Abstract

Elsinochromes (ESCs) are virulence factors produced by Elsinoë arachidis which is the cause of peanut scab. However, the biosynthesis pathway of ESCs in E. arachidis has not been elucidated and the potential pathogenic mechanism of E. arachidis is poorly understood. In this study, we report a high-quality genome sequence of E. arachidis. The size of the E. arachidis genome is 33.18Mb, which is comparable to the Ascomycota genome (average 36.91 Mb), encoding 9174 predicted genes. The self-detoxification family including transporters and cytochrome P450 enzymes were analysis, candidate effectors and cell wall degrading enzymes were investigated as the pathogenicity genes by using PHI and CAZy databases. Additionally, the E. arachidis genome contains 24 secondary metabolism gene clusters, in which ESCB1 was identified as the core gene of ESC biosynthesis. Taken together, the genome sequence of E. arachidis provides a new route to explore its potential pathogenic mechanism and the biosynthesis pathway of ESCs.

Highlights

  • Data Availability Statement: All relevant data are within the paper and its Supporting Information files

  • We report on the 33.18Mb genome sequence of E. arachidis, the secondary metabolism gene cluster, and the discovery of 6 polyketide synthases (PKSs) gene clusters in E. arachidis including the ESC biosynthetic gene cluster and the core gene ESCB1

  • In order to confirm the function of polyketide synthase (PKS), which is the core protein that responsible for the biosynthesis of mycotoxin in different organisms, PKS sequences were used to construct the phylogenetic tree by MEGA 10.0.5

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Summary

Introduction

Data Availability Statement: All relevant data are within the paper and its Supporting Information files. Potential pathogenic mechanism and the biosynthesis pathway of elsinochrome toxin (PKS) [11], and the other gene functions in the PKS gene clusters have been determined. The biosynthetic pathway of ESCs in E. arachidis and their potential pathogenic mechanism remain to be explored. It is unclear whether, in addition to ESCs, there exist cell wall degrading enzymes or effectors that act as virulence factors in E. arachidis [12]. Through our analysis of the whole genome, we show that E. arachidis has a complex pathogenesis, with, in addition to the toxin, several candidate virulence factors including effectors, enzymes, and transporters. The putative pathogenicity genes provide new horizons to unravel the pathogenic mechanism of E. arachidis

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