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Updated: Jul 15, 2026

Assessment of Social Cognition in Non-human Primates Using a Network of Computerized Automated Learning Device (ALDM) Test Systems
Published on: May 5, 2015
Abstract:
The goal of the International Alt/Self Project (IASP) is to determine the molecular basis of societal altruistic and selfish behaviour in primate societies. In order to solve this difficult problem, an International Consortium comprising genomists and psycho-biologists from the G-8 countries has been created. In a first step it was decided to concentrate on extreme opposite phenotypes manifesting in Homo sapiens sapiens: the hyper-altruism syndrome (HAS) and the hyper-selfishness syndrome (HSS). Conventional association methods, using the most powerful tools provided by the SNR, and the HumMap projects, resulted in the preliminary mapping of the ''altruist'' locus, and the ''selfish'' locus, both in the pseudo-autosomal region of the short arm of chromosome X. Transcriptional studies using 1000K chips showed that an unannotated sequence was overexpressed in HAS and underexpressed in HSS individuals. This mirror pattern of expression suggested that the two deviant states might be allelic. This hypothesis was substantiated by genome studies using GGH-array. Ultimately different mutations in expressed genomic sequences showed a striking genotype-phenotype correlation: gain-of-function (GOF) mutations were invariably found in the HAS group, whereas loss-of-function (LOF) mutations were invariably found in the HSS group. These results demonstrate that a same and unique novel gene, coined DARWIN, is involved in the two opposite deviant phenotypes, suggesting that the morbid locus is a GTL (quantitative trait locus). Preliminary comparative data obtained in non-human primates showed that the DARWIN gene is highly conserved. Like humans, chimpanzees (Pan troglodytes) have a single expressed gene copy located in a stable genomic domain, whereas the highly benevolent bonobo primate (Pan paniscus) has several expressed gene copies, located in a copy number variable region (CNVR), a situation that buffers phenotypic manifestation of LOF mutations.
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