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. 2022 Apr 22;50(8):4500–4514. doi: 10.1093/nar/gkac259

Figure 7.

Figure 7.

H3.3 S31Ph acts as a phosphorylation switch which regulates KDM4B binding and heterochromatin accessibility at the telomeres. (A) ATRX and KDM4B act to maintain telomeric heterochromatin integrity. ATRX complexes with DAXX to deposit H3.3 at telomeres to form H3K9me3 heterochromatin, enabling binding of HP1α via its interaction with H3K9me3. Despite being enriched with H3K9me3, telomeres are also enriched with KDM4B that demethylates H3K9me3. We propose that ATRX and KDM4B act to maintain the level of H3K9me3 at the telomere, and this is achieved via H3.3 S31Ph switch (B) During replication, the absence of H3.3 phosphorylation in S phase allows KDM4B to bind and demethylate H3K9me3 to promote heterochromatin accessibility at telomeres. (C) After replication and as cells progress into M phase, H3.3 S31 is phosphorylated, preventing removal of H3K9me3 by KDM4B and thereby maintaining a heterochromatic state from mitosis until the next G1/S phase. Figure made in BioRender.com.