Marine mollusks suffer harmful effects due to environmental organotin compounds such as tributyltin (TBT) and triphenyltin (TPT). It is known that gastropod imposex caused by organotins is mediated by a key nuclear receptor, retinoid X receptor (RXR). The organotin-mediated toxic effects on oysters grown in seawater include a thicker shell, incomplete growth, disrupted development and a high rate of mortality. However, few studies have been conducted to determine the role of RXR in the toxic effects of organotins on bivalves. Here, we cloned an RXR homolog (CgRXR) from the Pacific oyster (Crassostrea gigas) and characterized its molecular function. Expression of the CgRXR RNA transcripts was assessed in whole developmental stages and tissues, with the highest expression detected in the blastula and mantle, respectively. The subcellular localization experiment confirmed that CgRXR protein was expressed in the nucleus exclusively as a nuclear receptor. Electrophoretic mobility shift assay indicated that CgRXR could bind to the DNA motifs DR0-DR5. The dual-luciferase reporter assay demonstrated that the transcriptional activity of CgRXR was activated by conserved ligands (9-cis retinoic acid and cis-4,7,10,13,16,19-docosahexanoic acid) and endocrine-disrupting chemicals (TBT and TPT). These results revealed the conserved gene function involved in protein localization, ligand binding and heterodimer formation with thyroid hormone receptor. However, the DNA binding properties of CgRXR differed from those of other invertebrate and vertebrate RXRs. CgRXR had the highest expression level in the blastula and mantle, and the disrupted development or shell malformation induced by organotins suggested a possible correlation of CgRXR with shell formation in bivalves. The results indicated the potential involvement of CgRXR in the toxic effects of organotins (TBT and TPT) through signaling pathway disruption. Functional characterization of CgRXR will help us better understand the endocrinology of bivalves.

海洋软体动物由于环境有机锡化合物（例如三丁基锡（TBT）和三苯基锡（TPT））而遭受有害影响。众所周知，由有机锡引起的腹足动物的内爆是由关键的核受体类视黄醇X受体（RXR）介导的。有机锡介导的对海水中生长的牡蛎的毒性作用包括壳变厚，生长不完全，发育受阻和高死亡率。但是，很少有研究确定RXR在有机锡对双壳类动物的毒性作用中的作用。在这里，我们从太平洋牡蛎（Crassostrea gigas）克隆了RXR同源物（CgRXR））并表征其分子功能。评估了CgRXR RNA转录本在整个发育阶段和组织中的表达，其中囊胚和套膜中的表达最高。亚细胞定位实验证实CgRXR蛋白在核中仅作为核受体表达。电泳迁移率变动分析表明CgRXR可以结合DNA基序DR0-DR5。双重荧光素酶报告基因测定表明，CgRXR的转录活性被保守的配体（9-顺式视黄酸和顺式4,7,10,13,16,19-二十二碳六烯酸）和破坏内分泌的化学物质（TBT和TPT）。这些结果揭示了保守的基因功能，涉及蛋白质定位，配体结合和与甲状腺激素受体的异二聚体形成。然而，CgRXR的DNA结合特性不同于其他无脊椎动物和脊椎动物RXR。CgRXR在囊泡和地幔中具有最高的表达水平，并且由有机锡诱导的发育受破坏或壳畸形表明双壳类动物中CgRXR与壳的形成可能相关。结果表明，CgRXR可能通过信号传导途径的破坏参与有机锡（TBT和TPT）的毒性作用。CgRXR的功能表征将帮助我们更好地了解双壳类动物的内分泌学。有机锡诱导的发育中断或壳畸形表明，CgRXR与双壳类动物壳形成可能相关。结果表明，CgRXR可能通过信号传导途径的破坏参与有机锡（TBT和TPT）的毒性作用。CgRXR的功能表征将帮助我们更好地了解双壳类动物的内分泌学。有机锡诱导的发育中断或壳畸形表明，CgRXR与双壳类动物壳形成可能相关。结果表明，CgRXR可能通过信号传导途径的破坏参与有机锡（TBT和TPT）的毒性作用。CgRXR的功能表征将帮助我们更好地了解双壳类动物的内分泌学。