# Transcription Factor SsNdt80b Maintains Optimal Expression of SsSNF1 to Modulate Growth and Pathogenicity in Sclerotinia sclerotiorum

## TL;DR

This study shows how a transcription factor in a plant pathogen helps control growth and infection by regulating a key enzyme.

## Contribution

The novel finding is that SsNdt80b modulates SsSNF1 to regulate carbon utilization and pathogenicity in Sclerotinia sclerotiorum.

## Key findings

- SsNdt80b binds the promoter of SsSNF1 and modulates its transcriptional activity.
- Silencing SsSNF1 leads to reduced hyphal growth, infection cushion formation, and pathogenicity.
- A model is proposed where SsNdt80b responds to carbon sources to regulate development and virulence.

## Abstract

Microorganisms use versatile strategies to facilitate the colonisation of hosts, through remodelling transcription and metabolism to accommodate growth under harsh and hostile environments. Sclerotinia sclerotiorum is a typical necrotrophic pathogen that causes Sclerotinia stem rot in more than 700 species, resulting in serious economic losses. How S. sclerotiorum integrates mechanisms for nutrient acquisition and utilisation to maintain optimal growth and pathogenicity is still indistinct. Here, we demonstrate that Ndt80 family transcription factors (SsNdt80a,b,c) are involved in carbon source utilisation and have different roles in the growth, sclerotia formation, infection cushion development, and the virulence of S. sclerotiorum. SsNdt80b could bind the promoter of SsSNF1 and modulate the transcriptional activity of SsSNF1. Silencing SsSNF1 resulted in defects in hyphal growth and infection cushion formation, reduced cell wall‐degrading enzymes, and reduced pathogenicity of S. sclerotiorum. A model is proposed in which SsNdt80b responds to carbon sources and modulates SsSnf1 to regulate the development and pathogenicity of S. sclerotiorum.

This study reveals that SsNdt80b regulates carbon utilisation and pathogenicity in Sclerotinia sclerotiorum by modulating SsSNF1, affecting growth, development and virulence.