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RPA is a master regulator of DNA metabolism and RPA availability acts as a rate-limiting factor. While numerous studies focused on the post-translational regulations of RPA for its functions, little is known regarding how RPA availability is controlled. Here we identify a novel lncRNA  Discn  as the guardian of RPA availability in stem cells.  Discn  is induced upon genotoxic stress and binds to neucleolin (NCL) in the nucleolus. This prevents NCL from translocation into nucleoplasm and avoids undesirable NCL-mediated RPA sequestration. Thus,  Discn -NCL-RPA pathway preserves a sufficient RPA pool for DNA replication stress response and repair.  Discn  loss causes massive genome instability in mouse embryonic stem cells and neural stem/progenigor cells. Mice depleted of  Discn  display newborn death and brain dysfunctions due to DNA damage accumulation and associated inflammatory reactions. Our findings uncover a key regulator of DNA metabolism and provide new clue to understand the chemoresistance in cancer treatment.

A novel lncRNA Discn fine-tunes replication protein A (RPA) availability to promote genomic stability