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. Author manuscript; available in PMC: 2011 Oct 6.
Published in final edited form as: Cell Metab. 2010 Oct 6;12(4):398–410. doi: 10.1016/j.cmet.2010.08.013

Figure 2. acs-3 has a limited expression pattern, and expression of acs-3 in seam cells rescues the fat storage phenotype.

Figure 2

To examine the expression pattern of acs-3, we fused 2.5kb of upstream regulatory sequence to GFP. This construct yields high expression in a limited set of tissues. In L4 animals, strong expression is evident in seam cells, which are beginning to fuse at this stage, the excretory cell (marked Ex) and vulva (marked Vul) as well as cells in the head and tail (A). In an L2 animal, individual seam cells are clearly visible (B). We also generated constructs driving the acs-3 cDNA fused to GFP. We drove this construct with the previously characterized seam cell promoters wrt-2 (C) and grd-10 (D). With both constructs, ACS-3 is clearly localized to the cell membrane (C-D). When we drove the acs-3(ft5) mutant cDNA we observed misslocalization of the protein to seam cell nuclei (E). In panels A-E, arrows mark the position of seam cells. Elevated Nile Red staining of acs-3(ft5) animals can be rescued by expression of acs-3 cDNA with regulatory elements upstream of acs-3 start site, as well as with the wrt-2 and grd-10 seam cell specific promoters (E). Expression in the body-wall muscle, a tissue in which acs-3 is not normally expressed, driven by the myo-3 promoter, fails to rescue the high Nile Red staining of acs-3(ft5) animals (F). We quantified Nile Red intensity in these lines (G). Data are shown as a percentage of the wild-type average +/− SEM. ***p < 0.001 compared to acs-3(ft5).