Saur, Lesage et al. report that RNA:DNA hybrids arise at double-strand breaks in transcribed genes, independently of de novo recruitment of RNA polymerase II/III, as a result of DSB-induced transcriptional repression.

Funded by the National Cancer Institute (T32CA186895), the program at City of Hope provides exceptionally motivated, recent (2 years or less) postdoctoral fellows with scientific knowledge, researc

Department of Biochemistry, School of Medicine—Basic Sciences

Abstract. Accurate visualization and quantification of homologous recombination (HR)-associated foci in readily available patient samples are critical for

Overview of the Journal Nucleic Acids Research (NAR) is a leading open access molecular biology journal published by Oxford University Press. It provides rapid

A tight coordination between transcription and DNA replication is essential to maintain genome stability. Both excessive transcription and upregulated…

Structures associated with the final steps of non-homologous end joining (NHEJ) and gap filling present new targets for NHEJ inhibition to enhance efficacy of radiotherapy and accuracy of gene editing...

Ever since BRCA1 germline mutations were found to confer a strong predisposition to the development of breast and ovarian cancers, there has been great interest in determining how this protein suppresses tumor formation. Through more than two decades of research, it has become clear that BRCA1 safeguards our genome mainly by promoting DNA repair through homologous recombination (HR). This opinion article outlines our evolving view of BRCA1’s role in end resection, an upstream commitment step for HR, and highlights recent discoveries suggesting that the context in which DNA breaks are generated dictates whether BRCA1 is required for end resection. In addition, strong emerging evidence for the tumor-suppressive function of BRCA1 being mediated predominantly by its indispensable role in supporting RAD51-dependent recombination downstream of end resection is discussed.