Abstract
The two tobacco relatives of Nicotiana alata and Nicotiana longiflora display a high level of resistance against Colletotrichum nicotianae and the two genes NTF6 and NtPAL related to pathogen defense transcription were higher in N. alata and N. longiflora than the commercial cv. K326. Inoculation with C. nicotianae reduced the abundance of NTF6 and NtPAL transcript during the first 48 h post inoculation (hpi) when only biotrophic hyphae were present, but increased it over the following 24 h as necrotrophic hyphae began to predominate. Activity levels of phenylalanine ammonia lyase, peroxidase and polyphenol oxidase changed markedly at 72 hpi. The conclusion was that the pathogen enters the host leaf within 24 hpi, triggering the up-regulation of various defense-related genes in a resistant host plant. By 72 hpi, the pathogen switched to necrotrophic growth to avoid contact with the increasing presence of host defense compounds. Key words: Nicotiana alata, Nicotiana longiflora, tobacco anthracnose resistance-related gene, antioxidant enzyme activity.
Highlights
Plants have evolved a multifaceted system of defense against pathogens, some of which are highly specific to a particular microbial species (Doehlemann et al, 2008)
The two tobacco relatives of Nicotiana alata and Nicotiana longiflora display a high level of resistance against Colletotrichum nicotianae and the two genes NTF6 and NtPAL related to pathogen defense transcription were higher in N. alata and N. longiflora than the commercial cv
The results show that the disease index of cv. k326 was 74.17%, and the two tobacco relatives of N. alata and N. longiflora were 23.33 and 26.67%, which displayed high levels of resistance against the anthracnose pathogen (Table 1)
Summary
Plants have evolved a multifaceted system of defense against pathogens, some of which are highly specific to a particular microbial species (Doehlemann et al, 2008). Many components of the plant defense signal transduction pathway remain obscure, those responsible for both salicylic acid-dependent systemic acquired resistance and jasmonate- and ethylene-induced resistance are well documented (Hammond-Kosack and Parker, 2003; Bari and Jones, 2009). Effectors trigger the plant's defense responses and salicylic acid signaling is used to initiate apoptosis at the site of the pathogen's entry. The defense response has evolved such that the salicylic acid-dependent pathway is largely activated by biotrophic pathogens, while the jasmonate- and ethylene-dependent pathway operates against necrotrophic pathogens and insects (Qiu and Wang, 2007). Associated with the defense signal transduction network, plants have evolved a set of antioxidation strategies which are brought into play to miti-
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