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

José L. Maestro,Juliana Cobo,Xavier Bellés

doi:10.1074/jbc.m807042200

José L. Maestro, Juliana Cobo + Show 1 more

Open Access

https://doi.org/10.1074/jbc.m807042200

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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.

Highlights

The enzymes 3-hydroxy-3-methylglutaryl coenzyme A (HMGCoA) synthase and HMG-CoA reductase are key in the mevalonate pathway and in the synthesis of juvenile hormone (JH), and both have been cloned in B. germanica [3]
BgTOR mRNA levels in the corpora allata (CA) and the fat body of B. germanica adult females are practically constant throughout the first gonadotrophic cycle, in spite that during it there is a marked feeding cycle [2]
It is worth remembering that CA are the glands synthesizing JH, the gonadotrophic hormone in B. germanica

Summary

Introduction

Given that BgTOR RNAi treatment resulted in a dramatic reduction of JH production, we studied the knockdown effects on the expression of HMG-CoA synthase-1 and -2 [18, 19] and HMG-CoA reductase [20] in CA and fat body. We used CA and fat body tissues from 5-day-old control and BgTOR RNAi groups, and data were normalized by measuring mRNA levels of Actin 5C.

Results

Conclusion