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. 2021 Mar 1;35(5-6):379–391. doi: 10.1101/gad.343269.120

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© 2021 Innes et al.; Published by Cold Spring Harbor Laboratory Press

This article, published in Genes & Development, is available under a Creative Commons License (Attribution 4.0 International), as described at http://creativecommons.org/licenses/by/4.0/.

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Figure 3. — XPO7 depletion prevents senescence. (A) TRF2^ΔBΔM-induced senescence. Representative images of colony formation assay (crystal violet, top left) and SA-β-galactosidase (bottom left) in IMR90 Tet-TRF2^ΔBΔM cells infected with the indicated vectors. Quantification of the percentage of BrdU-positive (middle, n = 5 independent experiments) and SA-β-galactosidase-positive (right, n = 3 independent experiments) cells. (B) Replicative senescence. Representative images of colony formation assay (crystal violet, top left) and SA-β-galactosidase (bottom left) in old IMR90 cells (passage 24) infected with the indicated vectors. Quantification of the percentage of BrdU-positive (middle) and SA-β-galactosidase-positive (right) cells (n = 3 independent experiments). (C) Oncogene-induced senescence. Representative images of colony formation assay (crystal violet, top left) and SA-β-galactosidase (bottom left) in IMR90 ER:RAS cells infected with the indicated vectors. Quantification of the percentage of BrdU-positive (middle) and SA-β-galactosidase-positive (right) cells (n = 3 independent experiments). All scale bars, 50 µm. (****) P < 0.0001, (***) P < 0.001, (**) P < 0.01, (*) P < 0.05. All statistical significances were calculated using one-way ANOVA with multiple comparison with control senescent cells for each condition.