Department of Physiological Chemistry, BioMedical Center (BMC), Ludwig Maximilians University of Munich, Martinsried, Germany.
International Max Planck Research School for Molecular and Cellular Life Sciences, Martinsried, Germany.
Curr Genet. 2019 Oct;65(5):1153-1160. doi: 10.1007/s00294-019-00986-8. Epub 2019 May 7.
Chromosome ends are protected from erosion and chromosomal fusions through telomeric repeats and the telomere-binding protein complex shelterin. Imperfect repetitive sequences, known as telomere-associated sequences (TAS), flank the telomeres, yet their function is not well understood. In this perspective, we discuss our recent findings demonstrating that the TAS, in Schizosaccharomyces pombe, are organized into a distinct chromatin domain that is marked by low nucleosome levels and is highly recombinogenic (van Emden et al. in EMBO Rep 20:e47181. https://doi.org/10.15252/embr.201847181 , 2019). Low nucleosome abundance at the TAS is independent of the chromosomal position, but is an intrinsic property of the DNA sequence itself. Critical nucleosome levels are maintained through two heterochromatin complexes recruited by the shelterin subunit Ccq1, which together control gene repression and nucleosome stability. Furthermore, Ccq1 inhibits TAS-facilitated recombination between subtelomeres, yet independently of nucleosome stability. In conclusion, the TAS present a unique chromatin environment causing nucleosome loss and genome instability, which are both counteracted by Ccq1 through independent mechanisms. Given the antagonistic behavior, we hypothesize that Ccq1 co-evolved with the appearance of TAS to regulate nucleosome dynamics and recombination-based telomere maintenance in the absence of telomerase.
端粒通过端粒重复序列和端粒结合蛋白复合物 shelterin 保护染色体末端免受侵蚀和染色体融合。不完美的重复序列,称为端粒相关序列(TAS),侧翼端粒,但它们的功能尚不清楚。在这篇观点文章中,我们讨论了我们最近的发现,即在裂殖酵母中,TAS 被组织成一个独特的染色质域,其特征是核小体水平低,高度重组(van Emden 等人,EMBO Rep 20:e47181. https://doi.org/10.15252/embr.201847181 ,2019)。TAS 处的核小体丰度低与染色体位置无关,而是 DNA 序列本身的固有特性。通过 shelterin 亚基 Ccq1 募集的两个异染色质复合物维持关键核小体水平,这两个复合物共同控制基因抑制和核小体稳定性。此外,Ccq1 抑制 shelterin 亚基 Ccq1 抑制端粒间 TAS 促进的重组,但与核小体稳定性无关。总之,TAS 呈现出一种独特的染色质环境,导致核小体缺失和基因组不稳定性,而 Ccq1 通过独立的机制来对抗这两种情况。鉴于拮抗行为,我们假设 Ccq1 与 TAS 的出现共同进化,以调节无端粒酶时核小体动力学和基于重组的端粒维持。