natural-products-in-plant-pest-management
natural-products-in-plant-pest-management
natural-products-in-plant-pest-management
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154 H.N. Verma and V.K. BaranwalThe <strong>in</strong>duced antiviral state <strong>in</strong> N. glut<strong>in</strong>osa by SRI from C. aculeatumdecreased considerably after 3 days (Verma and Varsha, 1994). However, theresistance <strong>in</strong>duc<strong>in</strong>g ability of C. aculeatum SRI could be enhanced up to6 days by prim<strong>in</strong>g it with certa<strong>in</strong> prote<strong>in</strong>aceous additives (Verma and Versha,1994). The activity is probably enhanced by modification or enhanced stabilityof prote<strong>in</strong>aceous <strong>in</strong>ducers by these additives. Thus, one unexploitedapproach to eng<strong>in</strong>eer<strong>in</strong>g virus resistance is the manipulation of <strong>in</strong>ducibledefences <strong>in</strong> <strong>plant</strong>s. The production of systemic resistance by the use of botanicalswill be effective aga<strong>in</strong>st a broad spectrum of viruses and will not breakdown when <strong>plant</strong>s are exposed to high temperatures.Suppression of disease symptoms by true <strong>in</strong>hibitors may be accomplishedeither by act<strong>in</strong>g on the first stage of the <strong>in</strong>fection process, which is theadsorption of the virus <strong>in</strong>to the host cell, or by block<strong>in</strong>g or compet<strong>in</strong>g withthe virus receptor sites on the leaf surface (Ragetli, 1957; Ragetli andWei ntraub, 1962) or by affect<strong>in</strong>g the susceptibility of the host by alter<strong>in</strong>g hostcell metabolism (Verma and Awasthi, 1979). Bozarth and Ross (1964) suggestedthe phenomenon of SAR as a result of the <strong>in</strong>itial <strong>in</strong>fection by which asignal was generated at the site of application and transported throughoutthe <strong>plant</strong> to respond more effectively to the subsequent <strong>in</strong>fection.Induction of systemic resistance by resistance <strong>in</strong>ducers obta<strong>in</strong>ed from<strong>plant</strong> extracts was first detailed by Verma and Mukerjee (1975). Extracts froma few <strong>plant</strong>s <strong>in</strong>duce an antiviral state by act<strong>in</strong>g through an act<strong>in</strong>omyc<strong>in</strong> D(AMD) sensitive mechanism (Verma and Awasthi, 1979; Verma et al., 1984).AMD is an <strong>in</strong>hibitor of prote<strong>in</strong> synthesis at the transcription level. Concomitantapplication of AMD with SRI reversed the <strong>in</strong>duction of resistance <strong>in</strong>susceptible <strong>plant</strong>s. However, <strong>in</strong>duction of resistance rema<strong>in</strong>s unaffectedwhen AMD is applied 12 h post-treatment. This gives an <strong>in</strong>dication that<strong>plant</strong>-extract-<strong>in</strong>duced resistance is a host-mediated response (Verma et al.,1979).The activity at a distance from the po<strong>in</strong>t of application might be expla<strong>in</strong>edby the supposition that the SRI present <strong>in</strong> the <strong>plant</strong> extract selectively attachesat the surface, and a type of cha<strong>in</strong> reaction starts that elicits the transcriptionof defence-related genes, lead<strong>in</strong>g to the production of a new VIA (Verma andAwasthi, 1979).Ribosome <strong>in</strong>activat<strong>in</strong>g prote<strong>in</strong>s (RIPs)The basic prote<strong>in</strong>s that function by <strong>in</strong>activat<strong>in</strong>g the ribosome of the host havebeen called RIPs. The RIPs have been shown to be N-glycosidases, whichremove a specific aden<strong>in</strong>e base <strong>in</strong> a conserved loop of the 28s rRNA ofeukaryotic organisms (Endo and Tsurugi, 1987; Endo et al., 1987) or the 23srRNA of prokaryotes (Hartely et al., 1991). Such damaged ribosomes can nolonger b<strong>in</strong>d the elongation factor-2 (Gessner and Irv<strong>in</strong>, 1980; Rodes and Irv<strong>in</strong>,1981). The RIPs damage the ribosome, arrest prote<strong>in</strong> synthesis and cause celldeath. RIPs show antiviral activity aga<strong>in</strong>st both animal and <strong>plant</strong> viruses(Barbieri and Stirpe, 1982) and have been classified <strong>in</strong>to two types (Stirpe