کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
1982027 1539491 2015 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Frizzled 2 is a key component in the regulation of TOR signaling-mediated egg production in the mosquito Aedes aegypti
موضوعات مرتبط
علوم زیستی و بیوفناوری علوم کشاورزی و بیولوژیک دانش حشره شناسی
پیش نمایش صفحه اول مقاله
Frizzled 2 is a key component in the regulation of TOR signaling-mediated egg production in the mosquito Aedes aegypti
چکیده انگلیسی


• Silencing of AaFz2 resulted in the decrease of the mosquito fecundity.
• AaFz2 was highly expressed in the mosquito fat body post a blood meal.
• AaFz2 played important role in the regulation of TOR signaling.

The Wnt signaling pathway was first discovered as a key event in embryonic development and cell polarity in Drosophila. Recently, several reports have shown that Wnt stimulates translation and cell growth by activating the mTOR pathway in mammals. Previous studies have demonstrated that the Target of Rapamycin (TOR) pathway plays an important role in mosquito vitellogenesis. However, the interactions between these two pathways are poorly understood in the mosquito. In this study, we hypothesized that factors from the TOR and Wnt signaling pathways interacted synergistically in mosquito vitellogenesis. Our results showed that silencing Aedes aegypti Frizzled 2 (AaFz2), a transmembrane receptor of the Wnt signaling pathway, decreased the fecundity of mosquitoes. We showed that AaFz2 was highly expressed at the transcriptional and translational levels in the female mosquito 6 h after a blood meal, indicating amino acid-stimulated expression of AaFz2. Notably, the phosphorylation of S6K, a downstream target of the TOR pathway, and the expression of vitellogenin were inhibited in the absence of AaFz2. A direct link was found in this study between Wnt and TOR signaling in the regulation of mosquito reproduction.

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ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Insect Biochemistry and Molecular Biology - Volume 61, June 2015, Pages 17–24
نویسندگان
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