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ARS Home » Plains Area » College Station, Texas » Southern Plains Agricultural Research Center » Insect Control and Cotton Disease Research » Research » Publications at this Location » Publication #398371
Research Project: Molecular and Genetic Approaches to Manage Cotton and Sorghum Diseases

Location: Insect Control and Cotton Disease Research

Title: Effect of RNAi suppression of the gossypol pathway on resistance to necrotrophic fungal seedling disease pathogens in cotton

Author
item WAGNER, TANYA - Texas A&M University
item Bell, Alois - Al
item Puckhaber, Lorraine
item MAGILL, CLINT - Texas A&M University
item Liu, Jinggao

Submitted to: Journal of Phytopathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 6/22/2023
Publication Date: 6/27/2023
Citation: Wagner, T.A., Bell, A.A., Puckhaber, L.S., Magill, C., Liu, J. 2023. Effect of RNAi suppression of the gossypol pathway on resistance to necrotrophic fungal seedling disease pathogens in cotton. Journal of Phytopathology. 127. Article 102085. https://doi.org/10.1016/j.pmpp.2023.102085.
DOI: https://doi.org/10.1016/j.pmpp.2023.102085

Interpretive Summary: Cotton plants produce several chemical compounds such as gossypol and lacinilene to protect the plants against wilt and seedling diseases. We previously showed that suppressing the gene responsible for gossypol production resulted in increased production of lacinilene and enhanced cotton resistance to Fusarium wilt pathogens. Suppression of this gene also has been reported to increase cotton resistance to Verticillium wilt pathogens. However, in this study, we found that suppression of the gossypol gene made plants more susceptible to seedling diseases, such as those caused by the pathogen Rhizoctonia solani. Thus, further understanding of the mechanisms and interactions governing plant defense responses to wilt and seedling disease pathogens is needed to develop cotton plants that are resistant to wilt pathogens without compromising resistance to seedling pathogens.

Technical Abstract: We previously demonstrated that blocking the gossypol pathway by RNAi suppression of the early pathway biosynthetic enzyme CYP82D hydroxylase resulted in enhanced resistance to the Fusarium wilt pathogens, which was attributed to the induction of a linked lacinilene defense pathway. RNAi suppression of the same gene is reported to cause also a spontaneous hypersensitive response-like cell death resulting in a lesion mimic phenotype and increased resistance to Verticillium wilt pathogens. We found that RNAi suppression of CYP82D is not associated with spontaneous hypertensive-like cell death. No lesion formation on hypocotyls occurred when the CYP82D RNAi plants were grown in pasteurized soil at temperatures unfavorable to seedling disease development. However, when grown in unpasteurized soil at temperatures favorable for seedling disease development, more than 87% of the CYP82D RNAi plants developed necrotic hypocotyl lesions, whereas only 3% of wild type plants developed lesions. Furthermore, at least 83% of the necrotic CYP82D RNAi plants harbored at least one of the seedling disease pathogens Fusarium spp, Rhizopus spp., or Aspergillus spp. isolate(s). Pathogenicity assays with the seedling disease pathogen Rhizoctonia solani AG4 confirmed that blocking the gossypol defense pathway by CYP82D RNAi increased host susceptibility to the necrotrophic pathogen. Developing cotton host resistance to wilt diseases without compromising resistance to seedling disease pathogens requires further understanding of the interaction between signaling pathways involved in responses to hemibiotrophs and necrotrophs.