Unwrap RAP1's Mystery at Kinetoplastid Telomeres.
Unwrap RAP1's Mystery at Kinetoplastid Telomeres.
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DOI：
10.3390/biom14010067
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发表时间：
2024-01-04
期刊：
影响因子：
5.5
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中科院分区：
文献类型：
--
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虽然位于染色体末端，但端粒是一种重要的染色体组分，有助于维持从原生动物到哺乳动物的基因组完整性和染色体稳定性。端粒蛋白在染色体末端保护中的作用是保守的，它们抑制各种DNA损伤反应机制并阻断天然染色体末端的溶核降解，尽管详细的潜在机制并不相同。此外，特化的端粒结构对许多真核生物中位于亚端粒的基因的表达产生抑制性表观遗传效应。这种所谓的端粒沉默也影响许多经历抗原变异/表型转换的微生物病原体的毒力。端粒蛋白，特别是RAP 1同源物，已被证明是端粒沉默的关键参与者。RAP 1同源物还抑制含有端粒重复序列的RNA（TERRA）的表达，这与它们在端粒稳定性维持中的作用有关。RAP 1抑制端粒重组的功能在很大程度上是保守的动质体哺乳动物。然而，RAP 1介导的端粒沉默的潜在机制具有许多种属特异性特征。在这篇综述中，我将集中在布氏锥虫RAP 1的功能，在抑制端粒/亚端粒DNA重组和在调节单等位基因表达的亚端粒定位的主要表面抗原基因。共同和独特的机制将比较RAP 1同源物，并将讨论其影响。
Although located at the chromosome end, telomeres are an essential chromosome component that helps maintain genome integrity and chromosome stability from protozoa to mammals. The role of telomere proteins in chromosome end protection is conserved, where they suppress various DNA damage response machineries and block nucleolytic degradation of the natural chromosome ends, although the detailed underlying mechanisms are not identical. In addition, the specialized telomere structure exerts a repressive epigenetic effect on expression of genes located at subtelomeres in a number of eukaryotic organisms. This so-called telomeric silencing also affects virulence of a number of microbial pathogens that undergo antigenic variation/phenotypic switching. Telomere proteins, particularly the RAP1 homologs, have been shown to be a key player for telomeric silencing. RAP1 homologs also suppress the expression of Telomere Repeat-containing RNA (TERRA), which is linked to their roles in telomere stability maintenance. The functions of RAP1s in suppressing telomere recombination are largely conserved from kinetoplastids to mammals. However, the underlying mechanisms of RAP1-mediated telomeric silencing have many species-specific features. In this review, I will focus on Trypanosoma brucei RAP1’s functions in suppressing telomeric/subtelomeric DNA recombination and in the regulation of monoallelic expression of subtelomere-located major surface antigen genes. Common and unique mechanisms will be compared among RAP1 homologs, and their implications will be discussed.
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