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  • Hypersensitive reaction  (1)
  • Sclerotinia sclerotiorum  (1)
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  • 1
    ISSN: 1432-2048
    Keywords: Key words: Capsicein ; Cryptogein ; Gene regulation ; Hypersensitive reaction ; Nicotiana
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract. The induction of sesquiterpene cyclase, a key phytoalexin biosynthetic enzyme, and the accumulation of phytoalexins in relation to the induction of a hypersensitive response (HR) and cell necrosis in tobacco (Nicotiana tabacum L.) were investigated. When tobacco leaves were inoculated with virulent or avirulent isolates of Ralstonia solanacearum, steady-state levels of mRNA complementary to cDNA of the sensitivity-related (sts) gene str319 were dramatically induced. This cDNA clone is greater than 90% homologous with a gene coding for 5-epi-aristolochene synthase (EAS), previously described as a branch-point enzyme regulating the synthesis of capsidiol, the major sesquiterpenoid phytoalexin found in tobacco. Accumulation of EAS transcripts in leaves after inoculation with virulent and avirulent strains of R. solanacearum, or after treatment with necrotizing or non-necrotizing elicitins was rapid but transient, and restricted to the site of infiltration. Two highly similar sesquiterpene cyclase activities, 5-epi-aristolochene synthase and a vetispiradiene synthase-like activity, were found in extracts of elicitin-challenged and R. solanacearum-inoculated tobacco. Under all conditions tested, the induction of cyclase activity was closely correlated with induction of the cyclase mRNA level. In contrast, high levels of capsidiol were found only after treatment with the necrosis-inducing elicitin cryptogein, or after infiltration with HR-inducing bacterial strains. Low levels of capsidiol did accumulate after application of capsicein, an elicitin that induces little or no necrosis on tobacco, or after infection with a virulent bacterium. Hence, capsidiol accumulation, not 5-epi-aristolochene synthase gene expression or total sesquiterpene cyclase enzyme activity, appears to be a good marker for the HR of tobacco.
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    European journal of plant pathology 102 (1996), S. 181-192 
    ISSN: 1573-8469
    Keywords: dichloroisonicotinic acid ; necrosis induction ; Phytophthora spp. ; rape ; Sclerotinia sclerotiorum ; systemic acquired resistance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition
    Notes: Abstract Elicitins are a family of proteins excreted byPhytophthora spp. They exhibit high sequence homology but large net charge differences. They induce necrosis in tobacco plants which then become resistant to the tobacco pathogenPhytophthora parasitica var.nicotianae. In stem-treated plants, resistance was not restricted to the site of elicitin application, but could be demonstrated by petiole inoculation at all levels on the stem. Resistance was already maximum after two days and lasted for at least two weeks. It was effective not only towardsP. p. var.nicotianae infection, but also against the unrelated pathogenSclerotinia sclerotiorum. In contrast to dichloroisonicotinic acid, an artificial inducer of systemic acquired resistance, which was increasingly effective with doses ranging from 0.25 to 5Μmole per plant, the basic elicitin cryptogein exhibited a threshold effect, inducing near total resistance and extensive leaf necrosis above 0.1 nmole per plant. Between 1 and 5 nmole, acidic elicitins (capsicein and parasiticein) protected tobacco plants with hardly any necrotic symptom. Elicitins exhibited similar effects in various tobacco cultivars andNicotiana species, although with quantitative differences, but induced neither necrosis nor protection in other SolanaceÆ (tomato, petunia and pepper). Among 24 additional species tested belonging to 18 botanical families, only some BrassicaceÆ, noticeably rape, exhibited symptoms in response to elicitins, in a cultivar-specific manner. Elicitins appear to be natural specific triggers for systemic acquired resistance and provide a tool for unraveling the mechanisms leading to its establishment.
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