The Transcription Factor SsSR Mediates Ergosterol Biosynthesis and Virulence in Sclerotinia sclerotiorum

TL;DR

A new transcription factor, SsSR, was found to control ergosterol production and virulence in the fungus Sclerotinia sclerotiorum.

Contribution

The study identifies SsSR as a novel transcription factor regulating ergosterol biosynthesis and virulence in Sclerotinia sclerotiorum.

Findings

SsSR regulates virulence by modulating ergosterol biosynthesis through phosphorylation of SsCYP51.

Deleting SsSR or SsCYP51 reduces ergosterol levels, virulence, and hyphal stress tolerance.

SsSR does not affect growth or acid production in Sclerotinia sclerotiorum.

Abstract

Sclerotinia sclerotiorum, known as a typical necrotrophic pathogenic fungus, exhibits a complex pathogenic mechanism. Research on S. sclerotiorum has primarily focused on oxalic acid, pathogenicity-related enzymes, and secreted proteins. In this study, we identified a transcription factor, SsSR (S. sclerotiorum Sterol-Related transcription factor), which regulates S. sclerotiorum infection by modulating virulence through ergosterol biosynthesis. We characterized the transcriptional activity of SsSR and its downstream target gene, SsCYP51. SsSR undergoes phosphorylation induced by the host plant, subsequently regulating the expression of SsCYP51. The deletion of SsSR or SsCYP51 does not affect the growth or acid production of S. sclerotiorum, but it leads to a reduction in ergosterol, significantly diminishing virulence and impairing the stress tolerance of the hyphae. In summary, this study identifies a transcription factor, SsSR, that specifically regulates the virulence of S. sclerotiorum. SsSR upregulates the expression of SsCYP51 through phosphorylation during the infection phase, leading to the synthesis of ergosterol, which enhances hyphal stress tolerance and thereby promotes infection.

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