AI Networking Cookbook: Practical recipes for AI-assisted network automation and development
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It is shown that expression of AVR2 is strongly induced in root-and xylem-colonizing hyphae three days post inoculation, and it is found that Avr2 has to be nuclear localized to trigger an I-2 -dependent cell death response.
The use of pathogen-derived effectors as molecular probes to identify S genes is explored, finding that most effector targets identified so far are not applicable as S genes due to detrimental effects they have on other traits.
Plant cells can directly or indirectly detect bacterial effectors, triggering a hypersensitive response to defend against pathogen infection. One extensively studied effector, AvrB, is a Fido (Fic, Doc, AvrB) domain-containing protein that acts as a glycosyltransferase. AvrC is an elusive Pseudomonas syringae avirulence effector protein with significant sequence and structural similarity to AvrB. Combining biochemistry, mass spectrometry, and AlphaFold prediction tools, we show that AvrC is a glycosyltransferase with auto-rhamnosylation activity. Like AvrB, AvrC can rhamnosylate a threonine residue (T166) on the A. thaliana “guardee” protein RIN4. In vitro assays revealed rhamnosylation substrates for AvrC also include plant coatomer subunits COPE1 and COPZ1. Collectively, our findings indicate that AvrC is a rhamnosyltransferase with broad substrate specificity. Our experimental strategies and findings provide valuable insights into future studies on the characterization of other Fido proteins.
Fusarium pseudograminearum, the dominant causal agent of Fusarium crown rot (FCR), secretes numerous effectors to modulate host immunity during infection, but the functions of most remain unknown. In this study, we identified FpSP5, an effector from F. pseudograminearum, as a pathogen-associated molecular pattern (PAMP) that triggers plant immunity. FpSP5 induces cell death, oxidative burst, and PTI in Nicotiana benthamiana, conferring resistance against multiple pathogens. Furthermore, its perception specifically depends on the coreceptor BAK1 in N. benthamiana. Interestingly, FpSP5 is not only conserved among fungi and capable of activating defense responses in different plants but also essential for the full virulence of F. pseudograminearum on wheat. Collectively, these findings enhance our understanding of how F. pseudograminearum effectors modulate host immunity and contribute to pathogenicity, laying a foundation for developing targeted strategies to control FCR.
ABSTRACT Plant fungal pathogens secrete a plethora of effectors into host cells to facilitate their infection by interfering with the normal physiological processes of the host plant. However, the role of guanyl‐specific ribonuclease T1 effector protein in the virulence of fungal pathogens remains largely unexplored. Here, we show that an effector protein EC19, secreted by the soil‐borne fungus Fusarium oxysporum f. sp. lycopersici (Fol) that causes tomato wilt disease, contributes to the full virulence of Fol. In‐locus knockout of EC19 significantly reduced the virulence of Fol, while complementing EC19 in the knockout mutant restored the pathogenicity of Fol on tomato. EC19, which contains the ribonuclease T1‐like domain, is highly conserved across fungal species and exhibited the ability to cleave single‐stranded RNA isolated from tomato. EC19 was specifically induced during Fol infection. The AlphaFold3‐predicted structure of EC19 shows a high degree of structural similarity with ribonuclease T1 from Aspergillus oryzae, with limited similarity to RNase T2. Using Agrobacterium‐mediated transient assay in the leaves of Nicotiana benthamiana, we found that EC19 predominantly localised to the nucleus of plant cells. Stable transgenic susceptible tomato plants overexpressing EC19 exhibited increased susceptibility to Fol infection compared to wild‐type plants. RNA‐seq analysis of EC19‐overexpressing tomato lines revealed that downregulated differentially expressed genes were predominantly enriched in plant hormone signal transduction, phenylpropanoid biosynthesis, and plant–pathogen interaction pathways. Taken together, these findings indicate that EC19 with ribonuclease activity promotes Fol infection, expanding our understanding of the molecular mechanisms underlying Fol virulence.
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