Behavioral variation within and between populations and species of the genus Papio has been studied extensively, but little is known about the genetic causes of individual- or population-level differences. This study investigates the influence of genetic variation on personality (sometimes referred to as temperament) in baboons and identifies a candidate gene partially responsible for the variation in that phenotype. To accomplish these goals, we examined individual variation in response to both novel objects and an apparent novel social partner (using a mirror test) among pedigreed baboons (n = 578) from the Southwest National Primate Research Center. We investigated the frequency and duration of individual behaviors in response to novel objects and used multivariate factor analysis to identify trait-like dimensions of personality. Exploratory factor analysis identified two distinct dimensions of personality within this population. Factor 1 accounts for 46.8 % of the variance within the behavioral matrix, and consists primarily of behaviors related to the "boldness" of the subject. Factor 2 accounts for 18.8 % of the variation, and contains several "anxiety" like behaviors. Several specific behaviors, and the two personality factors, were significantly heritable, with the factors showing higher heritability than most individual behaviors. Subsequent analyses show that the behavioral reactions observed in the test protocol are associated with animals' social behavior observed later in their home social groups. Finally we used linkage analysis to map quantitative trait loci for the measured phenotypes. Single nucleotide polymorphisms in a positional candidate gene (SNAP25) are associated with variation in one of the personality factors, and CSF levels of homovanillic acid and 3-methoxy-4-hydroxyphenylglycol. This study documents heritable variation in personality among baboons and suggests that sequence variation in SNAP25 may influence differences in behavior and neurochemistry in these nonhuman primates.

An anxious temperament in both humans and monkeys is evident from infanthood, is an important risk factor for later psychopathology, and is known to be heritable. In a large-scale study combining imaging with genetics, Oler et al. characterize the neural circuitry associated with this trait and the extent to which the function of this circuit is heritable. They scanned more than 200 related monkeys from a single-family pedigree using positron emission tomography after exposing the monkeys to a mildly stressful situation. Activation in both the amygdala and hippocampus was predictive of anxious temperament, but heritability of hippocampal activity was greater than that for amygdala. This suggests that there may be different effects of genes and environment on the function of these two regions in anxious temperament, and provides new insights into the genetic risk for anxiety and depressive disorders. Anxious temperament in both humans and monkeys is an important early predictor of psychopathology and is known to be heritable. These authors characterize the neural circuitry associated with this trait and the extent to which its function is heritable. A scan of related monkeys after exposure to mild stress showed that activation in both the amygdala and hippocampus was predictive of anxious temperament, but that heritability of activity in hippocampus was greater than that in amygdala. Anxious temperament (AT) in human and non-human primates is a trait-like phenotype evident early in life that is characterized by increased behavioural and physiological reactivity to mildly threatening stimuli1,2,3,4. Studies in children demonstrate that AT is an important risk factor for the later development of anxiety disorders, depression and comorbid substance abuse5. Despite its importance as an early predictor of psychopathology, little is known about the factors that predispose vulnerable children to develop AT and the brain systems that underlie its expression. To characterize the neural circuitry associated with AT and the extent to which the function of this circuit is heritable, we studied a large sample of rhesus monkeys phenotyped for AT. Using 238 young monkeys from a multigenerational single-family pedigree, we simultaneously assessed brain metabolic activity and AT while monkeys were exposed to the relevant ethological condition that elicits the phenotype. High-resolution 18F-labelled deoxyglucose positron-emission tomography (FDG–PET) was selected as the imaging modality because it provides semi-quantitative indices of absolute glucose metabolic rate, allows for simultaneous measurement of behaviour and brain activity, and has a time course suited for assessing temperament-associated sustained brain responses. Here we demonstrate that the central nucleus region of the amygdala and the anterior hippocampus are key components of the neural circuit predictive of AT. We also show significant heritability of the AT phenotype by using quantitative genetic analysis. Additionally, using voxelwise analyses, we reveal significant heritability of metabolic activity in AT-associated hippocampal regions. However, activity in the amygdala region predictive of AT is not significantly heritable. Furthermore, the heritabilities of the hippocampal and amygdala regions significantly differ from each other. Even though these structures are closely linked, the results suggest differential influences of genes and environment on how these brain regions mediate AT and the ongoing risk of developing anxiety and depression.

Identification of polymorphic microsatellite loci in nonhuman primates is useful for various biomedical and evolutionary studies of these species. Prior methods for identifying microsatellites in nonhuman primates are inefficient. We describe a new strategy for marker development that uses the available whole genome sequence for rhesus macaques. Fifty-four novel rhesus-derived microsatellites were genotyped in large pedigrees of rhesus monkeys. Linkage analysis was used to place 51 of these loci into the existing rhesus linkage map. In addition, we find that microsatellites identified this way are polymorphic in other Old World monkeys such as baboons. This approach to marker development is more efficient than previous methods and produces polymorphisms with known locations in the rhesus genome assembly. Finally, we propose a nomenclature system that can be used for rhesus-derived microsatellites genotyped in any species or for novel loci derived from the genome sequence of any nonhuman primate.

Introduction Monodelphis ( Monodelphis domestica ) shows 20-fold differences, that may be under genetic control, in individual responses to a high-fat challenge diet. Two partially inbred lines of animals were derived by selectively breeding among high responders and low responders and we analysed data from these pedigreed animals and their F 1 progeny. A blood sample was taken from each animal while consuming the basal diet (basal sample). Each animal was then fed a high-fat, high-cholesterol challenge diet for 8 weeks prior to collection of a second blood sample (challenge sample). Lipoprotein measurements included cholesterol concentrations of high-density lipoproteins (HDL-C) and low-density lipoproteins (non-HDL-C) and particle size phenotypes for both. Quantitative genetic analyses indicated strong heritabilities (range, 0.382–0.827) for each of the eight traits. We also tested for single genes with large effects on each trait (major genes). Segregation analyses provided evidence of major genes for three traits: basal non-HDL-C, challenge non-HDL-C, and challenge HDL-C; no major genes were detected for the lipoprotein size traits. Tests for pleiotropy, using bivariate one-locus segregation analyses, showed that the major locus for challenge HDL-C had no effect on the basal HDL-C and that the major locus for challenge non-HDL-C had no effect on basal non-HDL-C. However, the major gene for basal non-HDL-C did significantly influence challenge non-HDL-C. We have found evidence for at least three genes influencing lipoprotein phenotypes under two dietary regimes. Identification of these genes may provide valuable insights into lipoprotein metabolism in other species, including man.