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Little is known about the genetic changes that distinguish domestic cat populations from their wild progenitors. Here we describe a high-quality domestic cat reference genome assembly and comparative inferences made with other cat breeds, wildcats, and other mammals. Based upon these comparisons, we identified positively selected genes enriched for genes involved in lipid metabolism that underpin adaptations to a hypercarnivorous diet. We also found positive selection signals within genes underlying sensory processes, especially those affecting vision and hearing in the carnivore lineage. We observed an evolutionary tradeoff between functional olfactory and vomeronasal receptor gene repertoires in the cat and dog genomes, with an expansion of the feline chemosensory system for detecting pheromones at the expense of odorant detection. Genomic regions harboring signatures of natural selection that distinguish domestic cats from their wild congeners are enriched in neural crest-related genes associated with behavior and reward in mouse models, as predicted by the domestication syndrome hypothesis. Our description of a previously unidentified allele for the gloving pigmentation pattern found in the Birman breed supports the hypothesis that cat breeds experienced strong selection on specific mutations drawn from random bred populations. Collectively, these findings provide insight into how the process of domestication altered the ancestral wildcat genome and build a resource for future disease mapping and phylogenomic studies across all members of the Felidae.Felis catus | domestication | genome T he domestic cat (Felis silvestris catus) is a popular pet species, with as many as 600 million individuals worldwide (1). Cats and other members of Carnivora last shared a common ancestor with humans ∼92 million years ago (2, 3). The cat family Felidae includes ∼38 species that are widely distributed across the world, inhabiting diverse ecological niches that have resulted in divergent morphological and behavioral adaptations (4). The earliest archaeological evidence for human coexistence with cats dates to ∼9.5 kya in Cyprus and ∼5 kya in central China (5, 6), during periods when human populations adopted more agricultural lifestyles. Given their sustained beneficial role surrounding vermin control since the human transition to agriculture, any selective forces acting on cats may have been minimal subsequent to their domestication. Unlike many other domesticated mammals bred for food, herding, hunting, or security, most of the 30-40 cat breeds originated recently, within the past 150 y, largely due to selection for aesthetic rather than functional traits.Previous studies have assessed breed differentiation (6, 7), phylogenetic origins of the domestic cat (8), and the extent of recent introgression between domestic cats and wildcats (9, 10). However, little is known regarding the impact of the domestication process within the genomes of modern cats and how this compares with genetic changes accompanying selection identified...

These data suggest a potential interaction between serotonin transporter gene variation and early experience in vulnerability to alcoholism.

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Variation in the serotonin transporter gene-linked polymorphic region (5-HTTLPR) has been associated with anxiety and harm avoidance and is weakly associated with a number of neuropsychiatric disorders, including Type II alcoholism, which has a high rate of comorbidity with antisocial personality disorder. Studies have also demonstrated interactions between 5-HTTLPR variation and environmental stress on the incidence of depression. As in humans, there is a serotonin transporter gene promoter length polymorphism in rhesus macaques that produces similar decreases in transcriptional efficiency. Macaques with histories of early-life stress have been shown to exhibit impulsive aggression, incompetent social behavior and increased behavioral and endocrine responsivity to stress. In this paper, we review studies performed previously in our lab and present preliminary data examininng interactions between early rearing and serotonin transporter gene promoter variation on the incidences of play behavior and aggression in infant rhesus macaques. The data presented here highlight the importance of considering gene-environment interactions when studying childhood risk factors for aggression, anxiety and related neuropsychiatric disorders and support the use of the nonhuman primate for studing gene by environment interactions in behavioral research.Keywords: Aggression, gene  environment interaction, nonhuman primate, play, serotonin transporter, stress The 'nature vs. nurture' controversy over the development of personality is long-standing (for reviews, see Balaban 2002;Plomin et al. 1988). While, historically, many scientists held that personality was subject to evolutionary pressures and therefore was probably of genetic etiology, others maintained that personality was probably more strongly influenced by the environment. This debate extended further to the development of psychopathology and neuropsychiatric disease (Balaban 2002;Rutter et al. 1997). Today, it is more widely accepted that the development of personality is driven by both nature and nurture and that, moreover, there are potential interactions between genes and environment (G ÂE interactions) that may be at the root of the development of some personality traits and neuropsychiatric diseases (for review, see Gunzerath & Goldman 2003). With the advent of modern molecular and statistical tools, we are now capable of refining our approach so that specific G ÂE interactions in the development of personality traits can be revealed.The non-human primate model is particularly useful for the study of G  E interactions in the development of psychopathology. Firstly, most psychopathology revolves around social functioning, and, compared to other laboratory animal species, non-human primates have complex behaviors and social structures that more closely approximate those present in humans. Secondly, because they are more closely related to humans than are the other laboratory animal species, they provide a useful model for the study of gene variation as it relates to ...

In a variety of species, development of attachment to a caregiver is crucial for infant survival and partly mediated by the endogenous opioids. Functional mu-opioid receptor gene polymorphisms are present in humans (OPRM1 A118G) and rhesus macaques (OPRM1 C77G). We hypothesized that rhesus infants carrying a gain-of-function OPRM1 77G allele would experience increased reward during maternal contact and would, therefore, display increased measures of attachment. We collected behavioral data from rhesus macaques (n ‫؍‬ 97) during early infancy and at 6 months of age, across four cycles of maternal separation (4 days) and reunion (3 days). Animals were genotyped for the OPRM1 C77G polymorphism, and the effects of this allele on attachmentrelated behaviors were analyzed. Infants carrying the G allele exhibited higher levels of attachment behavior during early infancy. During prolonged periods of maternal separation, although infant macaques homozygous for the C allele exhibited decreases in their levels of distress vocalization with repeated separation, this response persisted in G allele carriers. The OPRM1 77G allele also affected social preference during reunion. C/G infants spent increasing amounts of time in social contact with their mothers as a function of repeated separation and were less likely to interact with other individuals in the social group, a pattern not observed among infants with the C/C genotype. These findings suggest a role for OPRM1 variation in the expression of attachment behavior in human subjects, especially as a function of separation from the caregiver.genetic ͉ rhesus macaque ͉ mother-infant bond ͉ C77G ͉ A118G

Context Traumatic experiences in early childhood are associated with increased risk for developing stress-related disorders, which are linked to structural brain abnormalities. However, it is unclear if these volumetric brain changes are present before disease onset or reflect the consequences of the disease progression. Objective To identify structural abnormalities in the nonhuman primate brain that may predict increased risk for stress-related neuropsychiatric disorders in humans. Design Rhesus monkeys were divided in two groups at birth: a group raised with their mothers and other juvenile and adult animals (mother-reared, MR), and a group raised with three age-matched monkeys only (peer-reared, PR). Anatomical brain images were acquired in juvenile male and female rhesus monkeys using magnetic resonance imaging. Main Outcome Measures Volumetric measures of the anterior cingulate cortex, medial prefrontal cortex, hippocampus, corpus callosum and cerebellar vermis were compared between MR (n=15) and PR animals (n=13). Results Compared to MR monkeys, we found an enlarged vermis, dorsomedial prefrontal and dorsal anterior cingulate cortex in PR monkeys but no differences in the corpus callosum and hippocampus. Conclusions Peer-rearing during infancy induces enlargements in stress-sensitive brain regions. These changes may be a structural phenotype for an increased risk to stress-related neuropsychiatric disorders in humans.