Ss NEP2 Contributes to the Virulence of Sclerotinia sclerotiorum .
Chenghuizi YangWei LiXingchuan HuangXianyu TangLei QinYanan LiuYunong XiaZhihong PengShitou XiaPublished in: Pathogens (Basel, Switzerland) (2022)
Sclerotinia sclerotiorum is a notorious soilborne fungal pathogen that causes serious economic losses globally. The necrosis and ethylene-inducible peptide 1 (NEP1)-like proteins (NLPs) were previously shown to play an important role in pathogenicity in fungal and oomycete pathogens. Here, we generated S. sclerotiorum necrosis and ethylene-inducible peptide 2 ( SsNEP2 ) deletion mutant through homologous recombination and found that Ss NEP2 contributes to the virulence of S. sclerotiorum without affecting the development of mycelia, the formation of appressoria, or the secretion of oxalic acid. Although knocking out SsNEP2 did not affect fungal sensitivity to oxidative stress, it did lead to decreased accumulation of reactive oxygen species (ROS) in S. sclerotiorum . Furthermore, Ss nlp24 SsNEP2 peptide derived from SsNEP2 triggered host mitogen-activated protein kinase (MAPK) activation, increased defense marker gene expression, and enhanced resistance to Hyaloperonospora arabidopsidis Noco2. Taken together, our data suggest that Ss NEP2 is involved in fungal virulence by affecting ROS levels in S. sclerotiorum . It can serve as a pathogen-associated molecular pattern (PAMP) and trigger host pattern triggered immunity to promote the necrotrophic lifestyle of S. sclerotiorum .
Keyphrases
- reactive oxygen species
- dna damage
- oxidative stress
- gene expression
- escherichia coli
- pseudomonas aeruginosa
- biofilm formation
- staphylococcus aureus
- antimicrobial resistance
- cell death
- dna repair
- candida albicans
- cardiovascular disease
- metabolic syndrome
- dna methylation
- physical activity
- type diabetes
- tyrosine kinase
- artificial intelligence
- induced apoptosis
- heat shock protein