Raimondi Célia, Jagla Bernd, Proux Caroline, Waxin Hervé, Gangloff Serge, Arcangioli Benoit
Genomes and Genetics department, Genome Dynamics Unit, UMR 3525 CNRS, Institut Pasteur, 25-28 rue du docteur Roux, Paris, France. Sorbonne Universités, Université Pierre et Marie Curie, Institut de Formation Doctorale, 75252 Paris Cedex 05, France.
Center for Human Immunology, CRT & Hub de Bioinformatique et Biostatistiques, C3BI, Institut Pasteur, 25-28 rue du Docteur Roux, Paris, France.
Microb Cell. 2018 Jan 16;5(4):169-183. doi: 10.15698/mic2018.04.623.
Genetic and molecular studies have indicated that an epigenetic imprint at , the sexual locus of fission yeast, initiates mating type switching. The polar DNA replication of generates an imprint on the Watson strand. The process by which the imprint is formed and maintained through the cell cycle remains unclear. To understand better the mechanism of imprint formation and stability, we characterized the recruitment of early players of mating type switching at the region. We found that the switch activating protein 1 (Sap1) is preferentially recruited inside the allele on a sequence () that enhances the imprint. The lysine specific demethylases, Lsd1/2, that control the replication fork pause at and the formation of the imprint are specifically drafted inside of , regardless of the allele. The CENP-B homolog, Abp1, is highly enriched next to but it is not required in the process. Additionally, we established the computational signature of the imprint. Using this signature, we show that both sides of the imprinted molecule are bound by Lsd1/2 and Sap1, suggesting a nucleoprotein protective structure defined as imprintosome.
遗传和分子研究表明，在裂殖酵母的性位点处的一种表观遗传印记启动了交配型转换。该位点的极性DNA复制在沃森链上产生一个印记。印记在细胞周期中形成和维持的过程仍不清楚。为了更好地理解印记形成和稳定性的机制，我们对交配型转换早期参与者在该区域的募集情况进行了表征。我们发现，开关激活蛋白1（Sap1）优先在增强印记的序列（）上的等位基因内被募集。控制复制叉在该位点暂停和印记形成的赖氨酸特异性去甲基化酶Lsd1/2，无论等位基因如何，都被特异性地招募到该位点内部。CENP - B同源物Abp1在该位点旁边高度富集，但在这个过程中不是必需的。此外，我们建立了印记的计算特征。利用这个特征，我们表明印记分子的两侧都被Lsd1/2和Sap1结合，这表明存在一种定义为印记体的核蛋白保护结构。
