报告题目🚞：Dicer functions at sites of replication-transcription collisions to protect genome integrity 

报告人：任捷 博士

主持人：翁杰敏 教授

报告时间：2016年4月14日上午10:00

 

报告人简介🧚🏼‍♀️：任捷🐾，2000-2004年获得南京大学理学学士学位😦🛞， 2004-2010年在纽约州立大学石溪分校获得博士学位，主要研究内容为染色质结构的表观遗传调控，2010年起在冷泉港做博士后研究🕒，主要研究成果为Dicer对复制和转录的碰撞的调控及对基因组和表观遗传基因组稳定性的保护，发表在Nature, Cell等期刊上。

 

报告摘要🤹🏻‍♂️：

Maintaining genome stability and faithfully inheriting the epigenetic information are major challenges in all eukaryotes. Nuclear RNA interference (RNAi) is an important regulator of transcription and epigenetic modifications, however, its function in response to these challenges and the underlying mechanisms remain elusive.

I have found a novel role for the RNAi protein Dicer in resolving replication-transcription collisions via the release of RNA polymerase II (Pol II). This allows Dicer to couple the spreading of heterochromatin with replication fork progression, providing a mechanistic link between heterochromatin inheritance by RNAi and DNA replication. Using genome-wide approaches, I have also revealed that the role of Dicer in managing collisions is not limited to heterochromatin, but is also important at highly transcribed genes, rDNA and tDNA. These novel Dicer-regulated sites strongly correlates with replication stress, DNA damage and genome instability. A striking example of this is at the subtelomeric rDNA repeats, where Dicer is required to release Pol II to facilitate DNA replication and to prevent homologous recombination, which would otherwise lead to loss of rDNA repeats during mitosis and meiosis. These results now provide a paradigm for Dicer action at transcription-replication collisions in various genomic contexts. Such collisions have a profound impact in genome and epigenome stability, and contribute to the molecular basis of cancer and ageing.