转座因子(TE)的移动性有助于基因组的进化。它们不受控制的活动导致基因组不稳定;因此,TEs的表达被宿主基因组沉默。TEs用DNA和H3K9甲基化标记,这与开花植物的沉默有关,动物,和真菌。然而,在远缘相关的真核生物群体中,TE由Polycomb抑制复合物2(PRC2)沉积的H3K27me3标记,与开花植物和动物的基因沉默相关的表观遗传标记。迄今为止,PRC2对TE的直接沉默仅在一种纤毛虫中显示。为了测试PRC2是否在更广泛的真核生物中沉默TE,我们产生了PRC2活性降低的突变体,并分析了PRC2在古生菌谱系和硅藻P.tricornutum中的作用。在这种硅藻和红色藻类C.merolae中,PRC2抑制的TEs比例高于基因,而苔藓植物中PRC2抑制的基因比例高于TEs。在开花植物中,TE包含被转录因子识别并与邻近基因相关的潜在顺式元件,作为PRC2抑制的转录单位。因此,PRC2对TEs的沉默不仅在古细菌中观察到,而且在硅藻和纤毛虫中也观察到,表明PRC2在真核生物的最后一个共同祖先中沉积了H3K27me3以沉默TE。我们假设在古细菌的进化过程中,选择用H3K27me3标记的TE片段来塑造转录调控,控制PRC2调控的基因网络。
The mobility of transposable elements (TEs) contributes to evolution of genomes. Their uncontrolled activity causes genomic instability; therefore, expression of TEs is silenced by host genomes. TEs are marked with DNA and H3K9 methylation, which are associated with silencing in flowering plants, animals, and fungi. However, in distantly related groups of eukaryotes, TEs are marked by H3K27me3 deposited by the Polycomb repressive complex 2 (PRC2), an epigenetic mark associated with gene silencing in flowering plants and animals. The direct silencing of TEs by PRC2 has so far only been shown in one species of ciliates. To test if PRC2 silences TEs in a broader range of eukaryotes, we generated mutants with reduced PRC2 activity and analyzed the role of PRC2 in extant species along the lineage of Archaeplastida and in the diatom P. tricornutum. In this diatom and the red alga C. merolae, a greater proportion of TEs than genes were repressed by PRC2, whereas a greater proportion of genes than TEs were repressed by PRC2 in bryophytes. In flowering plants, TEs contained potential cis-elements recognized by transcription factors and associated with neighbor genes as transcriptional units repressed by PRC2. Thus, silencing of TEs by PRC2 is observed not only in Archaeplastida but also in diatoms and ciliates, suggesting that PRC2 deposited H3K27me3 to silence TEs in the last common ancestor of eukaryotes. We hypothesize that during the evolution of Archaeplastida, TE fragments marked with H3K27me3 were selected to shape transcriptional regulation, controlling networks of genes regulated by PRC2.