Location: Biological Control of Insects Research
Title: Rac1 mediates cytokine-stimulated hemocyte spreading via prostaglandin biosynthesis in the beet armyworm, Spodoptera exigua Authors
|Park, Jiyeong -|
|Kim, Yonggyun -|
Submitted to: Journal of Insect Physiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: April 23, 2013
Publication Date: May 6, 2013
Citation: Park, J., Stanley, D.W., Kim, Y. 2013. Rac1 mediates cytokine-stimulated hemocyte spreading via prostaglandin biosynthesis in the beet armyworm, Spodoptera exigua. Journal of Insect Physiology. 59:682-689. Interpretive Summary: Application of classical insecticides has introduced severe problems in 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. In this paper we report on identification of biological signals responsible for stimulating insect defenses to infection. 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 and users by supporting the long-term sustainability of agriculture.
Technical Abstract: Cell spreading is an integral component of insect hemocytic immune reactions to infections and invasions. Cell spreading is accomplished by cytoskeleton rearrangement, which is activated by three major immune mediators, biogenic monoamines, plasmatocyte-spreading peptide (PSP), and eicosanoids, particularly prostaglandin E2 (PGE2). However, little is known about how these immune mediators activate hemocyte spreading at the intra-cellular level. A small G protein, Rac1, acts in cytoskeleton arrangements in mammalian cells. Based on this information, we identified a Rac1 gene (SeRac1) in hemocytes prepared from Spodoptera exigua. It was expressed in most developmental stages and in the two main immunity-conferring tissues, hemocytes and fat body, in larvae. In response to bacterial challenge, its expression was up-regulated by >37-fold at 2 h post-injection and returned to a basal level about two h later. Silencing SeRac1 expression inhibited hemocyte spreading in response to three immune mediators, octopamine, 5-hydroxytryptamine, and PSP. Addition of PGE2 to SeRac1-silenced larvae rescued the influence of these three mediators on hemocyte spreading. These compounds also increased phospholipase A2 activity via SeRac1, which leads to prostaglandin biosynthesis. We infer that SeRac1 transduces OA, 5-HT, and PSP signaling via activating biosynthesis of prostaglandins and possibly other eicosanoids.