Institute of Microbial Technology, Sector 39A, Chandigarh 160 036, India.
J Biosci. 2021;46.
Gene silencing in occurs by heterochromatin formation at the centromere (), mating-type () and telomere loci. It is mediated by silencing factors including Swi6, Clr1-4, Rhp6 and Pola. RNAi pathway also plays a role in establishment of silencing at the and loci. Recently, the stress response factors, Atf1 and Pcr1were shown to play an RNAi-independent role in silencing at the locus through a -acting Atf1-binding site located within the repression element and recruitment of the silencing factors Clr3 and Clr6. Another -acting site, named repression element abutting the locus, also establishes heterochromatin structure through Clr5 and histone deacetylases but independently of H3-Lys9-methylation and RNAi. Here, we report the occurrence of binding sites for another oxidative response factor, the pombe AP1- like factor Pap1, at the mating-type, centromere and telomere loci. By genetic studies we show that these sites play a role in silencing at the outer repeats of centromeres as well as mating-type locus and this effect is mediated through Pap1 binding site and interaction with and recruitment of the HP1/Swi6. Importantly, Δ cells display a silencing defect even in absence of the oxidative stress. Such a role of Pap1 in heterochromatin formation may be evolutionarily conserved.
基因沉默在中心体（）、交配型（）和端粒位点发生通过异染色质形成。它由沉默因子介导，包括 Swi6、Clr1-4、Rhp6 和 Pola。RNAi 途径也在 和 位点的沉默建立中发挥作用。最近，应激反应因子 Atf1 和 Pcr1 被证明通过位于抑制元件内的与作用的 Atf1 结合位点和沉默因子 Clr3 和 Clr6 的募集，在 位点的沉默中发挥 RNAi 独立作用。另一个称为抑制元件的与作用位点，也通过 Clr5 和组蛋白去乙酰化酶建立异染色质结构，但不依赖于 H3-Lys9 甲基化和 RNAi。在这里，我们报道了另一个氧化应激因子，即 fission 酵母的 AP1 样因子 Pap1，在交配型、着丝粒和端粒位点结合位点的发生。通过遗传研究，我们表明这些位点在着丝粒的外环重复以及交配型位点的沉默中发挥作用，这种效应通过 Pap1 结合位点介导，并与 HP1/Swi6 的相互作用和募集有关。重要的是，Δ细胞即使在没有氧化应激的情况下也表现出沉默缺陷。Pap1 在异染色质形成中的这种作用可能是进化保守的。
