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. 2018 Aug 30;8(11):3515–3527. doi: 10.1534/g3.118.200586

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Copyright © 2018 Xu et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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skn-1c(mac53gf) transgenes under control of skn-1c or nhx-2 promoters can increase the gst-4p::GFP (dvIs19) reporter expression. (A) Structures of transgenes for phenocopying the survival-promoting effect of skn-1c(gf) mutations. The coding exons of skn-1c are delineated as alternating red and black boxes. (B, C, D) Left panels. skn-1c(wt) transgenes did not increase the expression of the gst-4p::GFP reporter. Non-transgenic (Non-Tg) animals are on left. Transgenic animals (Tg, red fluorescence in pharynxes expressed from the pCFJ90 co-injection marker) are on right. (B, C, D) Right panels, skn-1c(mac53gf) transgenes. Non-transgenic and transgenic animals are indicated on left and right, respectively. (D) Right panel, Tg: dpy-7p::skn-1c(mac53gf) transgenes did not increase the expression of the gst-4p::GFP reporter in most cases (animals on the left). Occasionally the transgene caused a strong Dpy phenotype with increased reporter expression in the intestine (animals on the right).