674 resultados para Primates.
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The diet and feeding ecology of a wild subpopulation of black-and-white snub-nosed monkeys (Rhinopithecus bieti) were studied at Xiaochangdu in Honglaxueshan Nature Reserve, Tibet. This region is climatologically harsher than any other inhabited by non-human primates. Black-and-white snub-nosed monkeys fed on 48 parts of 25 plant species, at least three species of lichens and seven species of invertebrates. The number of food items exploited varied markedly among seasons, with dietary diversity being greatest in spring and summer. In winter, black-and-white snub-nosed monkeys had to subsist on fallback foods such as dried grass and bark. Ubiquitous lichens formed a major dietary constituent throughout the year, contributing about 75% of feeding records. Even though lichens act as a staple, our findings signify that the monkeys at Xiaochangdu prefer feeding on foliage, which is higher in protein content than the former. We provide evidence that black-and-white snub-nosed monkeys are able to cope with an array of food items other than lichens and hence can be regarded as feeding generalists. We discuss the results with reference to previous studies on other subpopulations living in habitats that are floristically more diverse and offer more plant food items than the marginal habitat at Xiaochangdu.
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Background: Flying lemurs or Colugos (order Dermoptera) represent an ancient mammalian lineage that contains only two extant species. Although molecular evidence strongly supports that the orders Dermoptera, Scandentia, Lagomorpha, Rodentia and Primates form a superordinal clade called Supraprimates (or Euarchontoglires), the phylogenetic placement of Dermoptera within Supraprimates remains ambiguous. Results: To search for cytogenetic signatures that could help to clarify the evolutionary affinities within this superordinal group, we have established a genome-wide comparative map between human and the Malayan flying lemur (Galeopterus variegatus) by reciprocal chromosome painting using both human and G. variegatus chromosome-specific probes. The 22 human autosomal paints and the X chromosome paint defined 44 homologous segments in the G. variegatus genome. A putative inversion on GVA 11 was revealed by the hybridization patterns of human chromosome probes 16 and 19. Fifteen associations of human chromosome segments (HSA) were detected in the G. variegatus genome: HSA1/3, 1/10, 2/21, 3/ 21, 4/8, 4/18, 7/15, 7/16, 7/19, 10/16, 12/22 (twice), 14/15, 16/19 (twice). Reverse painting of G. variegatus chromosome-specific paints onto human chromosomes confirmed the above results, and defined the origin of the homologous human chromosomal segments in these associations. In total, G. variegatus paints revealed 49 homologous chromosomal segments in the HSA genome. Conclusion: Comparative analysis of our map with published maps from representative species of other placental orders, including Scandentia, Primates, Lagomorpha and Rodentia, suggests a signature rearrangement (HSA2q/21 association) that links Scandentia and Dermoptera to one sister clade. Our results thus provide new evidence for the hypothesis that Scandentia and Dermoptera have a closer phylogenetic relationship to each other than either of them has to Primates.
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人是生命演化的产物。然而由于具有一个超级大的大脑和高级的认知能力, 人类在自然界中又显得十分与众不同。在灵长类进化过程中,脑容量大小和认知 能力高低可以明显的分成几个等级,由高到低依次为人类、大猿和其它灵长类。 现在一般认为,人类超级大的大脑的形成是适应性选择(达尔文正选择)的结果。 但人类高级认知的起源一直还是个未解之谜。随着分子进化理论和比较基因组学 的发展,人们有可能从分子进化的角度去探讨高级认知的起源问题,并揭示其遗 传学机制。 本文从两个不同的角度入手,通过对认知相关的候选基因的分子进化研究来 探索高级认知起源的遗传学机制。1. 从表型出发,发现microcephalin 基因跟小 脑症相关。我们推测,该基因可能在人类起源过程中发生一些突变,导致脑容量 增大。2. 比较基因组学方法发现垂体腺苷酸环化酶激活肽(PACAP)前体基因在人 类支系中存在正选择。这类受正选择的神经相关基因可能在进化过程中对认知能 力的提高发挥重要作用。 Microcephalin 基因在人脑的发育过程中起重要作用。导致该基因蛋白质翻译 提前终止的突变,会引起人类小脑症,患者脑容量回复到早期原始人的大小。我 们对人群和12 个非人灵长类物种的microcephalin 基因编码区进行测序。所测的 非人灵长类物种包括大猿、小猿、旧大陆猴和新大陆猴。结果显示,microcephalin 基因在人群中具有较高的多态性。在人群中编码区有22 个多态位点,其中有15 个是错义突变位点。中性检验结果显示,microcephalin 基因的高多态性是人类群 体扩张和达尔文正选择共同作用的结果。灵长类各支系的进化分析表明, microcephalin 基因在大猿的起源过程中受到较强的正选择信号。这正好和小猿向 大猿进化过程中大脑容量急剧增大,认知能力大幅度提高的事实相符。单个氨基 酸编码位点检验显示,microcephalin 基因有五个氨基酸位点在灵长类的进化过程中存在正选择信号。这几个位点可能在灵长类进化和人类起源过程中,对脑容量 的增大和认知能力的提高起到了重要的作用。 PACAP 是一个神经系统中高表达的神经肽,与神经发生和神经信号传导有 关。该基因的氨基酸序列在脊椎动物的进化过程中非常保守,表明PACAP 前体 基因在这一进化历程中受到强烈的功能限制。然而比较序列分析显示,自从人与 黑猩猩分歧以后,人类支系中PACAP 前体基因有明显的加速进化。由于存在强 烈的正选择作用,人类支系的氨基酸替换速率是其它哺乳动物支系的至少7 倍。 PACAP 前体基因中有7 个人类特异的氨基酸改变,而这些氨基酸在从鼠类到大 猿的所有物种中都是保守的。蛋白质结构分析结果显示,人类起源过程中,PACAP 前体基因可能编码一个新的神经肽,并在人脑中具有功能。因此,在人类起源过 程中,PACAP 前体基因发生了适应性的改变,可能对人类认知能力的产生起到 了重要作用。这个新神经肽是否存在及其功能还有待于进一步功能实验的验证。 总之,本文通过分子进化分析,发现了两个在灵长类进化过程中对认知能力 的提高起关键作用的基因(Microcephalin 基因、PACAP 前体基因)。Microcephalin 基因,在1400-1800 万年前,从小猿向大猿的进化过程中,可能对脑容量的增大 和认知能力的提高发挥了重要的作用。PACAP 前体基因则在最近的几百万年内, 现代人的起源过程中,对人脑的形成以及人类高级认知能力的产生可能发挥了重 要的作用。
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大约5一7百万年前,从大猿中分出来的一支,走上了以大脑容量快速扩增为特征的演化道路,并最终进化成具有高级认知能力的物种-人。一直以来古人类学家和生物学家经过不懈努力,向我们揭示了人与灵长类其他物种的亲缘关系,并且让我们知道黑猩猩是同人类亲缘关系最近的现生物种。然而人口的爆炸增长和黑猩猩种群数目的急剧减少形成的鲜明对比,让我们迷惑于为何在进化地位上如此相近的物种,命运却截然不同。通过比较两个物种,科学家们发现问题的关键在于:人具有高度发达的大脑和相伴而生的高级认知能力。高度发达的认知能力使得人类获得了对环境强大的适应力,从而能够从众多生物中脱颖而出成为统治地球的智慧生物。通过比较黑猩猩和人基因组序列,生物学家发现人和黑猩猩DNA序列相似度接近99%。这个结果提示我们:1)只有很少数目的基因在一级结构上的变化和认知差异有关;2)认知差异可能更多是由调控相关元件变化导致的基因表达水平上的差异引起的。基于此,我们试图通过比较两个物种目前所知的在人脑中表达的基因的一级结构差异,找寻那些在人起源过程中受到较强正选择的基因。我们检测了近万个基因,结果显示只有大约1.38%的基因有明显的正选择迹象。接着我们从中选取了一个基因-MrgX2,测了全世界范围内的代表性人群以及非人灵长类中的代表性物种,结果显示MrgX2在人这一支受到了很强的适应选择作用,这一适应又很有可能和人类起源过程中感觉神经系统的适应有关。神经生物学的研究表明,大脑皮层前额叶是行使高级认知功能的主要区域。大脑在发育的过程中有一个神经网络重新搭建的过程,而这一过程和基因表达是密切相关的。基于此我们采用基因芯片的方法,通过比较称猴大脑发育各个关键时期的前额叶基因表达图谱,以期了解与大脑神经网络构建相关基因的活动情况。
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microRNAs(miRNAs)是基因组中广泛编码的一类小RNA 基因,存在于绝大多数多细胞生物中,而且在各种生物学过程中都起着举足轻重的作用。miRNAs 在转录后水平通过与mRNAs 的3’UTRs 序列互补识别靶基因,并引起靶基因的降解或阻遏其翻译。在动物中,一个miRNA 可以调控数百个靶基因的表达。大多数miRNAs 在物种间高度保守,暗示了其功能的重要性。然而,非保守的miRNAs可能对物种特有新功能的产生有贡献。为了回答miRNAs是如何起源,如何进化的问题,我们研究了两个非保守miRNA 家族在灵长类中的进化历史。第一个miRNA 家族位于X 染色体上,在灵长类中的数目比狗或啮齿类中的多。我们比较了这一家族在灵长类主要分支-人、大猿、小猿、旧大陆猴和新大陆猴中的序列情况,发现了这一家族在灵长类中的快速进化。这种快速进化包括频繁的串联重复和碱基替换现象。此外,在人和黑猩猩中还发现了相应进化分支特有的替换,可能会导致分支特有的新miRNAs 的产生。对这一miRNA 家族在不同发育阶段恒河猴睾丸中的表达分析揭示了miRNA 表达变化和雄性性成熟之间的负相关,暗示这一家族在睾丸发育和精子成熟中可能起的调节作用。最后,我们认为,像蛋白编码基因一样,与雄性生殖功能相关的miRNAs 容易受到性选择而发生适应性进化。第二个miRNA 家族是位于19 号染色体上的一个灵长类特有的家族。通过分析和比较这一家族以及其临近区域在9 个不同灵长类物种中的序列,我们发现了 Alu 介导的这一家族的产生和扩张。序列比较表明,物种内和物种间miRNAs 的序列分歧相似;同时,在各个灵长类分支中均存在基因拷贝的获得和丢失,也存在基因的假基因化。由此表明,这一家族在灵长类中经历了典型的“生-死”进化历程,暗示这个家族的miRNA 基因在灵长类的进化中其功能可能发生了多样化,以适应不同灵长类物种在发育过程中的需要。此外,二级结构的保守性和前体miRNAs 区域的低SNP 密度都表明这一家族受到功能性约束。最后,我们进一步分析了这一家族在胎盘和胎儿大脑中的表达,揭示其对灵长类胚胎发育可能的重要性。除了研究miRNAs 在灵长类中的进化,我们还探讨了miRNAs 对基因表达变异度的影响。通过对已发表的193 例人类大脑基因表达谱的分析发现,基因在人群中的表达变异的大小和调控它的miRNA 数目呈正比,这暗示了miRNAs 对基因表达变异度的直接影响。相比于不受miRNA 调控的基因,受到两个以上 miRNA 核心区调控的基因有较高的表达变异度,不受miRNA 类型的影响。同时,我们还证明,人群中靶基因miRNA 识别序列上的变异(SNPs)会进一步导致靶基因表达变异的增加。我们的研究表明miRNAs 是影响人群中基因表达变异度的因素之一。
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Ebolaviruses (EBOVs) are among the most virulent and deadly pathogens ever known, causing fulminant haemorrhagic fevers in humans and non-human primates. The 2014 outbreak of Ebola virus disease (EVD) in West Africa has claimed more lives than all previous EVD outbreaks combined. The EBOV high mortality rates have been related to the virus-induced impairment of the host innate immunity reaction due to two virus-coded proteins, VP24 and VP35. EBOV VP35 is a multifunctional protein, it is essential for viral replication as a component of the viral RNA polymerase and it also participates in nucleocapsid assembly. Early during EBOV infection, alpha-beta interferon (IFN-α/β) production would be triggered upon recognition of viral dsRNA products by cytoplasmic retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs). However, this recognition is efficiently prevented by the double-stranded RNA (dsRNA) binding activity of the EBOV VP35 protein, which hides RLRs binding sites on the dsRNA phosphate backbone as well the 5’-triphosphate (5’-ppp) dsRNA ends to RIG-I recognition. In addition to dsRNA binding and sequestration, EBOV VP35 inhibits IFN-α/β production preventing the activation of the IFN regulatory factor 3 (IRF-3) by direct interaction with cellular proteins. Previous studies demonstrated that single amino acid changes in the VP35 dsRNA binding domain reduce EBOV virulence, indicating that VP35 is an attractive target for antiviral drugs development. Within this context, here we report the establishment of a novel method to characterize the EBOV VP35 inhibitory function of the dsRNA-dependent RIG-I-mediated IFN-β signaling pathway in a BLS2 cell culture setting. In such system, a plasmid containing the promoter region of IFN-β gene linked with a luciferase reporter gene was transfected, together with a EBOV VP35 mammalian expression plasmid, into the IFN-sensitive A549 cell line, and the IFN-induction was stimulated through dsRNA transfection. Through alanine scanning mutational studies with biochemical, cellular and computational methods we highlighted the importance of some VP35 residues involved in dsRNA end-capping binding, such as R312, K282 and R322, that may serve as target for the development of small-molecule inhibitors against EBOV. Furthermore, we identified a synthetic compound that increased IFN-induction only under antiviral response stimulation and subverted VP35 inhibition, proving to be very attractive for the development of an antiviral drug. In conclusion, our results provide the establishment of a new assay as a straightforward tool for the screening of antiviral compounds that target i) dsRNA-VP35 or cellular protein-VP35 interaction and ii) dsRNA-dependent RIG-I-mediated IFN signaling pathway, in order to potentiate the IFN response against VP35 inhibition, setting the bases for further drug development.
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Neuroinflammation is a key component of Parkinson’s disease (PD) neuropathology. Skewed microglia activation with pro-inflammatory prevailing over anti-inflammatory phenotypes may contribute to neurotoxicity via the production of cytokines and neurotoxic species. Therefore, microglia polarization has been proposed as a target for neuroprotection. The peroxisome proliferator-activated receptor gamma (PPARγ) is expressed in microglia and peripheral immune cells, where it is involved in macrophages polarization and in the control of inflammatory responses, by modulating gene transcription. Several studies have shown that PPARγ agonists are neuroprotective in experimental PD models in rodents and primates. however safety concerns have been raised about PPARγ agonists thiazolidinediones (TZD) currently available, prompting for the development of non-TZD compounds. Aim of this study was to characterize a novel PPARγ agonist non TZD, MDG548, for its potential neuroprotective effect in PD models and its immunomodulatory activity as the underlying mechanism of neuroprotection. The neuroprotective activity of MDG548 was assessed in vivo in the subacute MPTP model and in the chronic MPTP/probenecid (MPTPp) model of PD. MDG548 activity on microglia activation and phenotype was investigated in the substantia nigra pars compacta (SNc) via the evaluation of pro- (TNF-α and iNOS) and anti-inflammatory (CD206) molecules, with fluorescent immunohistochemistry. Moreover, cultured murine microglia MMGT12 were treated with MDG548 in association with the inflammagen LPS, pro- and anti-inflammatory molecules were measured in the medium by ELISA assay and phagocytosis was evaluated by fluorescent immunohistochemistry for CD68. MDG548 arrested dopaminergic cells degeneration in the SNc in both the subacute MPTP and the chronic MPTPp models of PD, and reverted MPTPp-induced motor impairment. Moreover, MDG548 reduced microglia activation, iNOS and TNF-α production, while induced CD206 in microglia. In cultured unstimulated microglia, LPS increased TNF-α production and CD68 expression, while decreased CD206 expression. MDG548 reverted LPS effect on TNF-α and CD206 restoring physiological levels, while strongly increased CD68 expression. Results suggest that the PPARγ agonist MDG548 is neuroprotective in experimental models of PD. MDG548 targets microglia polarization by correcting the imbalance between pro- over antiinflammatory molecules, offering a novel immunomodulatory approach to neuroprotection.
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Oculomotor tracking of moving objects is an important component of visually based cognition and planning. Such tracking is achieved by a combination of saccades and smooth pursuit eye movements. In particular, the saccadic and smooth pursuit systems interact to often choose the same target, and to maximize its visibility through time. How do multiple brain regions interact, including frontal cortical areas, to decide the choice of a target among several competing moving stimuli? How is target selection information that is created by a bias (e.g., electrical stimulation) transferred from one movement system to another? These saccade-pursuit interactions are clarified by a new computational neural model, which describes interactions among motion processing areas MT, MST, FPA, DLPN; saccade specification, selection, and planning areas LIP, FEF, SNr, SC; the saccadic generator in the brain stem; and the cerebellum. Model simulations explain a broad range of neuroanatomical and neurophysiological data. These results are in contrast with the simplest parallel model with no interactions between saccades and pursuit than common-target selection and recruitment of shared motoneurons. Actual tracking episodes in primates reveal multiple systematic deviations from predictions of the simplest parallel model, which are explained by the current model.
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The processes by which humans and other primates learn to recognize objects have been the subject of many models. Processes such as learning, categorization, attention, memory search, expectation, and novelty detection work together at different stages to realize object recognition. In this article, Gail Carpenter and Stephen Grossberg describe one such model class (Adaptive Resonance Theory, ART) and discuss how its structure and function might relate to known neurological learning and memory processes, such as how inferotemporal cortex can recognize both specialized and abstract information, and how medial temporal amnesia may be caused by lesions in the hippocampal formation. The model also suggests how hippocampal and inferotemporal processing may be linked during recognition learning.
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RNA editing is a biological phenomena that alters nascent RNA transcripts by insertion, deletion and/or substitution of one or a few nucleotides. It is ubiquitous in all kingdoms of life and in viruses. The predominant editing event in organisms with a developed central nervous system is Adenosine to Inosine deamination. Inosine is recognized as Guanosine by the translational machinery and reverse-transcriptase. In primates, RNA editing occurs frequently in transcripts from repetitive regions of the genome. In humans, more than 500,000 editing instances have been identified, by applying computational pipelines on available ESTs and high-throughput sequencing data, and by using chemical methods. However, the functions of only a small number of cases have been studied thoroughly. RNA editing instances have been found to have roles in peptide variants synthesis by non-synonymous codon substitutions, transcript variants by alterations in splicing sites and gene silencing by miRNAs sequence modifications. We established the Database of RNA EDiting (DARNED) to accommo-date the reference genomic coordinates of substitution editing in human, mouse and fly transcripts from published literatures, with additional information on edited genomic coordinates collected from various databases e.g. UCSC, NCBI. DARNED contains mostly Adenosine to Inosine editing and allows searches based on genomic region, gene ID, and user provided sequence. The Database is accessible at http://darned.ucc.ie RNA editing instances in coding region are likely to result in recoding in protein synthesis. This encouraged me to focus my research on the occurrences of RNA editing specific CDS and non-Alu exonic regions. By applying various filters on discrepancies between available ESTs and their corresponding reference genomic sequences, putative RNA editing candidates were identified. High-throughput sequencing was used to validate these candidates. All predicted coordinates appeared to be either SNPs or unedited.
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In a stochastic environment, long-term fitness can be influenced by variation, covariation, and serial correlation in vital rates (survival and fertility). Yet no study of an animal population has parsed the contributions of these three aspects of variability to long-term fitness. We do so using a unique database that includes complete life-history information for wild-living individuals of seven primate species that have been the subjects of long-term (22-45 years) behavioral studies. Overall, the estimated levels of vital rate variation had only minor effects on long-term fitness, and the effects of vital rate covariation and serial correlation were even weaker. To explore why, we compared estimated variances of adult survival in primates with values for other vertebrates in the literature and found that adult survival is significantly less variable in primates than it is in the other vertebrates. Finally, we tested the prediction that adult survival, because it more strongly influences fitness in a constant environment, will be less variable than newborn survival, and we found only mixed support for the prediction. Our results suggest that wild primates may be buffered against detrimental fitness effects of environmental stochasticity by their highly developed cognitive abilities, social networks, and broad, flexible diets.
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Calorie restriction (CR) has been established as the only non-genetic method of altering longevity and attenuating biological changes associated with aging. This nutritional paradigm has been effective in nematodes, flies, rodents, dogs and possibly non-human primates. Its long history notwithstanding, little is known regarding the exact mechanism(s) of CR action or its potential impact on the hypothalamic-pituitary-gonadal (HPG) axis. The objectives of this project were to: 1) analyze neuroendocrine changes to the HPG axis that occur with aging and 2) evaluate the effects of moderate CR on reproductive function in male rhesus macaques. Pituitary gene expression profiling, semi-quantitative RT-PCR (sqRT-PCR) and immunohistochemistry showed circadian clock mechanism components present in three age categories of macaques, demonstrated age differences in expression for Per2, indicated differential expression of Per2 and Bmal1 at opposing time points and revealed daily rhythmic expression of REV-ERBα protein. These data indicate the ability of the macaque pituitary to express core-clock genes, their protein products, and to do so in a 24-hour rhythm. Young Adult CON and CR pituitary gene expression profiles detected potential differential expression in <150 probesets. A decline in>TSHR and CGA was detected in CR macaques as measured by sqRT-PCR. Other genes investigated showed no diet-induced changes. Young Adult CON and CR testicular gene expression profiles detected potential differential expression in <300 probesets although mRNA expression was not altered based on sqRT-PCR and real-time RT-PCR. Age-related>and/or diet-induced changes in HSD17β3, INSL3, CSNK1E and CGA were observed in a separate experiment with CGA in Old Adult CR subjects returning to youthful levels. Semen samples were collected from Young Adult CON and CR macaques. Normal spermiogram measures, ZP-binding, AR assay and SCSA® were conducted and indicated no differences between CON and CR-treated animals. Both groups exhibited similar daily testosterone profiles with no differences in mean or maximum levels; however, daily minimum testosterone levels were lower in CON animals. It appears that moderate CR had limited impact on neuroendocrine or reproductive function in male rhesus macaques based on our selected endpoints. Thus, advantageous CR health benefits can be achieved without obvious negative consequences to the HPG axis.
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BACKGROUND: Like other vertebrates, primates recognize their relatives, primarily to minimize inbreeding, but also to facilitate nepotism. Although associative, social learning is typically credited for discrimination of familiar kin, discrimination of unfamiliar kin remains unexplained. As sex-biased dispersal in long-lived species cannot consistently prevent encounters between unfamiliar kin, inbreeding remains a threat and mechanisms to avoid it beg explanation. Using a molecular approach that combined analyses of biochemical and microsatellite markers in 17 female and 19 male ring-tailed lemurs (Lemur catta), we describe odor-gene covariance to establish the feasibility of olfactory-mediated kin recognition. RESULTS: Despite derivation from different genital glands, labial and scrotal secretions shared about 170 of their respective 338 and 203 semiochemicals. In addition, these semiochemicals encoded information about genetic relatedness within and between the sexes. Although the sexes showed opposite seasonal patterns in signal complexity, the odor profiles of related individuals (whether same-sex or mixed-sex dyads) converged most strongly in the competitive breeding season. Thus, a strong, mutual olfactory signal of genetic relatedness appeared specifically when such information would be crucial for preventing inbreeding. That weaker signals of genetic relatedness might exist year round could provide a mechanism to explain nepotism between unfamiliar kin. CONCLUSION: We suggest that signal convergence between the sexes may reflect strong selective pressures on kin recognition, whereas signal convergence within the sexes may arise as its by-product or function independently to prevent competition between unfamiliar relatives. The link between an individual's genome and its olfactory signals could be mediated by biosynthetic pathways producing polymorphic semiochemicals or by carrier proteins modifying the individual bouquet of olfactory cues. In conclusion, we unveil a possible olfactory mechanism of kin recognition that has specific relevance to understanding inbreeding avoidance and nepotistic behavior observed in free-ranging primates, and broader relevance to understanding the mechanisms of vertebrate olfactory communication.
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Background: Serotonin signaling influences social behavior in both human and nonhuman primates. In humans, variation upstream of the promoter region of the serotonin transporter gene (5-HTTLPR) has recently been shown to influence both behavioral measures of social anxiety and amygdala response to social threats. Here we show that length polymorphisms in 5-HTTLPR predict social reward and punishment in rhesus macaques, a species in which 5-HTTLPR variation is analogous to that of humans. Methodology/Principal Findings: In contrast to monkeys with two copies of the long allele (L/L), monkeys with one copy of the short allele of this gene (S/L) spent less time gazing at face than non-face images, less time looking in the eye region of faces, and had larger pupil diameters when gazing at photos of a high versus low status male macaques. Moreover, in a novel primed gambling task, presentation of photos of high status male macaques promoted risk-aversion in S/L monkeys but promoted risk-seeking in L/L monkeys. Finally, as measured by a "pay-per-view" task, S/L monkeys required juice payment to view photos of high status males, whereas L/L monkeys sacrificed fluid to see the same photos. Conclusions/Significance: These data indicate that genetic variation in serotonin function contributes to social reward and punishment in rhesus macaques, and thus shapes social behavior in humans and rhesus macaques alike. © 2009 Watson et al.