Target of rapamycin (TOR) controls vitellogenesis via activation of the S6 kinase in the fat body of the tick, Haemaphysalis longicornis

• Published in: International journal for parasitology 2012-10, Vol.42 (11), p.991-998
• Main Authors: Umemiya-Shirafuji, Rika, Boldbaatar, Damdinsuren, Liao, Min, Battur, Banzragch, Rahman, Md. Morshedur, Kuboki, Thasaneeya, Galay, Remil Linggatong, Tanaka, Tetsuya, Fujisaki, Kozo
• Format: Article
• Language: English
• Subjects: 1-Phosphatidylinositol 3-kinase; Animals; Biological and medical sciences; Cloning, Molecular; Enzyme Activation - physiology; Fat body; Fat Body - enzymology; Female; Fundamental and applied biological sciences. Psychology; GATA; Gene silencing; Haemaphysalis longicornis; Hemolymph; Ixodidae; Life cycle. Host-agent relationship. Pathogenesis; Molecular Sequence Data; mRNA; Nutrient availability; Oocytes; Ovaries; Phosphorylation; Protozoa; Rapamycin; Reproduction; Ribosomal Protein S6 Kinases - genetics; Ribosomal Protein S6 Kinases - metabolism; RNA Interference; RNA, Messenger - genetics; RNA, Messenger - metabolism; RNA-mediated interference; S6K; Sirolimus - pharmacology; Target of rapamycin; Tick; Ticks - enzymology; Ticks - metabolism; TOR protein; TOR Serine-Threonine Kinases - antagonists & inhibitors; TOR Serine-Threonine Kinases - genetics; TOR Serine-Threonine Kinases - metabolism; Transcriptome; Vitellogenesis; Vitellogenesis - drug effects; Vitellogenesis - physiology; Vitellogenin
• ISSN: 0020-7519; 1879-0135
• DOI: 10.1016/j.ijpara.2012.08.002

[Display omitted] ► Target of rapamycin (TOR) RNA interference (RNAi) inhibited S6K phosphorylation in the tick fat body. ► TOR RNAi led to decreased expression of GATA and vitellogenins (Vgs). ► TOR RNAi delayed oocyte development. ► Rapamycin inhibited S6K phosphorylation and reduced Vg expression in the fat body. ► Vgs were not detected in rapamycin-treated fat bodies in the presence of 20E. Vitellogenin (Vg) synthesis, vitellogenesis, is an essential process for the development and reproduction of ticks. Our previous finding led to the hypothesis that target of rapamycin (TOR) pathway is important for vitellogenesis in the hard tick, Haemaphysalis longicornis. The TOR pathway controls cellular activity according to nutrient availability in eukaryotes. TOR, a member of the phosphatidylinositol 3-kinase family, is a central player in this pathway. Here, we present preliminary evidence that H. longicornis TOR (HlTOR) controls vitellogenesis via activation of S6 kinase (S6K) in the fat body. RNA interference (RNAi)-mediated gene silencing of HlTOR was undertaken to elucidate the involvement of HlTOR in the vitellogenesis of the tick. HlTOR-RNAi caused inhibition of S6K phosphorylation in the fat body. HlTOR-RNAi also altered not only the expression levels of GATA mRNA and protein but also the intracellular localisation of GATA in the fat body. The expression levels of Vg mRNA and protein in the fat body of HlTOR-RNAi ticks were significantly lower than those in control ticks. In the pre-ovipositional stage, the ovaries of control ticks had brown oocytes developing, but those of HlTOR-RNAi ticks were white and immature. The haemolymph colour indicated that the amount of Vg was lower in HlTOR-RNAi ticks than in the controls. Furthermore, rapamycin inhibited S6K phosphorylation and reduced the expression levels of Vg mRNA and protein in the fat bodies. Vg proteins were not detected in rapamycin-treated fat bodies in the presence of 20-hydroxyecdysone. These results suggest that HlTOR activity is critical for vitellogenesis stimulated by 20-hydroxyecdysone.