RT Journal Article
SR Electronic
T1 Ancient duplication and horizontal transfer of a toxin gene cluster reveals novel mechanisms in the cercosporin biosynthesis pathway
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 100545
DO 10.1101/100545
A1 Ronnie de Jonge
A1 Malaika K. Ebert
A1 Callie R. Huitt-Roehl
A1 Paramita Pal
A1 Jeffrey C. Suttle
A1 Jonathan D. Neubauer
A1 Wayne M. Jurick II
A1 Gary A. Secor
A1 Bart P.H.J Thomma
A1 Yves Van de Peer
A1 Craig A. Townsend
A1 Melvin D. Bolton
YR 2017
UL http://biorxiv.org/content/early/2017/01/15/100545.abstract
AB Cercospora species have a global distribution and are best known as the causal agents of leaf spot diseases of many crops. Cercospora leaf spot (CLS) is an economically devastating disease of sugar beet caused by C. beticola. The C. beticola genome encodes 63 biosynthetic gene clusters, including the cercosporin toxin biosynthesis (CTB) cluster. Studies spanning nearly 60 years have shown that cercosporin is photoactivated, critical for disease development, and toxic to most organisms except Cercospora spp. themselves, which exhibit cercosporin auto-resistance. We show that the CTB gene cluster has experienced an unprecedented number of duplications, losses, and horizontal transfers across a spectrum of plant pathogenic fungi. Although cercosporin biosynthesis has been widely assumed to rely on the eight gene CTB cluster, our comparative genomic analysis revealed extensive gene collinearity adjacent to the established cluster in all CTB cluster-harboring species. We demonstrate that the CTB cluster is larger than previously recognized and includes the extracellular proteins fasciclin and laccase required for cercosporin biosynthesis and the final pathway enzyme that installs the unusual cercosporin methylenedioxy bridge. Additionally, the expanded cluster contains CFP, which contributes to cercosporin auto-resistance in C. beticola. Together, our results give new insight on the intricate evolution of the CTB cluster.