These authors contributed equally to this work.
Complex regulation of secondary metabolism controlling pathogenicity in the phytopathogenic fungus Alternaria alternata
Article first published online: 10 MAR 2014
© 2014 The Authors. New Phytologist © 2014 New Phytologist Trust
Volume 202, Issue 4, pages 1297–1309, June 2014
How to Cite
Takaoka, S., Kurata, M., Harimoto, Y., Hatta, R., Yamamoto, M., Akimitsu, K. and Tsuge, T. (2014), Complex regulation of secondary metabolism controlling pathogenicity in the phytopathogenic fungus Alternaria alternata. New Phytologist, 202: 1297–1309. doi: 10.1111/nph.12754
- Issue published online: 8 MAY 2014
- Article first published online: 10 MAR 2014
- Manuscript Accepted: 3 FEB 2014
- Manuscript Received: 22 NOV 2013
- Grants-in-Aids for Scientific Research (A). Grant Number: 23248007
- Scientific Research (S). Grant Numbers: 19108001, 21228001
- Japanese Society for Promotion of Sciences and Special Coordination Funds
- Ministry of Education, Culture, Sports, Science, and Technology of Japan
- Alternaria alternata ;
- biosynthetic gene cluster;
- cytochrome P450 monooxygenase;
- host-selective toxin;
- secondary metabolism;
- splicing error
- 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.