تأثیر سیلیکون و نانو ذرات سیلیکون بر بیماری‌ لکه‌موجی سیب‌زمینی و گوجه‌فرنگی در شرایط گلخانه‌ای و آزمایشگاهی

Early blight is one of the most important diseases of potato and tomato which causes the great damage to yield of potato and tomato in the fields of East Azerbaijan province. In this research, the influence of some plant disease resistance inducers including silicon and nanoparticles of silicon in induction of systemic acquired resistance (SAR) in potato and tomato plants and control of early blight on them was studied in vitro and in vivo conditions. In glasshouse experiment, first the plants were treated two times in 5 days intervals with different concentrations of silicon and nanosilicon and after 48 hours were inoculated with spore suspension of Alternaria alternata. This experiment was conducted as a completely randomized design with three replications at three concentrations of 1, 2 and 4 milliliter per liter of silicon and three concentrations of 1, 2 and 4 milli molar (mM) of nanosilicon in Primo Early cultivar of tomato and in Agria cultivar of potato. In laboratory conditions, none of the applied silicon concentrations could reduce mycelial growth of the pathogen in compare with control treatment but nanosilicon at three applied concentrations inhibited mycelial growth as 43, 40 and 56% respectively. These two inducers did not inhibit the germination of pathogen conidia and 100 percent of conidial germination was observed in all treatments. At glasshouse conditions, the concentrations of 1, 2 and 4 ml liter-1 of silicon, were reduced early blight severity of potato as 25, 39 and 40 % respectively and disease severity of tomato as 25, 25 and 50% respectively. Disease severity reduction at concentrations of 1, 2 and 4 mM of nanosilicon in potato was evaluated as 30, 30 and 30% respectively and in tomato as 50, 50 and 25% respectively. According to the results, silicon and nanoparticles of silicon induce resistance by affecting the host plants and cause the disease control but silicon did not have direct effect on pathogen.