The interaction between a sexually transferred steroid hormone and a female protein regulates oogenesis in the malaria mosquito Anopheles gambiae.
The interaction between a sexually transferred steroid hormone and a female protein regulates oogenesis in the malaria mosquito Anopheles gambiae.
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DOI：
10.1371/journal.pbio.1001695
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发表时间：
2013-10
期刊：
影响因子：
9.8
通讯作者：
Catteruccia F
中科院分区：
文献类型：
--
作者：
Baldini F;Gabrieli P;South A;Valim C;Mancini F;Catteruccia F
在冈比亚按蚊中，雄性在性交过程中转移的类固醇激素会触发一系列分子级联事件，从而增加雌性蚊子的生殖成功。交配过程中雌雄因子之间的分子相互作用深刻地影响着雌虫的生殖行为和生理。在冈比亚按蚊的自然种群中，吸血的雌性蚊子只有在受精时才会将营养资源用于卵子发生。在这里，我们发现这些蚊子的卵子发育依赖于交配的途径是由雄性在交配过程中转移的类固醇激素20-羟基蜕皮激素(20E)和雌性交配诱导的卵子发生刺激蛋白(MISO)之间的相互作用来调节的。MISO的RNAi沉默消除了吸血雌性动物交配导致的卵子发生增加，导致卵母细胞发育延迟，并损害了雄性转移的20E的功能。免疫共沉淀实验表明，MISO和20E在雌性生殖道内相互作用。此外，20E通过蜕皮激素受体诱导交配后MISO的表达，表明这两个因子之间存在密切的协同作用。因此，雄性转移的20E起到了交配信号的作用，雌性通过MISO依赖的途径转化为对卵子发育的更多投资。这种雄性-雌性生殖相互作用的确定为控制传播疟疾的蚊子种群提供了新的机会。冈比亚按蚊是人类疟疾最致命的媒介。这些蚊子的繁殖能力有助于它们作为疾病媒介的作用，因为它确保了疟疾传播的高人口密度。雌性在吸血后发育的卵子数量取决于它们以前是否交配过。事实上，在自然蚊子种群中，处女雌性蚊子在吸血时很少产卵。20-羟基蜕皮激素(20E)是雄性在性交过程中传递的一种类固醇激素，而交配诱导的卵子发生刺激物(MISO)是一种雌性生殖蛋白，它的表达由交配触发并导致产卵量增加。我们发现交配后MISO的表达受20E通过蜕皮激素受体(ECR)调节。实验中沉默的MISO通过减少卵黄生成脂质转运蛋白的表达，降低了交配的雌性在吸血后发育卵子的能力。通过展示雄性蚊子如何促进雌性蚊子的卵子发生，我们确定了一种分子途径，可以有针对性地减少自然蚊子种群的繁殖成功，以帮助控制疟疾。
Steroid hormones transferred by the male during sex trigger a molecular cascade of events that increases the reproductive success of females in Anopheles gambiae mosquitoes. Molecular interactions between male and female factors during mating profoundly affect the reproductive behavior and physiology of female insects. In natural populations of the malaria mosquito Anopheles gambiae, blood-fed females direct nutritional resources towards oogenesis only when inseminated. Here we show that the mating-dependent pathway of egg development in these mosquitoes is regulated by the interaction between the steroid hormone 20-hydroxy-ecdysone (20E) transferred by males during copulation and a female Mating-Induced Stimulator of Oogenesis (MISO) protein. RNAi silencing of MISO abolishes the increase in oogenesis caused by mating in blood-fed females, causes a delay in oocyte development, and impairs the function of male-transferred 20E. Co-immunoprecipitation experiments show that MISO and 20E interact in the female reproductive tract. Moreover MISO expression after mating is induced by 20E via the Ecdysone Receptor, demonstrating a close cooperation between the two factors. Male-transferred 20E therefore acts as a mating signal that females translate into an increased investment in egg development via a MISO-dependent pathway. The identification of this male–female reproductive interaction offers novel opportunities for the control of mosquito populations that transmit malaria. Anopheles gambiae mosquitoes are the most deadly vectors of human malaria. The reproductive ability of these mosquitoes contributes to their role as disease vectors as it ensures high population densities for malaria transmission. The number of eggs developed by females after blood feeding depends on whether they have previously mated. Indeed in natural mosquito populations, virgin females rarely develop eggs when blood fed. Here we report on the identification of a molecular interaction between 20-hydroxy-ecdysone (20E), a steroid hormone transferred by the male during sex, and the Mating-Induced Stimulator of Oogenesis (MISO), a female reproductive protein, expression of which is triggered by mating and leads to increased egg production. We show that the expression of MISO after mating is regulated by 20E via the Ecdysone receptor (EcR). Experimental silencing of MISO reduces the ability of mated females to develop eggs after blood feeding, by reducing expression of a vitellogenic lipid transporter. By showing how male mosquitoes contribute to oogenesis in females, we identify a molecular pathway that can be targeted to reduce the reproductive success of natural mosquito populations to aid malaria control.
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影响因子：
3.4
作者：
Dottorini, Tania;Persampieri, Tania;Crisanti, Andrea
通讯作者：
Crisanti, Andrea
影响因子：
3.8
作者：
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影响因子：
4.8
作者：
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影响因子：
3
作者：
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Rosario, VD
影响因子：
2.2
作者：
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通讯作者：
Noriega, Fernando G.