Sugar is attractive to human and almost all other animals. In nature, Sweet indicates sugar, the one of essential nutrients and the source of energy. It influences the choice of what to eat. To meet the demand of good taste with low-calorie addition, various sweeteners with diversity in both structure and resource are developed and applied in food industries. How do they inspire sweet sensory and how sweet signal is transducted to brain? To solve these problems, far before the discovery of sweet receptor genes, effords were made to build binding model for sweeteners and receptors via the shared structure of known sweet substance, as well as to uncover the signal pathway in cell and between neurons. Human beings are so arrogant that we took the idea all animals were supposed to share our sensation for granted for a very long time. fortunately，people noticed the differences of sweet perception between species gradually. The whole picture of how sweet taste sensation works and evolves is still obsure. The discovery of sweet taste receptor provides a new angle to this problem. Althought sweet taste receptor is conserve in mammal, several spiecse over the phylogenetic tree abtain sweet receptor genes pseudogenized. That might explain why animals like cat cannot detect sweet taste. Primates, animals most closed to human and well studied phylogeneticly, shows differences in sweet perception. It is found that, not like old world monkey, new world monkeys and prosimians cannot detect sweet proteins and artificial sweeteners. Glaser and Norfre regarded that it was a main change happened at the divergent node for old world monkey, to prepare them have a higher sweet taste grade “simian grade”,departuring from ancestory “primitive grade” . We report an overall pattren of the evolution of sweet receptor in primates for the first time by construct common ancestors’ sequences. We find no gather of changes on any branch. It might refer an unexpected complexity existing in the evolution process. Both of Tas1r2 and Tas1r3 are suffered purifying selection, but in different ways. The difference of amino acid substitutions on every branch shows significance in Tas1r3, not in Tas1r2. Positive selection sites (pr > 0.5) are found distributing in binding region. It consists with previous study in other GPCR genes. Then we map the proved functional sites to the phylogenetic tree and find out there are different reason for Aspartame nontasters in primates and a relatively cleared process of evolution is shown in Tas1r3. To sum up, we find out two regular patterns. The one is the ability of detection sweeteners are strengthened via an extremly complicated way. The other is the evolution of Tas1r2 and Tas1r3 is imbanlanced. Co-evolution sites within and between Tas1r2 and Tas1r3 are scaned to provide additional reason for the different evolution details between these two genes. Finally, we construct sweet taste receptor gene expression vectors in five primates; enable the colletction of response data of primate sweet receptors to sweeteners on cell level. Key words: sweet receptor, natural selection, adaptive evolution, coevolution
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