The cross-pathway control system regulates production of the secondary metabolite toxin, sirodesmin PL, in the ascomycete, <it>Leptosphaeria maculans</it>

• Main Authors: Fox Ellen M, Elliott Candace E, Jarvis Renee S, Howlett Barbara J
• Format: Article
• Language: English
• Published: BMC 2011-07-01
• Series: BMC Microbiology
• Online Access: http://www.biomedcentral.com/1471-2180/11/169

<p>Abstract</p> <p>Background</p> <p>Sirodesmin PL is a secondary metabolite toxin made by the ascomycetous plant pathogen, <it>Leptosphaeria maculans</it>. The sirodesmin biosynthetic genes are clustered in the genome. The key genes are a non-ribosomal peptide synthetase, <it>sirP</it>, and a pathway-specific transcription factor, <it>sirZ</it>. Little is known about regulation of sirodesmin production.</p> <p>Results</p> <p>Genes involved in regulation of sirodesmin PL in <it>L. maculans </it>have been identified. Two hundred random insertional T-DNA mutants were screened with an antibacterial assay for ones producing low levels of sirodesmin PL. Three such mutants were isolated and each transcribed <it>sirZ </it>at very low levels. One of the affected genes had high sequence similarity to <it>Aspergillus fumigatus cpcA</it>, which regulates the cross-pathway control system in response to amino acid availability. This gene was silenced in <it>L. maculans </it>and the resultant mutant characterised. When amino acid starvation was artificially-induced by addition of 3-aminotriazole for 5 h, transcript levels of <it>sirP </it>and <it>sirZ </it>did not change in the wild type. In contrast, levels of <it>sirP </it>and <it>sirZ </it>transcripts increased in the silenced <it>cpcA </it>mutant. After prolonged amino acid starvation the silenced <it>cpcA </it>mutant produced much higher amounts of sirodesmin PL than the wild type.</p> <p>Conclusions</p> <p>Production of sirodesmin PL in <it>L. maculans </it>is regulated by the cross pathway control gene, <it>cpcA</it>, either directly or indirectly via the pathway-specific transcription factor, <it>sirZ</it>.</p>