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Activation-induced deaminase (AID) initiates hypermutation of Ig genes in activated B cells by converting C:G into U:G base pairs. G 1 -phase variants of uracil base excision repair (BER) and mismatch repair (MMR) then deploy translesion polymerases including REV1 and Pol η, which exacerbates mutation. dNTP paucity may contribute to hypermutation, because dNTP levels are reduced in G 1 phase to inhibit viral replication. To derestrict G 1 -phase dNTP supply, we CRISPR-inactivated SAMHD1 (which degrades dNTPs) in germinal center B cells. Samhd1 inactivation increased B cell virus susceptibility, increased transition mutations at C:G base pairs, and substantially decreased transversion mutations at A:T and C:G base pairs in both strands. We conclude that SAMHD1's restriction of dNTP supply enhances AID's mutagenicity and that the evolution of Ig hypermutation included the repurposing of antiviral mechanisms based on dNTP starvation., Competing Interests: The authors declare no conflict of interest.

In the endeavor to associate genetic variation with complex traits, closely related taxa are particularly fruitful for understanding the neurophysiological and genetic underpinnings of species-specific attributes. Similarity to humans has motivated research into nonhuman primate models, yet few studies of wild primates have investigated immediate causal factors of evolutionarily diverged social behaviors. Neurotransmitter differences have been invoked to explain the distinct behavioral suites of two baboon species in Awash, Ethiopia, which differ markedly in social behavior despite evolutionary propinquity. With this natural experiment, we test the hypothesis that genomic regions associated with monoamine neurotransmitters would be highly differentiated, and we identify a dopamine pathway as an outlier, highlighting the system as a potential cause of species-specific social behaviors. Dopamine levels and resultant variation in impulsivity were likely under differential selection in the species due to social system structure differences, with either brash or circumspect social behavior advantageous to secure mating opportunities depending on the social backdrop. Such comparative studies into the causes of the behavioral agendas that create and interact with social systems are of particular interest, and differences in temperament related to boldness and associated with dopamine variation likely played important roles in the evolution of all social, behaviorally complex animals, including baboons and humans.

An important determinant of wheat grain quality is the hardness of the grain. The trait is controlled by a major locus, Ha, on the short arm of chromosome 5D. Purified starch granules from soft-grained wheats have associated with them 15-kDa polypeptides called grain softness proteins (GSPs) or "friabilins." Genes that encode one family of closely related GSP polypeptides - GSP-1 genes - were mapped using chromosome substitution lines to the group 5 chromosomes. An F2 population segregating for hard and soft alleles at the Ha locus on a near-isogenic background was used in a single-seed study of the inheritance of grain softness and of GSP-1 alleles. Grain softness versus grain hardness was inherited in a 3:1 ratio. The presence versus absence of GSPs in single seed starch preparations was coinherited with grain softness versus hardness. This showed that grain softness is primarily determined by seed, and not by maternal, genotype. In addition, no recombination was detected in 44 F2 plants between GSP-1 restriction fragment length polymorphisms and Ha alleles. Differences between hard and soft wheat grains in membrane structure and lipid extractability have been described and, of the three characterized proteins that are part of the mixture of 15-kDa polypeptides called GSPs, at least two, and probably all three, are proteins that bind polar lipids. The data are interpreted to suggest that the Ha locus may encode one or more members of a large family of lipid-binding proteins.