Fig. 10

Proposed, putative mode of CFSH action in crustaceans based on the previous and present findings. First, CFSH is produced in the X-organ, temporally stored in the sinus glands, and released into the hemolymph. Then, binding of CFSH to CFSHR activates the intracellular signal transduction factors, which further triggers the rapid activation of the Wnt signaling and steroidogenesis. In the Wnt signaling cascade, the activated Wnt ligands bind to Frizzled and LRP6 receptors, leading to the phosphorylation of LRP6 and the disassembly of the destruction complex (DVL/AXIN/GSK3β/CK1/β-catenin), allowing the release of the stabilized β-catenin to cytoplasm. The free β-catenin is subsequently translocated into cell nucleus, stimulating cyclin D expression in concert with TCF. The up-regulated cyclin D expression promotes cell cycle progression, cell proliferation and tissue differentiation. On the other hand, with the increase in hemolymph cholesterol level, CFSH may increase E2 synthesis and release in the ovigerous setae via up-regulating StAR3 expression. The elevated E2 levels may trigger tissue differentiation via activating the transcription of cuticle and tubulin genes. The identification of CFSHR and CFSH signal transduction factors, the regulatory interaction among CFSH, the Wnt signaling and cell cycle pathways, and cuticle and tubulin genes, and ‘?’ requiring a further study. Abbreviations: TCF (T-cell factor), P450scc (P450 side-chain cleavage); StAR3 (StAR-related lipid transfer protein 3); 3βHSD (3β-hydroxysteroid dehydrogenase); P450c17 (17α-hydroxylase/17, 20-lyase); 17βHSD (17β-hydroxysteroid dehydrogenase); P450arom (P450 aromatase); and DHEA (dehydroepiandrosterone)