## 1 Introduction  
Reproductive physiology in animals is strictly regulated by hormones. However, depending on the species, these hormones and their specific contributions may differ. This is illustrated nicely by reports on the endocrine regulation of the female reproductive physiology in a wide variety of insect species (as reviewed by [1]). Two important players in this process are the sesquiterpenoid, juvenile hormone (JH), and the ecdysteroid, 20-hydroxycedysone (20E). Both lipophilic hormones are also key in the control of larval development and metamorphosis of insects. Whereas 20E triggers successive molts throughout the insect's life cycle, JH, as its name indicates, represses metamorphosis and thus keeps the insect in a juvenile stage. Ecdysone is synthesized in the prothoracic glands of juvenile insects. These glands degenerate in adult insects and ecdysteroid synthesis takesplace in the reproductive system [2; 3; 4]. JH on the other hand is produced in the _corpora allata_ (CA), small paired endocrine glands situated in the head [3; 4; 5]. Important enzymes catalyzing the final steps of JH biosynthesis in the desert locust's CA are juvenile hormone acid O-methyltransferaseasferase (JHAMT) and methyl farnesoate epoxidase (CYP15A1) [6]. The 20E signaling pathway with its heterodimeric receptor complex, consisting of ecdysone receptor (EcR) and retinoid X receptor/ultraspiracle (RXR/USP), and downstream transcription factors, many belonging to the nuclear receptor superfamily, has been widely researched [7]. However, for a long time the JH signaling pathway remained elusive. Methoprene-tolerant (Met), a member of the basic-helix-loop-helix (bHLH)/Per-Arnt-Sim (PAS) family of transcription factors, was first described in 1986 as a crucial factor in the resistance to the commercially available JH analog, Methoprene [8]. The possibility that Met might act as a JH receptor was later confirmed by [PERSON] _et al._, who showed that the recombinant _Drosophila melanogaster_ Met protein can bind JH with high affinity [9]. The study by [PERSON] et al. later showed that a _Tribolium castaneum_ Met contains a conserved hydrophobic binding pocket within the PAS-B domain, which binds JH and its analogs with high affinity, and that this capacity is necessary for interaction of Met with its partner, another member of the bHLH-PAS family named SRC (homologous to the mammalian steroid receptor coactivator 1) or Taiman (Tai), following FlyBase nomenclature [10]. Tai had previously been shown in yeast two-hybrid studies to interact with Met [11; 12]. Further downstream of the Met-Tai complex, the JH signal was later found to be transduced by Kruppel-homolog 1 (Kr-h1), a C2H2 zinc-finger containing transcription factor [13]. In various insect species, RNA interference (RNAi) based reverse genetics studies showed that Met, its binding partner Tai, and their downstream transcription factor Kr-h1 are indeed transducing the anti-metamorphic JH signal [14; 15; 16; 17; 18; 19; 20]. Key regulators of metamorphosis are often referred to as the MEKRE93 pathway, composed of the JH receptor Met and the transcription factors Kr-h1 and E93. Expression of E93, a key determinant promoting adult morphogenesis, is repressed by Kr-h1 during larval-to-larval transitions but will rise once JH titers drop and Kr-h1 expression is lowered before the onset of metamorphosis [21; 22; 23]. Studies on Met, Tai and Kr-h1 were further elaborated towards other processes in which JH was reported to play a role, such as the developmental maturation of the female reproductive system and the reproductive diapause that is observed in a variety of insect species [24; 25; 26; 27; 28; 29; 30; 31]. A recent study in the migratory locust, _Locusta migratoria_, has shown that one isoform of Tai contains a PRD-repeat motif that is essential for the induction of vitellogenesis by JH [32].