15:45 - 17:15
Tue-P1
Room: Waalsprong 4
Synchronized expansion and contraction of olfactory, vomeronasal, and taste receptor gene families in hystricomorph rodents
Tue-P1-012
Presented by: Yoshihito Niimura
Yoshihito Niimura 1, Bhim Biswa 2, 3, Takushi Kishida 4, Atsushi Toyoda 2, Masato Ito 5, Kazushige Touhara 5, Miho Inoue-Murayama 6, Scott Jenkins 6, Christopher Adenyo 7, Boniface Kayang 7, Tsuyoshi Koide 2, 3
1 University of Miyazaki, 2 National Institute of Genetics, 3 SOKENDAI (The Graduate University for Advanced Studies), 4 Nihon University, 5 The University of Tokyo, 6 Kyoto University, 7 University of Ghana
Chemical senses, olfaction, pheromone, and taste, are essential for the survival of most animals. It is well known that different modalities of senses compensate for each other, e.g., primates with a well-developed vision have retrogressed olfaction. However, it is unclear whether such compensation occurs in evolution between different modalities of chemical senses. To address this question, we examined three receptor gene families for olfaction, pheromone, and taste, with a similar structure: olfactory receptor (OR), vomeronasal receptor type 1 (V1R), and bitter taste receptor (T2R) genes in Hystricomorpha, which is morphologically and ecologically the most diverse group of rodents. We also newly sequenced a high-quality genome assembly for the grasscutter, Thryonomys swinderianus. We identified orthologous gene groups among hystricomorph rodents for these gene families to separate the gene gain and loss events that occurred in each phylogenetic branch during Hystricomorpha evolution. The analyses revealed that the three gene families have expanded or contracted synchronously rather than compensatorily, suggesting that the development of one chemical sense cannot compensate for another. The results also showed that V1R genes evolved the most rapidly, followed by OR genes, and T2R genes were the most evolutionarily stable, reflecting the biological significance of each receptor family’s ligands.
This work was supported by a Grant-in-Aid for Scientific Research (JSPS KAKENHI Grant Number 18K06359 to Y. N. and 19KK0177 to T. Koide) and by JST aXis Grant Number JPMJAS2017 to Y. N., A. T., M. I-M., and T. Koide and by National Institute of Genetics, NIG-Joint (1B2020) to M. I-M.