Biology subjects

Rufian, J. S.

Publications and source records attributed to Rufian, J. S..

5 recordsLinked to original sources

bioRxiv2025

The Ralstonia solanacearum effector RipAV targets Plant U-box proteins and induces proteasomal-dependent degradation of BIK1

Plants have developed a complex immune system to detect and respond to invading pathogens. A critical aspect of this defence relies on regulatory mechanisms that control the activation of immune responses, ensuring these are efficient yet do not compromise overall plant performance. Many pathogens secrete proteins called effectors to manipulate plant cellular functions, suppressing plant immunity and promoting infection. Here, we show that the bacterial effector RipAV, secreted by the soil-borne bacterial pathogen Ralstonia solanacearum, hijacks a major immune signalling hub to suppress immune responses. RipAV targets members of the plant-specific ubiquitin ligase (PUB) family and calcium-dependent protein kinase 28 (CPK28), which has been shown to phosphorylate a set of PUBs to enhance their activity and regulate the stability of the key immune regulator BIK1. RipAV association enhances the CPK28-mediated phosphorylation of PUBs, inducing the proteasome-mediated degradation of BIK1 and the suppression of immunity. Importantly, we found that RipAV is required for maintaining a low accumulation of BIK1 during a R. solanacearum infection. These findings provide new insights into the sophisticated strategies employed by pathogens to subvert plant immunity.

plant biology↗

bioRxiv2024

Cooperative colonization of the host and pathogen dissemination involves stochastic and spatially structured expression of virulence traits

Bacteria respond to changing environments by altering gene expression. Some responses display probabilistic cell-to-cell variation within isogenic populations. A few paradigmatic examples in animal pathogens have demonstrated that this phenotypic heterogeneity has biological relevance for virulence. We investigate single-cell flagellar expression in relation to type III secretion expression in the plant pathogen Pseudomonas syringae and describe that both systems undergo phenotypic heterogeneity throughout plant colonization. We establish that high expression of these system carries growth penalties. Stochastic, spatial and time factors shape dynamics of a phenotypically diverse population which displays division of labor during colonization: T3SSON bacteria effectors act as common goods to suppress immunity, allowing the increase of motile bacteria that actively leave the infected tissue before necrosis. This study provides a comprehensive view of how processes underlying bacterial specialization play out in the context of complex and changing environments of biological and applied relevance such as host colonization.

microbiology↗

bioRxiv2020

The Arabidopsis E3 ubiquitin ligase PUB4 regulates BIK1 homeostasis and is targeted by a bacterial type-III effector

Plant immunity is tightly controlled by a complex and dynamic regulatory network, which ensures optimal activation upon detection of potential pathogens. Accordingly, each component of this network is a potential target for manipulation by pathogens. Here, we report that RipAC, a type III-secreted effector from the bacterial pathogen Ralstonia solanacearum, targets the plant E3 ubiquitin ligase PUB4 to inhibit pattern-triggered immunity (PTI). PUB4 plays a positive role in PTI by regulating the homeostasis of the central immune kinase BIK1. Before PAMP perception, PUB4 promotes the degradation of non-activated BIK1, while, after PAMP perception, PUB4 contributes to the accumulation of activated BIK1. RipAC leads to BIK1 degradation, which correlates with its PTI-inhibitory activity. RipAC causes a reduction in pathogen-associated molecular pattern (PAMP)-induced PUB4 accumulation and phosphorylation. Our results shed light on the role played by PUB4 in immune regulation, and illustrate an indirect targeting of the immune signalling hub BIK1 by a bacterial effector.

plant biology↗

bioRxiv2020

A bacterial effector uncovers a metabolic pathway involved in resistance to bacterial wilt disease

Bacterial wilt caused by the soil-borne pathogen Ralstonia solanacearum is a devastating disease worldwide. Upon plant colonization, R. solanacearum replicates massively, causing plant wilting and death; collapsed infected tissues then serve as a source of inoculum. In this work, we show that the metabolic pathway mediated by pyruvate decarboxylases (PDCs), activated in response to low oxygen and involved in drought stress tolerance, contributes to resistance against bacterial wilt disease. Arabidopsis and tomato plants with deficient PDC activity are more susceptible to bacterial wilt, and treatment with either pyruvic acid or acetic acid (substrate and product of the PDC pathway, respectively) enhances resistance. An effector protein secreted by R. solanacearum, RipAK, interacts with PDCs and inhibits their oligomerisation and enzymatic activity. This work reveals a metabolic pathway involved in resistance to biotic and abiotic stresses, and a bacterial virulence strategy to promote disease and the completion of the pathogenic life cycle.

plant biology↗

bioRxiv2020

The bacterial effector HopZ1a acetylates MKK7 to suppress plant immunity

The Pseudomonas syringae type III secretion system translocates effector proteins into the host cell cytosol, suppressing plant basal immunity triggered upon recognition of pathogen-associated molecular patterns (PAMPs), and effector-triggered immunity. Effector HopZ1a suppresses local and systemic immunity triggered by PAMPs and effectors, through target acetylation. HopZ1a has been shown to target several plant proteins, but none fully substantiates HopZ1a-associated immune suppression. Here, we investigate Arabidopsis thaliana mitogen-activated protein kinase kinases (MKKs) as potential targets, focusing on AtMKK7, a positive regulator of local and systemic immunity. We analyse HopZ1a interference with AtMKK7 by translocation of HopZ1a from bacteria inoculated into Arabidopsis expressing MKK7 from an inducible promoter. Reciprocal phenotypes are analysed on plants expressing a construct quenching MKK7 native expression. We analyse HopZ1a-MKK7 interaction by three independent methods, and the relevance of acetylation by in vitro kinase and in planta functional assays. We demonstrate AtMKK7 contribution to immune signalling showing MKK7-dependent flg22-induced ROS burst, MAPK activation, and callose accumulation, plus AvrRpt2-triggered MKK7-dependent signalling. Further, we demonstrate HopZ1a suppression of all MKK7-dependent responses, HopZ1a-MKK7 interaction in planta, and HopZ1a acetylation of MKK7 in a lysine required for full kinase activity. We demonstrate that HopZ1a targets AtMKK7 to suppress local and systemic plant immunity.

plant biology↗