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唾液腺肥大病毒对家蝇(Musca domestica)生殖行为的影响。

Effects of salivary gland hypertrophy virus on the reproductive behavior of the housefly, Musca domestica.

作者信息

Lietze Verena-Ulrike, Geden Christopher J, Blackburn Patrick, Boucias Drion G

机构信息

Department of Entomology and Nematology, University of Florida, PO Box 110620, Gainesville, FL 32611, USA.

出版信息

Appl Environ Microbiol. 2007 Nov;73(21):6811-8. doi: 10.1128/AEM.02694-06. Epub 2007 Sep 7.

Abstract

Pathological studies demonstrated that the salivary gland hypertrophy virus of houseflies (MdSGHV) shuts down reproduction in infected females. The mechanism that underlay the disruption of reproduction functioned on several levels. Females infected at the previtellogenic stage did not produce eggs, reflecting a block in the gonadotropic cycle. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western blot analysis of hemolymph samples demonstrated that MdSGHV infection reduced the levels of both the female-specific hexamerin and egg yolk proteins. Furthermore, reverse transcriptase quantitative real-time PCR data demonstrated that infection blocked hexamerin and yolk protein gene transcription. When females were allowed to develop eggs prior to infection (postvitellogenic stage), the outcome of mating attempts depended upon when mating took place. If egg-containing, virus-infected females were mated within 24 h of infection, they copulated and deposited a single batch of fertilized eggs. However, if mating was delayed for a longer period, the egg-containing females refused to copulate with healthy males. Both of these results suggested that a virus-induced signal influenced the central nervous system, shutting down female receptivity and egg production. All experiments demonstrated that MdSGHV-infected males did not display azoospermia and were fertile. Both healthy females mated with infected males, and the resulting F1 progeny were free of salivary gland hypertrophy symptoms, which suggests that the virus is not sexually or vertically transmitted.

摘要

病理学研究表明,家蝇唾液腺肥大病毒(MdSGHV)会使受感染雌性家蝇停止繁殖。生殖功能受到破坏的机制在多个层面上发挥作用。在前卵黄生成阶段受感染的雌性家蝇不产卵,这反映出促性腺激素周期受阻。对血淋巴样本进行的十二烷基硫酸钠-聚丙烯酰胺凝胶电泳和蛋白质免疫印迹分析表明,MdSGHV感染降低了雌性特异性六聚蛋白和卵黄蛋白的水平。此外,逆转录酶定量实时PCR数据表明,感染会阻断六聚蛋白和卵黄蛋白基因的转录。当雌性家蝇在感染前已发育出卵(卵黄生成后期)时,交配尝试的结果取决于交配发生的时间。如果含有卵的、受病毒感染的雌性家蝇在感染后24小时内交配,它们会交配并产下一批受精卵。然而,如果交配延迟更长时间,含有卵的雌性家蝇会拒绝与健康雄性家蝇交配。这两个结果都表明,病毒诱导的信号影响中枢神经系统,从而抑制雌性家蝇的接受性和产卵。所有实验均表明,受MdSGHV感染的雄性家蝇没有出现无精子症,且具有生育能力。健康雌性家蝇与受感染雄性家蝇交配后,产生的F1后代没有唾液腺肥大症状,这表明该病毒不会通过性传播或垂直传播。

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