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Rhizoctonia solani Secretes RsCAP3 to Target Nb14–3–3b, Interfering with Hormone-Mediated Resistance in Tobacco

Summary

A fungal disease that damages tobacco plants produces a protein called RsCAP3 that helps it evade plant immune defenses. This protein hijacks a plant defense regulator, causing the plant to activate the wrong defense pathway while suppressing another crucial defense mechanism. By manipulating these natural plant defenses, the fungus can infect the tobacco more easily, leading to disease.

Background

Rhizoctonia solani is a necrotrophic phytopathogen that causes significant leaf spot and root rot disease in tobacco crops. Plant defense against pathogens relies on complex phytohormone signaling cascades involving salicylic acid (SA) and jasmonic acid (JA). Pathogens have evolved secreted effectors that interfere with these defense pathways to promote infection.

Objective

This study aimed to identify and characterize CAP domain-containing proteins from R. solani and determine their role in interfering with tobacco’s hormone-mediated defense responses. The researchers focused on elucidating the molecular mechanism by which these effectors suppress plant immunity.

Results

RsCAP3 was identified as a secreted effector that induces cell death and dramatically activates SA signaling while suppressing JA signaling in tobacco. RsCAP3 physically interacts with Nb14–3–3b, a negative regulator of tobacco immunity. RsCAP3-treated plants showed enhanced susceptibility to R. solani infection with lesions spreading significantly faster and higher fungal biomass.

Conclusion

R. solani hijacks Nb14–3–3b through RsCAP3 to disrupt the balance between SA and JA defense pathways, facilitating fungal infection. This study reveals a novel virulence strategy where the pathogen manipulates plant hormone signaling to overcome host immune defenses. The findings provide insights into necrotrophic fungal pathogenesis mechanisms.
  • Published in:Journal of Agricultural and Food Chemistry,
  • Study Type:Experimental Research,
  • Source: PMID: 40549997, DOI: 10.1021/acs.jafc.5c00921
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