Gene regulation of Sclerotinia sclerotiorum during infection of Glycine max: on the road to pathogenesis.

Abstract:

BACKGROUND:Sclerotinia sclerotiorum is a broad-host range necrotrophic pathogen which is the causative agent of Sclerotinia stem rot (SSR), and a major disease of soybean (Glycine max). A time course transcriptomic analysis was performed in both compatible and incompatible soybean lines to identify pathogenicity and developmental factors utilized by S. sclerotiorum to achieve pathogenic success. RESULTS:A comparison of genes expressed during early infection identified the potential importance of toxin efflux and nitrogen metabolism during the early stages of disease establishment. The later stages of infection were characterized by an apparent shift to survival structure formation. Analysis of genes highly upregulated in-planta revealed a temporal regulation of hydrolytic and detoxification enzymes, putative secreted effectors, and secondary metabolite synthesis genes. Redox regulation also appears to play a key role during the course of infection, as suggested by the high expression of genes involved in reactive oxygen species production and scavenging. Finally, distinct differences in early gene expression were noted based on the comparison of S. sclerotiorum infection of resistant and susceptible soybean lines. CONCLUSIONS:Although many potential virulence factors have been noted in the S. sclerotiorum pathosystem, this study serves to highlight soybean specific processes most likely to be critical in successful infection. Functional studies of genes identified in this work are needed to confirm their importance to disease development, and may constitute valuable targets of RNAi approaches to improve resistance to SSR.

journal_name

BMC Genomics

journal_title

BMC genomics

authors

Westrick NM,Ranjan A,Jain S,Grau CR,Smith DL,Kabbage M

doi

10.1186/s12864-019-5517-4

subject

Has Abstract

pub_date

2019-02-26 00:00:00

pages

157

issue

1

issn

1471-2164

pii

10.1186/s12864-019-5517-4

journal_volume

20

pub_type

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