|DONG, SHENGZHANG - University Of Missouri|
|ZHANG, HONGWEI - University Of Missouri|
|CHEN, XI - University Of Missouri|
|YU, XIAOPING - China Jiliang University|
|SONG, QISHENG - University Of Missouri|
Submitted to: Archives of Insect Biochemistry and Physiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/27/2015
Publication Date: 3/27/2015
Citation: Dong, S., Zhang, H., Chen, X., Stanley, D.W., Yu, X., Song, Q. 2015. THE NEUROPEPTIDE BURSICON ACTS IN CUTICLE METABOLISM. Archives of Insect Biochemistry and Physiology. doi:10.1002/arch.21227.
Interpretive Summary: Application of classical insecticides has introduced severe problems into agricultural sustainability. The concept of biological control of insects is a potentially powerful alternative to classical insecticides. Biological control is based on the idea that direct application of insect-specific pathogens and parasites can reduce pest insect populations and the economic damage due to pest insects. The problem, however, is the efficiency of these organisms in biological control programs is limited by insect immune defense reactions to challenge. One approach to improving the efficiency of biocontrol agents would be to somehow disable insect immune reactions to viral, bacterial, fungal and parasitic infections. With this goal, we are investigating how insect immune reactions to infection are signaled within insect bodies. In this paper we report on identification of biological signals that are responsible for stimulating insect defenses prior to infection, that is, in a prophylactic manner. This new research will be directly useful to scientists who are working to improve the efficacy of biological control methods. The ensuing improved biological control methods will benefit a wide range of agricultural producers by supporting the long-term sustainability of agriculture.
Technical Abstract: Bursicon is a neuropeptide composed of two cysteine knot proteins, bursicon a (burs a) and bursicon b (burs b), responsible for cuticle tanning (melanization and sclerotization) and for wing expansion in newly-eclosed adult Drosophila melanogaster, and probably most insect species. Aside from forming the heterodimeric bursicon neuropeptide, the bursicon subunits also form burs a-a and burs b-b homodimers. The homodimers act through unidentified novel receptors and the NF-kB transcription factor, Relish, to induce expression of genes encoding antimicrobial peptides during molting. In this paper, we posed the hypothesis that the bursicon homodimers stimulate expression of genes encoding two stress proteins via the pleiotropic JAK/STAT signal pathway. Here, we show that neck-ligating newly-eclosed adult flies repressed expression of TotA and Tep1 and phosphorylation of the transcription factor STAT92E. Treating ligated adults with rburs b'b homodimers restored phosphorylation of STAT92E, leading to increased expression of TotA and Tep1. The homodimers also increased expression of the endogenous cytokines Unpaired 2 (Upd2) and Upd3, upstream of JAK/STAT in the first 30 min post-treatment. We infer that bursicon homodimers act via the Drosophila JAK/STAT pathway.