Dataset Information

Oryza sativa extracellular vesicles proteins

ABSTRACT: Cross-kingdom molecular exchange between hosts and interacting microbes is essential for the survival of both plants and their pathogens. Recent studies showed plants transfer their small RNAs (sRNAs) and massager RNAs (mRNAs) into fungal pathogens to suppress infection. However, whether and how plants send defense proteins into pathogen cells remains unknown. Here, we show that rice plants send defense proteins into the fungal pathogen Rhizoctonia solani via extracellular vesicles (EVs). These vesicles enrich host defense proteins and are taken up by the fungal cells. Reducing EV-mediated host protein transfer leads to increased disease susceptibility. Thus, plants send defense proteins via EVs into fungal pathogens to combat infection, providing a mechanism of protein exchange between plants and pathogens that helps reduce crop disease.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Oryza Sativa (rice)

TISSUE(S): Shoot

SUBMITTER: Wei Li

LAB HEAD: Qiang Cai

PROVIDER: PXD048458 | Pride | 2025-01-06

REPOSITORIES: pride

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Rice extracellular vesicles send defense proteins into fungus Rhizoctonia solani to reduce disease.

Huang Yifan Y Li Wei W Liu Tiangu T Lin Xiaoli X Xia Yanhui Y Zhu Wenjing W Jin Hailing H Cai Qiang Q

Developmental cell 20241228

The exchange of molecular information across kingdoms is crucial for the survival of both plants and their pathogens. Recent research has identified that plants transfer their small RNAs and microRNAs into fungal pathogens to suppress infection. However, whether and how plants send defense proteins into pathogens remains unknown. Here, we report that rice (Oryza sativa) plants package defense proteins into extracellular vesicles (EVs) and deliver them to the fungal pathogen Rhizoctonia solani. T ...[more]

PMID: 39755117

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Project description:A LysM Receptor-like Kinase Mediates Chitin Perception and Fungal Resistance in Arabidopsis; Jinrong Wan,1 Xuecheng Zhang,1 David Neece,2 Katrina M. Ramonell,3 Steve Clough,2,4 Sung-yong Kim,1 Minviluz Stacey,1 and Gary Stacey1*; 1Division of Plant Sciences, National Center for Soybean Biotechnology, C.S. Bond Life Sciences Center, University of Missouri-Columbia, Columbia, MO 65211, USA; 2Department of Crop Sciences, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA; 3Department of Biological Sciences, University of Alabama, Tuscaloosa, AL 35487, USA; 4US Department of Agriculture, Soybean/Maize Germplasm, Pathology and Genetics Research, Urbana, IL 61801, USA; *To whom correspondence should be addressed. E-mail: staceyg@missouri.edu; Abstract: Chitin, a polymer of N-acetyl-D-glucosamine, is found in fungal cell walls, but not in plants. Plant cells are capable of perceiving chitin fragments (chitooligosaccharides) to trigger various defense responses. We identified a LysM receptor-like protein (AtLysM RLK1) that is required for the perception of chitooligosaccharides in Arabidopsis. Mutation of this gene blocked the induction of almost all chitooligosaccharide-responsive genes (CRGs) and led to more susceptibility to fungal pathogens, but not to a bacterial pathogen. In addition, exogenously applied chitooligosaccharides enhanced resistance against both fungal and bacterial pathogens in the wild-type plants, but not in the mutant. Together, our data strongly suggest AtLysM RLK1 is the chitin receptor or a key part of the receptor complex and chitin is a PAMP (pathogen-associated molecular pattern) in fungi recognized by the receptor leading to the induction of plant innate immunity against fungal pathogens. Since LysM RLKs were also recently shown to be critical for the perception of the rhizobial lipo-chitin Nod signals, our data suggest that LysM RLKs not just recognize friendly symbiotic rhizobia (via their lipo-chitin Nod signals), but also hostile fungal pathogens (via their cell wall chitin). These data suggest a possible evolutionary relationship between the perception mechanisms of Nod signals and chitin by plants. Experiment Overall Design: wild type Col-0 and chitin receptor mutants treated with or without chitooctaose

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