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Ruiz-Albert, J.

Publications and source records attributed to Ruiz-Albert, J..

5 recordsLinked to original sources

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↗

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↗

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↗

MiRNA and phasiRNAs-mediated regulation of TIR-NBS-LRR defense genes in Arabidopsis thaliana

Plants encode large numbers of intracellular immune receptors known as resistance (R) proteins or nucleotide-binding (NB) leucine-rich repeat (LRR) receptors (NLRs), involved in perception of pathogen-derived effectors and activation of immunity. Here, we report a two-tiered regulatory network mediated by microRNA and secondary phased small RNAs (phasiRNA) that targets the silencing of dozens of NLR genes encoding yet uncharacterized members of the Toll/interleukin-1 (TIR)-NBS-LRR (TNLs) subfamily in Arabidopsis. We show that miR825-5p downregulates expression of Arabidopsis AT5G38850 gene (renamed as microRNA-silenced TNL 1 or MIST1) by targeting the sequence coding for a highly conserved functional amino acid motif (TIR2) within the TIR domain of the receptor. Further, we show that MIST1 functions as a regulatory hub, since miRNA825-5p triggers RDR6-mediated processing of MIST1 transcripts, to generate trans-acting phasiRNAs that in turn target, a wide network of TNL genes for gene silencing. Regulation through MIST1 affects disease resistance against the model bacterial pathogen Pseudomonas syringae, since altered levels of miRNA825-5p lead to changes in Arabidopsis ability to establish basal defenses against this pathogen. MiR825-5p is expressed in unchallenged adult leaves and its production is down regulated in response to PAMPs such as bacterial flagellin but also fungal chitin.

plant biology↗

Geminivirus Replication Protein impairs SUMO conjugation of PCNA at two acceptor sites

Geminiviruses are DNA viruses that replicate in nuclei of infected plant cells using the plant DNA replication machinery, including PCNA (Proliferating cellular nuclear antigen), a cofactor that orchestrates genome duplication and maintenance by recruiting crucial players to replication forks. These viruses encode a multifunctional protein, Rep, which is essential for viral replication, induces the accumulation of the host replication machinery and interacts with several host proteins, including PCNA and the SUMO E2 conjugation enzyme (SCE1). Post-translational modification of PCNA by ubiquitin or SUMO plays an essential role in the switching of PCNA between interacting partners during DNA metabolism processes (e.g. replication, recombination, repair, etc.). In yeast, PCNA sumoylation has been associated to DNA repair involving homologous recombination (HR). Previously, we reported that ectopic Rep expression results in very specific changes in the sumoylation pattern of plant cells. In this work, we show, using a reconstituted sumoylation system in Escherichia coli, that tomato PCNA is sumoylated at two residues, K254 and K164, and that co-expression of the geminivirus protein Rep suppresses sumoylation at these lysines. Finally, we confirm that PCNA is sumoylated in planta and that Rep also interferes with PCNA sumoylation in plant cells.\n\nImportanceSUMO adducts have a key role in regulating the activity of animal and yeast PCNA on DNA repair and replication. Our work demonstrates for the first time that sumoylation of plant PCNA occurs in plant cells and that a plant virus interferes with this modification. This work marks the importance of sumoylation in allowing viral infection and replication in plants. Moreover, it constitutes a prime example of viral proteins interfering with post-translational modifications of selected host factors to create a proper environment for infection.

plant biology↗