Genes encoding allatostatin CC (AST-CC) were discovered relatively recently following a search of various arthropod genomes (Veenstra, 2009). The gene encoding AST-CC is a paralog of the allatostatin C (AST-C) gene. Both these genes are homologous to the vertebrate somatostatins. Interestingly, AST-CC encoding precursors have a signal anchor instead of the N-terminal signal peptide in several arthropods including Drosophila, tsetse flies, Zootermopsis nevadensis and Procambarus clarkii (Veenstra, 2015). Thus, AST-CC may function in a juxtacrine manner as opposed to an endocrine or paracrine factor in these species. However, AST-CC precursors in other species such as Tribolium castaneum, Rhodnius prolixus and Apis mellifera have a classical signal peptide. Like AST-C, arthropod AST-CCs contains two cysteine residues, which suggests that the peptide becomes cyclized by a disulfide bridge. In T. castaneum, there is a single somatostatin-like GPCR, which is activated by both AST-C and AST-CC; however, T. castaneum AST-C is a bit more potent (EC50 value = 25 nM) than AST-CC (EC50 value = 105.7 nM) (Audsley et al., 2013).
In D. melanogaster, AST-CC is co-expressed with CCAP, AstB and bursicon in bilaterally paired neurons in each of the four abdominal neuromeres in the larvae. These neurons are important in initiating the switch from pre-ecdysis to ecdysis behavior (Kim et al., 2015).
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