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LaeA regulation of secondary metabolism modulates virulence in Penicillium expansum and is mediated by sucrose
Author(s) -
Kumar Dilip,
Barad Shiri,
Chen Yong,
Luo Xingyu,
Tannous Joanna,
Dubey Amit,
Glam Mataofar,
Tian Shiping,
Li Boqiang,
Keller Nancy,
Prusky Dov
Publication year - 2017
Publication title -
molecular plant pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.945
H-Index - 103
eISSN - 1364-3703
pISSN - 1464-6722
DOI - 10.1111/mpp.12469
Subject(s) - patulin , penicillium expansum , biology , virulence , microbiology and biotechnology , mycotoxin , blue mold , catabolite repression , sucrose , repressor , secondary metabolism , mutant , botany , gene , biochemistry , biosynthesis , gene expression , postharvest
Summary Penicillium expansum , the causal agent of blue mould rot, is a critical health concern because of the production of the mycotoxin patulin in colonized apple fruit tissue. Although patulin is produced by many Penicillium species, the factor(s) activating its biosynthesis are not clear. Sucrose, a key sugar component of apple fruit, was found to modulate patulin accumulation in a dose‐responsive pattern. An increase in sucrose culture amendment from 15 to 175 m m decreased both patulin accumulation and expression of the global regulator laeA by 175‐ and five‐fold, respectively, whilst increasing expression of the carbon catabolite repressor creA . LaeA was found to regulate several secondary metabolite genes, including the patulin gene cluster and concomitant patulin synthesis in vitro . Virulence studies of Δ laeA mutants of two geographically distant P. expansum isolates (Pe‐21 from Israel and Pe‐T01 from China) showed differential reduction in disease severity in freshly harvested fruit, ranging from no reduction for Ch‐Pe‐T01 strains to 15%–25% reduction for both strains in mature fruit, with the Δ laeA strains of Is‐Pe‐21 always showing a greater loss in virulence. The results suggest the importance of abiotic factors in LaeA regulation of patulin and other secondary metabolites that contribute to pathogenicity.

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