Complex regulation of secondary metabolism controlling pathogenicity in the phytopathogenic fungus Alternaria alternata

© 2014 The Authors. New Phytologist © 2014 New Phytologist Trust.

Bibliographische Detailangaben
Veröffentlicht in:The New phytologist. - 1979. - 202(2014), 4 vom: 23. Juni, Seite 1297-1309
1. Verfasser: Takaoka, Shinya (VerfasserIn)
Weitere Verfasser: Kurata, Mariko, Harimoto, Yoshiaki, Hatta, Rieko, Yamamoto, Mikihiro, Akimitsu, Kazuya, Tsuge, Takashi
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2014
Zugriff auf das übergeordnete Werk:The New phytologist
Schlagworte:Journal Article Research Support, Non-U.S. Gov't Alternaria alternata biosynthetic gene cluster cytochrome P450 monooxygenase host-selective toxin secondary metabolism splicing error Fungal Proteins Mycotoxins
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520 |a The filamentous fungus Alternaria alternata includes seven pathogenic variants (pathotypes), which produce different host-selective toxins and cause disease on different plants. The Japanese pear, strawberry and tangerine pathotypes produce AK-toxin, AF-toxin and ACT-toxin, respectively, which have a common structural moiety, 9,10-epoxy-8-hydroxy-9-methyl-decatrienoic acid (EDA). Here, we identified a new gene, AKT7 (AK-toxin biosynthetic gene 7), from the Japanese pear pathotype, which encodes a cytochrome P450 monooxygenase and functions to limit AK-toxin production. AKT7 homologs were found in the strawberry pathotype, but not the tangerine pathotype. However, the strawberry pathotype homolog appeared to include a premature stop codon. Although the Japanese pear pathotype strain has multiple copies of AKT7, a single-copy disruption resulted in mutants with increased production of AK-toxin and EDA. AKT7 overexpression in the three pathotypes caused marked reductions of toxin and EDA production, suggesting that Akt7 catalyzes a side reaction of EDA or its precursor. AKT7 overexpression caused reduced virulence in these pathotypes. We also found that AKT7 transcripts predominantly include misspliced mRNAs, which have premature stop codons. Our observations suggest that the AK-toxin production required for full virulence is regulated in a complex way by the copy number and intron information content of AKT7 
650 4 |a Journal Article 
650 4 |a Research Support, Non-U.S. Gov't 
650 4 |a Alternaria alternata 
650 4 |a biosynthetic gene cluster 
650 4 |a cytochrome P450 monooxygenase 
650 4 |a host-selective toxin 
650 4 |a secondary metabolism 
650 4 |a splicing error 
650 7 |a Fungal Proteins  |2 NLM 
650 7 |a Mycotoxins  |2 NLM 
700 1 |a Kurata, Mariko  |e verfasserin  |4 aut 
700 1 |a Harimoto, Yoshiaki  |e verfasserin  |4 aut 
700 1 |a Hatta, Rieko  |e verfasserin  |4 aut 
700 1 |a Yamamoto, Mikihiro  |e verfasserin  |4 aut 
700 1 |a Akimitsu, Kazuya  |e verfasserin  |4 aut 
700 1 |a Tsuge, Takashi  |e verfasserin  |4 aut 
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773 1 8 |g volume:202  |g year:2014  |g number:4  |g day:23  |g month:06  |g pages:1297-1309 
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