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. 2020 May 28;11(6):595. doi: 10.3390/genes11060595

Figure 4.

Figure 4

Human PCH organization in health and disease. (A) Under normal physiological conditions, satellite II (SATII) at the 1q12 locus (left) and at other chromosomal loci (right) is highly methylated at the DNA level and binds the PRC1 complex, which mediates H2A ubiquitination. This molecular landscape leads to the maintenance of the transcriptionally inactive state [151]. (B) In cancer cells, the loss of methylation across SATII loci causes hyper-accumulation of PRC1 proteins at SATII at the 1q12 locus, which leads to the formation of cancer-associated polycomb (CAP) bodies (top-left). This mechanism maintains the silencing of 1q12-SATII, which is reinforced by increased H2A ubiquitination. At other loci, SATII shows less accumulation of ubiquitinated H2A, and becomes transcriptionally active (top right). This leads to the formation of cancer-associated satellite transcript (CAST) bodies, in which there is an aberrant accumulation of SATII RNAs. These aggregates sequester epigenetic factors, including MeCP2. Adapted from [151].