DNA double-strand breaks (DSBs) are cytotoxic lesions that threaten genome integrity and
cell viability. Typically, cells repair DSBs by either nonhomologous end joining (NHEJ) or …

Although transcription is an essential cellular process, it is paradoxically also a well-
recognized cause of genomic instability. R-loops, non-B DNA structures formed when …

R-loops are non-B DNA structures with intriguing dual consequences for gene expression
and genome stability. In addition to their recognized roles in triggering DNA double-strand …

DNA double-strand breaks (DSBs) are the most harmful DNA lesions and their repair is
crucial for cell viability and genome integrity. The readout of DSB repair may depend on …

Nonhomologous end-joining (NHEJ) factors act in replication-fork protection, restart, and
repair. Here, we identified a mechanism related to RNA: DNA hybrids to establish the NHEJ …

At critically short telomeres, stabilized TERRA RNA-DNA hybrids drive homology-directed
repair (HDR) to delay replicative senescence. However, even at long-and intermediate …

Stalled DNA replication fork restart after stress as orchestrated by ATR kinase, BLM
helicase, and structure-specific nucleases enables replication, cell survival, and genome …

The regulation of DNA double-strand breaks (DSBs) and telomeres are diametrically
opposed in the cell. DSBs are considered one of the most deleterious forms of DNA damage …

Double‐strand breaks (DSBs) are the most harmful DNA lesions, with a strong impact on cell
proliferation and genome integrity. Depending on cell cycle stage, DSBs are preferentially …

DNA resection—the nucleolytic processing of broken DNA ends—is the first step of
homologous recombination. Resection is catalyzed by the resectosome, a multienzyme …