Silicon reduces bacterial speck development on tomato leaves

• Autor(a) principal: Andrade,Camila Cristina Lage
• Data de Publicação: 2013
• Outros Autores: Resende,Renata Sousa, Rodrigues,Fabrício Ávila, Ferraz,Hélvio Gledson Maciel, Moreira,Wiler Ribas, Oliveira,José Rogério, Mariano,Rosa Lima Ramos
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Tropical plant pathology (Online)
• Texto Completo: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1982-56762013000500009
• topic: Pseudomonas syringae pv. tomato; Solanum lycopersicum; host resistance; plant nutrition

This study aimed to evaluate the effect of silicon (Si) on the resistance of tomato plants (cv. Santa Clara) to bacterial speck, caused by Pseudomonas syringae pv. tomato (Pst). Tomatoes were grown in soil without calcium silicate (control), in soil without calcium silicate and sprayed with Supa Sílica® (2 mL/L) (SS) and in soil with calcium silicate (0.16 g/kg of soil) (CS). The effect of SS on the growth of Pst was evaluated in vitro. There was no significant difference among the treatments for foliar Si concentration and incubation period. No significant differences were observed between the control and CS for the number of lesions per plant (NLP) and bacterial speck severity estimated by the software QUANT. The NLP was significantly reduced with SS spray. There was a negative linear response of in vitro Pst growth to the SS rates. Peroxidase, polyphenoloxidase and glucanase activities were significantly higher for plants sprayed with SS and grown in soil with CS compared to the control treatment. Phenylalanine ammonia-lyase and lypoxygenase activities were significantly higher for plants grown in soil with CS compared to the control. The concentration of malondialdehyde was significantly higher for plants sprayed with SS compared to the control at 0 and 7 dai. The results of this study indicate that the symptoms of bacterial speck are reduced when plants are sprayed with SS, which can be linked to the direct effect of this product against Pst rather than the potentation of host defense responses.