Premium
Funktion pflanzlicher und pilzlicher Metaboliten in der Abwehrreaktion der Banane im Pathosystem ‘Schwarze Sigatokakrankheit’ ( Musa spp. – Mycosphaerella fijiensis )
Author(s) -
Hoss R.,
Helbig J.,
Bochow H.
Publication year - 2000
Publication title -
journal of phytopathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.53
H-Index - 60
eISSN - 1439-0434
pISSN - 0931-1785
DOI - 10.1046/j.1439-0434.2000.00530.x
Subject(s) - pathosystem , mycosphaerella , biology , cultivar , phenylalanine ammonia lyase , plant disease resistance , musaceae , botany , pathogen , black spot , host (biology) , inoculation , fungus , fungicide , horticulture , microbiology and biotechnology , gene , biochemistry , enzyme , genetics , peroxidase
The host–pathogen interactions of Musa spp. and Mycosphaerella fijiensis were investigated in order to determine the function of secondary metabolites within the pathosystem of the Black Sigatoka disease. The pentaketide metabolites flaviolin, 2‐hydroxyjuglone, juglone and 2,4,8‐trihydroxytetralone (2,4,8‐THT) of the pathogen were identified. The concentration of 2,4,8‐THT was significantly increased by application of the synthetic compound tricyclazole and by natural activators extracted from the intercellular space of leaf tissue of resistant Musa cultivars. When inoculated host plants were treated with tricyclazole, extensive necrosis of both susceptible and resistant Musa cultivar leaves were observed. Plant defence mechanisms of resistant Musa cultivars were first detected as an activation of phenylalanine–ammonia lyase and the subsequent accumulation of post‐infectional substances which blocked fungal growth. These results indicated the bivalent importance of 2,4,8‐THT for host‐specific reactions, depending on its concentration at different stages of pathogenesis. Early activation of fungal 2,4,8‐THT metabolism by resistant Musa cultivars caused necrotic micro‐lesions and elicitation of post‐infectional defence reactions leading to incompatibility between pathogen and host plant; growth of the fungus on susceptible cultivars caused necrotizing doses of 2,4,8‐THT only after the establishment of a compatible interaction and development of typical symptoms at late stages of pathogenesis.