Target of Rapamycin (TOR) Mediates the Transduction of Nutritional Signals into Juvenile Hormone Production

Abstract

Anautogeny is a reproductive strategy by which females do not reproduce until they feed. Therefore, nutritional signals must inform the reproductive tissues, and cells that the organism has reached a nutritional status suitable for triggering reproductive processes. One of the possible pathways involved in anautogeny is the "target of rapamycin" (TOR) pathway, which has been described as connecting the nutritional status with growth, proliferation, and cancer. The German cockroach, Blattella germanica, is an anautogenous species whose vitellogenesis is governed by juvenile hormone. In the present report, we describe the cloning of TOR cDNA from B. germanica (BgTOR). Expression studies showed that BgTOR is expressed in adult female corpora allata and fat body. BgTOR knockdown using systemic RNAi in vivo produced a severe inhibition of juvenile hormone synthesis in adult female corpora allata, together with a reduction of mRNA levels corresponding to 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) synthase-1, HMG-CoA synthase-2, and HMG-CoA reductase. In addition, there was a reduction of vitellogenin mRNA in the fat body, and ovaries did not grow. Analysis of TOR expression in corpora allata of fed and starved females suggested that TOR is not regulated at the transcriptional level. Nevertheless, there was a reduction in HMG-CoA synthases and reductase mRNA in corpora allata (but not in the fat body) of starved females, together with a dramatic reduction of juvenile hormone production and ovary development. Taken together, our results indicate that TOR knockdown mimics starvation in terms of corpora allata activity, and suggest that nutritional signals that activate juvenile hormone biosynthesis and vitellogenin production are mediated by the TOR pathway.

IRS and TOR nutrient-signaling pathways act via juvenile hormone to influence honey bee caste fate

“…An in vitro experiment using cultured corpora allata (the glands that produce JH) from Blatella germanica showed that downregulation of TOR leads to reduced JH production (Maestro et al, 2009). Our results take this insight a step forward to establish the interactions between IRS, TOR and JH at an organismal level.…”

The ontogenetic saga of a social brain

“…(Barchuk et al 2007). This model has proven to be useful, and virtually, all interactions have been supported experimentally (Patel et al 2007;Kucharski et al 2008;Maestro et al 2009;Mutti et al 2011). All, that is, except for the confounding data on nervous system development that have been obtained from microarray experiments using whole body samples.…”

“…These differences promote the establishment of caste-specific hormonal environments, which in turn drive the expression of different groups of effector genes (Ulrich and Rembold 1983;Hartfelder and Engels 1998;Barchuk et al 2007;Maestro et al 2009;Mutti et al 2011;Moda et al 2013). These may be considered to be the molecular responsible for the development of the initially larger brain seen in queen larvae.…”

Juvenile Hormone Regulates Vitellogenin Gene Expression through Insulin-like Peptide Signaling Pathway in the Red Flour Beetle, Tribolium castaneum

“…Application of JH III to these small mosquitoes could initiate vitellogenesis with only one blood meal (15). Recent work in B. germanica also showed that TOR mediated nutrition status affects Vg gene expression and JH levels (16). In lubber grasshoppers, a cumulative feeding threshold is required for vitellogenesis and can be obviated with JH treatment (17).…”

“…D, shown is the time-course of Vg2 mRNA induction by insulin (Ins). Vg2 mRNA levels were measured by qRT-PCR in the fat body isolated from day 2 PAE beetles at 8,16, and 24 h after injection of 100 nl of H 2 O or 10 mg/ml bovine insulin. E, insulin induces Vg2 mRNA even in starved beetles.…”