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Figure 7 | Cell Division

Figure 7

From: Differential distribution of HP1 proteins after trichostatin a treatment influences chromosomal stability in HCT116 and WI-38 cells

Figure 7

The effect of TSA exposure on HP1α/β localization and centromeric and pericentromeric chromatin modifications, as well as on the relationship with CIN in WI-38 and HCT116 cells. Upper panel: Untreated WI-38 and HCT116 cells presented a similar localization of HP1α and HP1β along centromeric (CC) and pericentromeric chromatin (PC). At PC, H3K9me2/3 were enriched together with HP1 proteins; at CC, CENP-A was enriched during mitosis, whereas H3K4me2, H3K9me2/3 and H3K9ac modifications, as well as HP1α and HP1β and Mis12 proteins, fluctuate through interphase and mitosis. Lower panel: After treatment of HCT116 cells with TSA, H3K9me3 was significantly reduced at PC and CC, resulting in increased H3K4me2 and H3K9ac at PC satellite-2 regions; HP1α/β were initially significantly reduced. However, they later recovered by an unknown mechanism that could include other proteins or could involve an ncRNA PC transcript [43]-[45]. CC was enriched with H3K9ac and CENP-A, together with HP1α/β and Mis12 proteins. HCT116 cells proliferated with low levels of cell arrest and exhibited CIN in 50% of the cells. In both WI-38 and HCT116 cells, PC presented reduced H3K9me3, whereas H3K9ac and HP1 were enriched; moreover, CC was depleted of CENP-A and HP1, and no significant reduction in H3K9me3 was observed, even though H3K9ac was increased. While CIN was still generated, it was reduced compared with HCT116 cells.

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