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High-order chromatin structure and the epigenome in SAHFs

机译：SAHFs中的高级染色质结构和表观基因组

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It is almost ten years since senescence associated heterochromatic foci (SAHFs) were first described in human diploid fibroblasts (HDFs). Since then, a number of factors have been identified that affect SAHF formation, including HMGA proteins, structural components of SAHFs. However, the involvement of epigenetic marks in SAHF formation remains unclear. Our recent study, combining microscopy and ChIP-seq approaches, revealed that SAHFs are formed through spatial repositioning of the genome. This occurs according to certain chromatin features that are correlated with, but do not require, the repressive marks histone H3 trimethylated on lysine 9 (H3K9me3) and H3K27me3. These repressive marks are segregated from each other within SAHFs, forming layered high-order chromatin structures (HOCS). During the dynamic change in HOCS as SAHFs form, the linear epigenomic profiles of these repressive marks are highly static. This is in marked contrast to the spreading of repressive marks occurring during embryonic cell differentiation. Thus the layered HOCS of SAHFs is likely achieved mainly through the spatial rearrangement of pre-existing heterochromatin, rather than spreading of heterochromatin. Evidence for the co-association of similar types of chromatin is emerging and SAHFs may provide a unique model system to study the correlation between HOCS and chromatin types, which are readily visible and regulable.
机译：自从人类二倍体成纤维细胞（HDF）中首次描述衰老相关的异色病灶（SAHF）以来，已经快十年了。从那时起，已经确定了许多影响SAHF形成的因素，包括HMGA蛋白，SAHF的结构成分。然而，尚不清楚表观遗传标记是否参与SAHF的形成。我们最近的研究结合了显微镜和ChIP-seq方法，发现SAHF是通过基因组的空间重新定位而形成的。这是根据某些染色质特征发生的，这些染色质特征与赖氨酸9（H3K9me3）和H3K27me3上三甲基化的组氨酸H3相关但不相关。这些抑制标记在SAHF中彼此隔离，形成分层的高级染色质结构（HOCS）。在SACS形式的HOCS动态变化期间，这些阻抑标记的线性表观基因组图谱是高度静态的。这与在胚胎细胞分化期间发生的阻抑性标记的扩散形成鲜明对比。因此，SAHFs的分层HOCS可能主要是通过预先存在的异染色质的空间重排而不是分散异染色质来实现的。相似类型的染色质发生共缔合的证据不断涌现，SAHF可能会提供一个独特的模型系统来研究HOCS和染色质类型之间的相关性，它们之间很容易看到且可调节。

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