July 7, 2019  |  

Scallop genome reveals molecular adaptations to semi-sessile life and neurotoxins.

Authors: Li, Yuli and Sun, Xiaoqing and Hu, Xiaoli and Xun, Xiaogang and Zhang, Jinbo and Guo, Ximing and Jiao, Wenqian and Zhang, Lingling and Liu, Weizhi and Wang, Jing and Li, Ji and Sun, Yan and Miao, Yan and Zhang, Xiaokang and Cheng, Taoran and Xu, Guoliang and Fu, Xiaoteng and Wang, Yangfan and Yu, Xinran and Huang, Xiaoting and Lu, Wei and Lv, Jia and Mu, Chuang and Wang, Dawei and Li, Xu and Xia, Yu and Li, Yajuan and Yang, Zhihui and Wang, Fengliang and Zhang, Lu and Xing, Qiang and Dou, Huaiqian and Ning, Xianhui and Dou, Jinzhuang and Li, Yangping and Kong, Dexu and Liu, Yaran and Jiang, Zhi and Li, Ruiqiang and Wang, Shi and Bao, Zhenmin

Bivalve molluscs are descendants of an early-Cambrian lineage superbly adapted to benthic filter feeding. Adaptations in form and behavior are well recognized, but the underlying molecular mechanisms are largely unknown. Here, we investigate the genome, various transcriptomes, and proteomes of the scallop Chlamys farreri, a semi-sessile bivalve with well-developed adductor muscle, sophisticated eyes, and remarkable neurotoxin resistance. The scallop's large striated muscle is energy-dynamic but not fully differentiated from smooth muscle. Its eyes are supported by highly diverse, intronless opsins expanded by retroposition for broadened spectral sensitivity. Rapid byssal secretion is enabled by a specialized foot and multiple proteins including expanded tyrosinases. The scallop uses hepatopancreas to accumulate neurotoxins and kidney to transform to high-toxicity forms through expanded sulfotransferases, probably as deterrence against predation, while it achieves neurotoxin resistance through point mutations in sodium channels. These findings suggest that expansion and mutation of those genes may have profound effects on scallop's phenotype and adaptation.

Journal: Nature communications
DOI: 10.1038/s41467-017-01927-0
Year: 2017

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