RAD52 is a structurally and functionally conserved component of the DNA double-strand break (DSB) repair apparatus from budding yeast to humans. We recently showed that expressing the human gene, HsRAD52 in rad52 mutant budding yeast cells can suppress both their ionizing radiation (IR) sensitivity and homologous recombination repair (HRR) defects. Intriguingly, we observed that HsRAD52 supports DSB repair by a mechanism of HRR that conserves genome structure and is independent of the canonical HR machinery. In this study we report that naturally occurring variants of HsRAD52, one of which suppresses the pathogenicity of BRCA2 mutations, were unable to suppress the IR sensitivity and HRR defects of rad52 mutant yeast cells, but fully suppressed a defect in DSB repair by single-strand annealing (SSA). This failure to suppress both IR sensitivity and the HRR defect correlated with an inability of HsRAD52 protein to associate with and drive an interaction between genomic sequences during DSB repair by HRR. These results suggest that HsRAD52 supports multiple, distinct DSB repair apparatuses in budding yeast cells and help further define its mechanism of action in HRR. They also imply that disruption of HsRAD52-dependent HRR in BRCA2defective human cells may contribute to protection against tumorigenesis and provide a target for killing BRCA2-defective cancers.

Adaptations for predator defense are often complex traits with integrated display components spanning multiple signaling modalities. For antipredator coloration like deimatic or startle coloration, behavioral variation controlling dynamic color displays is an important but poorly understood component of the predator defense in most taxa. We studied antipredator behavior in North American ringneck snakes (Diadophis punctatus), which possess a brightly colored (red to yellow) ventral surface of the body and the tail compared to the mostly gray dorsal coloration. We sought to (a) characterize intraspecific variation in antipredator behaviors in ringneck snakes and (b) test which stimuli can induce antipredator displays. First, we assessed antipredator displays in the field and during routine handling during data collection by comparing categorical classifications of all displayed behavior across 25 individuals. Second, we performed experimental assays with tactile and visual stimuli to determine the cues that can elicit an antipredator display in ringneck snakes. We found that antipredator displays include ventral displays and tail‐coiling and that these components were induced by tactile cues in the field and the lab, but not visual cues. Our work is the first to show that a snake species with bright ventral coloration uses this behavior in response to tactile cues from a potential predator, but only in response to relatively strong stimuli (i.e., handling). This experimental evidence that tactile stimuli can induce a behavior revealing bright ventral coloration highlights the importance of correlated evolution of antipredator coloration and behavior.

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