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. 2021 Dec 15;41(50):10365–10381. doi: 10.1523/JNEUROSCI.1475-21.2021

Figure 7.

Figure 7.

Endolysosome localization of ERα is responsible for the endolysosome-enhancing effects of 17αE2. A, Confocal images show the codistribution of ERα with Rab7-positive endolysosomes in CLU199 cells. In cells expressing wild-type ERα-GFP, the distribution of ERα WT exhibited a distinct puncta pattern, and ERα WT was localized primarily on Rab7-positive endolysosomes; however, in cells transfected with ERα palmitoylation deficit mutant (ERα C451A-GFP), ERα C451A-GFP lacked a puncta pattern, and showed a diffuse cytoplasmic localization. Scale bar, 10 µm. B, Confocal images and bar graphs show 17αE2-induced (10 nm for 10 min) changes in the percentage of CatD lysosomes in CLU199 cells expressing wild-type ERα (ERα WT-HA) and the ERα C451A-HA mutant that lacks endolysosome localization (ERα C451A). Scale bar, 10 µm. Bar graph at the bottom shows that the overexpressing ERα C451A mutant significantly reduced 17αE2-induced changes in the percentage of cathepsin D-positive endolysosomes.