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. 2021 Mar 17;12:1703. doi: 10.1038/s41467-021-21882-1

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© The Author(s) 2021

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. 9 — a Representative confocal images of endogenous YAP/TAZ and F-actin immunostaining in MCF10A cells. MCF10A cells were initially exposed to ATG7/10 siRNAs for 48 h, and only after, followed by α-catenin depletion using CTNNA1/CTNNA3 siRNAs (together with ATG7/10 siRNAs) for other 48 h. Scale bars are 10 µm. The experiment was repeated with similar results. b YAP/TAZ localisation in MCF10A cells treated as in (a). CTNNA1/3 KD partially rescues the YAP/TAZ localisation phenotype in ATG7/10 KD cells. The experiment was repeated with similar results (n (from left to right) = 280/304/299/333 cells; **P < 0.01, ****P < 0.0001; chi-square test). c Quantification of percentages of MCF10A cells with F-actin stress fibres. MCF10A cells were initially exposed to ATG7/10 siRNAs for 48 h, followed by α-catenin depletion using CTNNA1/CTNNA3 siRNAs for other 48 h. The experiment was repeated with similar results (n (from left to right) = 202/ 200/ 206/ 233 cells; *P < 0.05, ****P < 0.0001; chi-square test). d Size of MCF10A cells initially exposed to ATG7/10 siRNAs for 48 h, followed by α-catenin depletion using CTNNA1/CTNNA3 siRNAs for other 48 h. Confocal images of 25 cells per condition were analysed for measuring cell area using ZEN software. Bars represent the mean ± s.e.m (****P < 0.0001, **P < 0.01; two-tailed t-test). e Mathematical modelling of YAP/TAZ activity when reducing autophagy levels. The graph shows the dependency of YAP/TAZ activity on the initial levels of α-catenins and the strength of the feedback loop involving YAP/TAZ control of autophagy v_Y²¹. f Representative immunoblot of α-catenin in various cell lines. Bars represent the mean ± s.d. (n = 3 independent experiments; ***P < 0.001, **P < 0.01, *P < 0.05; two-tailed one sample t-test). g Model for the autophagy-dependent YAP/TAZ activity in two initial conditions: low and high α-catenin levels. Autophagy inhibition in cells with high initial α-catenin levels promotes α-catenin accumulation which sequester YAP/TAZ into the cytosol (Hippo signalling is ON). However, autophagy inhibition in cells with low initial α-catenin levels causes only a small increase in these proteins, increase unable to sequester YAP/TAZ into the cytosol (as their levels also increase, being also autophagy substrates)—Hippo signalling is OFF. The feedback loop of YAP/TAZ controlling autophagy accentuates these effects. Exact P values for asterisks: b 0.0023; c 0.0105; d 0.0082; f (from left to right) <0.0001, 0.0027, <0.0001, 0.0027, 0.0276.