A Rhamnogalacturonan Acetylesterase Effector FsRGAE1 Enhances the Virulence of Fusarium sacchari by Localizing to the Nucleus and Suppressing Plant Immunity
Aug 2026· Journal of Fungi· 0 citations· 39 references
TL;DR
Findings indicate that FsRGAE1 promotes F. sacchari virulence by suppressing host immune responses in a nuclear localization-dependent manner, providing new insights into effector-mediated F. sacchari pathogenesis and potential target for resistance breeding in sugarcane.
Abstract
Fusarium sacchari is one of the major pathogenic fungi that cause sugarcane Pokkah Boeng disease (PBD). Effectors play pivotal roles in F. sacchari–sugarcane interaction; thus, characterizing these effectors is essential for elucidating the molecular mechanisms underlying F. sacchari pathogenicity and for developing effective strategies to control PBD. However, only a limited number of effectors have been functionally validated to date. Here, we report FsRGAE1, a candidate effector protein from F. sacchari predicted to encode a rhamnogalacturonan acetylesterase (RGAE). FsRGAE1 exhibits high expression during the early stages of infection and maintains relatively elevated expression levels throughout the F. sacchari–sugarcane interaction. Targeted deletion of the FsRGAE1 gene in F. sacchari had no discernible impact on mycelial growth, conidiation, or carbon-source utilization, yet it significantly attenuated fungal virulence. FsRGAE1 possesses both a signal peptide conferring secretory capacity and a transit peptide enabling its translocation into the host cytoplasm and nucleus. Using the Agrobacterium tumefaciens-mediated transient expression system in Nicotiana benthamiana, FsRGAE1 was confirmed to suppress cell death induced by Bcl-2-associated X protein (BAX), as well as ROS accumulation and callose deposition, and its nuclear localization is indispensable for this immunosuppressive activity. Collectively, these findings indicate that FsRGAE1 promotes F. sacchari virulence by suppressing host immune responses in a nuclear localization-dependent manner, providing new insights into effector-mediated F. sacchari pathogenesis and potential target for resistance breeding in sugarcane.
Pokkah Boeng disease caused by Fusarium sacchari seriously threatens the yield and quality of sugarcane worldwide. Effectors play a crucial role in the infection and colonization of pathogens. However, there were few reports on the virulence functions of F. sacchari effectors. To characterize effector functions and unravel the pathogenic mechanisms of F. sacchari, we identified an effector FsSCR6, which was vital for the virulence of F. sacchari. Gene knockout mutants showed no difference in growth rates and colony morphology from wild-type. However, the virulence of knockout mutants was severely impaired. Agrobacterium-mediated transient expression assays in Nicotiana benthamiana showed that FsSCR6 and FsSCR6Δsp (without signal peptide) performed cell death-suppressive activity inside plant cells. 3'3-diaminobenzidine staining and aniline blue staining assays showed that FsSCR6 significantly reduced the accumulation of reactive oxygen species and callose deposition triggered by BCL-2-Associated X protein (BAX) in N. benthamiana leaves. FsSCR6 significantly suppressed the relative expression of the marker genes of the hypersensitive responses and salicylic acid (SA)-, jasmonic acid (JA)-, and ethylene-dependent immunity in N. benthamiana. Overall, FsSCR6 is required for F. sacchari virulence; it performs a function inside plant cells and suppresses the plant immune responses by regulating the SA-, JA- and ethylene-mediated defense pathways. These results clarify the function of this effector from F. sacchari and assist in dissecting the interaction between sugarcane and F. sacchari, ultimately contributing to sugarcane production.
Minyan Lu, Lixiang Zhu, Liuyu Yin et al.· Plant physiology and biochem...· 0 citations
It is reported that the methyltransferase FpLaeA is a global regulator essential for F. proliferatum pathogenicity and a target for integrated control of F. proliferatum and its associated mycotoxin risk.
Ling Wang, Shaoqing Tang, Weiyang Liao et al.· Journal of Agricultural and...· 0 citations
It is revealed that CfMBZ1 plays a critical role in the pathogenesis of Glomerella leaf spot caused by C. fructicola and regulates appressorium-mediated penetration by modulating genes involved in peroxisome biogenesis, lipid droplet metabolism, and other penetration-related pathways.
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Chinese hickory (Carya cathayensis Sarg.) is an economically important tree species widely cultivated in southeastern China, where trunk canker disease caused by Botryosphaeria dothidea poses a serious threat to tree health and production. Pectin-degrading enzymes are important virulence-associated factors that facilitate fungal colonization and host tissue maceration, but their evolutionary diversification and functional roles in B. dothidea during woody host infection remain poorly understood. Comparative genomic analysis revealed lineage-specific variation in the GH28 glycoside hydrolase family among the examined Botryosphaeriaceae species, with B. dothidea exhibiting an expanded GH28 repertoire relative to the analyzed species. Expression analysis and functional assays revealed that BdGH28_3 showed the highest transcript abundance during infection stage and contributed to the full virulence of B. dothidea. A predicted protein–protein interaction (PPI) network suggested potential associations between BdGH28_3 and other pectinolytic enzymes, including polygalacturonases, pectin lyases, and pectinesterases. Collectively, these findings identify GH28 diversification as a distinctive feature of the B. dothidea genome and establish BdGH28_3 as a virulence-associated member, providing a foundation for investigating GH28-mediated pathogenicity in woody hosts.
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.
Xin-Long Wang, Zhe-Ran Liu, Fei-Fei Zan et al.· Journal of Agricultural and...· 0 citations
Cassava bacterial blight (CBB), caused by Xanthomonas phaseoli pv. manihotis (Xpm), is a major disease constraining cassava production. Although overexpression of the Xpm effector XopAG enhances Arabidopsis susceptibility to Pseudomonas syringae pv. tomato DC3000, its virulence mechanism in cassava remains unclear. The study showed that deletion of XopAG did not affect morphology or extracellular enzyme production of Xpm, but significantly attenuated its virulence on cassava. Quantitative proteomic analysis revealed that 267 differentially accumulated proteins (DAPs) at 6 hours post-inoculation (hpi) and 429 DAPs at 6 days post-inoculation (dpi) were identified in cassava leaves inoculated with ΔxopAG mutant compared with Xpm. KEGG enrichment analysis showed that DAPs were significantly enriched in phenylpropanoid and flavonoid biosynthesis pathways. In the absence of XopAG, flavonoid biosynthesis-related proteins and genes (DFR, ANR, ANS, CYP75A1, FLS) were up-regulated, accompanied by increased total flavonoid content in cassava leaves during early infection. Furthermore, cassava small heat shock protein MeHSP26 was identified as a host target of XopAG, and two proteins interact in both cytoplasm and nucleus in N. benthamiana. Importantly, degradation assay reveals that XopAG promotes MeHSP26 degradation in N. benthamiana. Silencing MeHSP26 compromised cassava resistance to Xpm, following reducing flavonoid content and suppressing flavonoid gene expression. Together, these results demonstrate that XopAG promotes MeHSP26 degradation to suppress flavonoid biosynthesis, thereby attenuating cassava immunity during early Xpm inoculation. This work provides insights into cassava-Xpm interactions by revealing effector manipulation of metabolic pathways facilitates inoculation.
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