Mutation of Drosophila dopamine receptor DopR leads to male-male courtship behavior

Mutation of Drosophila dopamine receptor DopR leads to male-male courtship behavior
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果蝇多巴胺受体 DopR 的突变导致雄性之间的求偶行为。

DOI:
10.1016/j.bbrc.2012.06.003
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发表时间:
2012-07-06
影响因子:
3.1
通讯作者:
Guo, Aike
Guo, Aike
中科院分区:
生物学4区
文献类型:
--
作者:
Chen, Bin;Liu, He;Guo, Aike

文献摘要

被引文献

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在果蝇中,多巴胺作为一种神经调节剂在许多生物过程中起着重要作用。先前的研究表明,多巴胺水平会影响苍蝇的求偶行为。多巴胺水平紊乱会以两种不同的方式导致不正常的求爱行为。多巴胺水平上调导致雄性果蝇的求偶行为,而多巴胺水平下调导致雄性果蝇对其他雄性果蝇的性吸引力增加。直到现在,多巴胺受体的身份参与这种不正常的雄性雄性求爱行为仍然是未知的。本文采用遗传方法研究了多巴胺受体在果蝇求偶行为中的作用。我们发现一种多巴胺d -1样受体DopR参与了果蝇的求偶行为。DopR突变雄性果蝇表现出雄性与雄性之间的求偶行为。这种行为主要是由于雄性越来越倾向于向其他雄性求爱。功能性DopR的表达成功地挽救了这种突变表型。d -2样受体D2R和另一个d -1样受体DAMB的敲除不会诱导雄性雄性的求爱行为,这表明了这种现象的受体类型特异性。我们的发现为多巴胺水平紊乱与诱导的雄性求爱行为之间的可能联系提供了见解。(C) 2012爱思唯尔公司版权所有。
In Drosophila, dopamine plays important roles in many biological processes as a neuromodulator. Previous studies showed that dopamine level could affect fly courtship behaviors. Disturbed dopamine level leads to abnormal courtship behavior in two different ways. Dopamine up-regulation induces male-male courtship behavior, while down-regulation of dopamine level results in increased sexual attractiveness of males towards other male flies. Until now, the identity of the dopamine receptor involved in this abnormal male-male courtship behavior remains unknown. Here we used genetic approaches to investigate the role of dopamine receptors in fly courtship behavior. We found that a dopamine D-1-like receptor, DopR, was involved in fly courtship behavior. DopR mutant male flies display male-male courtship behavior. This behavior is mainly due to the male's increased propensity to court other males. Expression of functional DopR successfully rescued this mutant phenotype. Knock-down of D-2-like receptor D2R and another D-1-like receptor, DAMB, did not induce male-male courtship behavior, indicating the receptor-type specificity of this phenomenon. Our findings provide insight into a possible link between dopamine level disturbance and the induced male-male courtship behavior. (C) 2012 Elsevier Inc. All rights reserved.