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 หัวเรื่อง:ไม่มีชื่อไทย (ชื่ออังกฤษ : Pectate lyase from Xanthomonas axonopodis pv. glycines 12-2 and Associated Pili Transporter Constitute a Key Virulence Factor) ผู้เขียน: วิลาวรรณ์ เชื้อบุญ, ดุสิต อธินุวัฒน์,  ดร.สุดฤดี ประเทืองวงศ์, ศาสตราจารย์ สื่อสิ่งพิมพ์:pdf AbstractA recent study has demonstrated that XagP in xagP of Xanthomonas axonopodis pv. glycines 12-2 )Xag 12-2), the causal agent of soybean bacterial pustule, is required to induce a hypersensitive response (HR) in tobacco (Nicotiana rustica). Until now, its role in virulence on soybean was unknown and whether the general secretion pathway (GSP) is different from other bacteria. To understand the possible relationship between functions, xagP and T4P operon-corresponding to XagP secretion and type IV pili of Xag 12-2, respectively- were mutated using the site-directed method. XagP secretion into media associated with ?xagP and ?T4Pmutants was reduced by 100 and 24.8% respectively. Pili mutants were less reduced in the Pel secretion than by other GSPs which might be necessary for an XagP transporter. Both mutants elicited HR-like typically necrotic symptoms which were the same as the wildtype, that is, within 48 hr after infiltration on susceptible soybean cv. Spencer. On this same host plant, disease severity induced by ?xagP and ?T4P mutants was highly reduced by 82.8 and 55.9%, respectively. It is also interesting to note that the HR and disease symptoms produced by the mutants were different from the wildtype. The mutants neither expressed haloes surrounding the HR nor scattered lesions over spray-inoculated leaves but revealed pustules around the leaf margin at hydathode pores. Complemented mutants showed enhanced secretion, transportation, HR and disease severity similar to the wildtype. This is the first report of a co-regulation mechanism of xagP and type IV pili secretion pathway in Xag 12-2 with bacterial pustule disease in soybean. Details involved in these interactions are discussed. The minimal translocation of XagP that is less coincident with the pili transporter should be further elucidated to determine if it is more dependent on other GSPs and can suppress secretion output of other virulence factors associated with Xag 12-2 pathogenesis. |
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