PhTx application. Note that while mEPSC amplitude is reduced in all three genotypes after PhTx application, PHP fails to be expressed in pef^C295 and muscle > Pef RNAi. e Quantification of mEPSC and quantal content values in the indicated genotypes normalized to baseline values (–PhTx: wild type, n = 8; pef^C295, n = 7; muscle > Pef RNAi, n = 10; + PhTx: wild type, n = 7; pef^C295, n = 8; muscle > Pef RNAi, n = 9). Representative traces (f and h) and quantification (g and i) of genetic interaction experiments between Cul3^EY11031/pef^C295 (Cul3^EY11031/ + , n = 8 ( – PhTx, + PhTx); pef^C295/ + , n = 8; Cul3^EY11031/ + ,pef^C295/ + , n = 21), inc^kk3/dmp²⁵³ (inc^kk3/ + , n = 8; dmp²⁵³/ + , n = 8; inc^kk3/ + ;dmp²⁵³/ + , n = 9) and Cul3^EY11031/dmp²⁵³ (Cul3^EY11031/ + ;dmp²⁵³/ + , n = 10). j Schematic illustrating a speculative but plausible model linking Cul3/Inc and Pef in retrograde homeostatic signaling. Asterisks indicate statistical significance using a Student’s t-test: (**) p < 0.01; (***) p < 0.001; (****) p < 0.0001, (ns) not significant. Error bars indicate ± SEM. n values indicate biologically independent cells. Additional statistical information and absolute values for normalized data can be found in Supplementary Table 2. Source data are provided as a Source Data file