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Homologous recombination (HR) is a key pathway to repair complex DNA damage, such as DNA gaps, double-strand breaks, and interstrand cross-links (1) (Fig. 1). Moreover, HR supports the recovery of stalled or broken replication forks and ensures faithful chromosome segregation during meiosis. The RAD52 gene in the budding yeast Saccharomyces cerevisiae encodes the lynchpin of HR in this organism. Hence, the genes of the HR pathway are called the RAD52 epistasis group. However, much to everybody's surprise, the RAD52 gene knockout in mice exhibits minimal to no phenotypes in recombination, repair, and meiosis (2). Instead, the breast and ovarian tumor suppressor protein BRCA2 maintains a central HR function, a protein that is missing in budding yeast. Analyzing HR in BRCA2-deficient human cells, a study reported in PNAS (3) redefines human RAD52 by showing that it plays a critical role in HR in BRCA2-deficient cells. This important result mandates a reexamination of vertebrate RAD52 and its functions, which opens perplexing mechanistic conundrums. Roles of BRCA2 and RAD52 in homologous recombination. Upper: Schematic representation of the mediator and annealing functions during recombination involving (A) invasion of both ends, (B) invasion of the first end and second end capture by annealing, or (C) invasion of the first end, D-loop disruption, and annealing of the extended first end to the second end (SDSA, synthesis-dependent strand annealing). Lower: BRCA2 and RAD52 functions and phenotypes in selected organisms. Checkmark denotes presence of the biochemical activity, − denotes absence of phenotype, ++ denotes a strong and (+) a weak phenotype. In the study (3), Feng et al. manipulate the BRCA2 and RAD52 status by mutation, complementation, …

Who's who in human recombination: BRCA2 and RAD52