research on plant resistance gene for disease
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Rescooped by tianxing84 from Plant-Microbe Symbiosis
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Bacillus amyloliquefaciens T-5 may prevent Ralstonia solanacearum infection through competitive exclusion

Investigation of the properties and mechanisms of the interactions of root-colonizing biocontrol bacteria and plant pathogens is necessary to optimize the biocontrol strategies. In the present study, the interaction of a biocontrol strain Bacillus amyloliquefaciens T-5 tagged with a green fluorescent protein marker and a bacterial wilt pathogen Ralstonia solanacearum QL-Rs1115 tagged with red fluorescent protein marker was studied on tomato roots using different inoculation methods. The results showed that in the co-culture experiment, the population of pathogen QL-RFP was decreased by increasing the initial inoculum concentration of biocontrol strain. In the greenhouse experiment, both strains T-5-GFP and QL-RFP colonized tomato roots (root tips, root hairs, primary roots, and root junctions) and formed a biofilm on the root surfaces as determined by dilution plating and confocal laser scanning microscopy (CLSM) techniques. However, the root colonization of pathogen strain QL-RFP was almost completely suppressed in the presence of biocontrol strain T-5-GFP when both soil and plant seedlings were treated with T-5-GFP. The results of this study revealed the effectiveness of strain B. amyloliquefaciens T-5 as a biocontrol agent against tomato wilt pathogen and the significance of inoculation method used to inoculate biocontrol strain.

Via Jean-Michel Ané
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Rescooped by tianxing84 from Plants and Microbes
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MPMI: The Fusarium oxysporum Effector Six6 Contributes to Virulence and Suppresses I-2-Mediated Cell Death (2014)

MPMI: The Fusarium oxysporum Effector Six6 Contributes to Virulence and Suppresses I-2-Mediated Cell Death (2014) | research on plant resistance gene for disease | Scoop.it

Plant pathogens secrete effectors to manipulate their host and facilitate colonization. Fusarium oxysporum f. sp. lycopersici is the causal agent of Fusarium wilt disease in tomato. Upon infection, F. oxysporum f. sp.lycopersici secretes numerous small proteins into the xylem sap (Six proteins). Most Six proteins are unique to F. oxysporum, but Six6 is an exception; a homolog is also present in two Colletotrichum spp. SIX6expression was found to require living host cells and a knockout ofSIX6 in F. oxysporum f. sp. lycopersici compromised virulence, classifying it as a genuine effector. Heterologous expression of SIX6did not affect growth of Agrobacterium tumefaciens in Nicotiana benthamiana leaves or susceptibility of Arabidopsis thaliana towardVerticillium dahliae, Pseudomonas syringae, or F. oxysporum, suggesting a specific function for F. oxysporum f. sp. lycopersici Six6 in the F. oxysporum f. sp. lycopersici– tomato pathosystem. Remarkably, Six6 was found to specifically suppress I-2-mediated cell death (I2CD) upon transient expression in N. benthamiana, whereas it did not compromise the activity of other cell-death-inducing genes. Still, this I2CD suppressing activity of Six6 does not allow the fungus to overcome I-2 resistance in tomato, suggesting that I-2-mediated resistance is independent from cell death.


Via Kamoun Lab @ TSL
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Rescooped by tianxing84 from Plant-microbe interaction
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Arabidopsis HSP90 protein modulates RPP4-mediated temperature-dependent cell death and defense responses

Arabidopsis HSP90 protein modulates RPP4-mediated temperature-dependent cell death and defense responses | research on plant resistance gene for disease | Scoop.it

Plant defense responses are regulated by temperature. In Arabidopsis, the chilling-sensitive mutant chs2-1 (rpp4-1d) contains a gain-of-function mutation in the TIR-NB-LRR (Toll and interleukin 1 transmembrane receptor-nucleotide binding-leucine-rich repeat) gene, RPP4 (RECOGNITION OF PERONOSPORA PARASITICA 4), which leads to constitutive activation of the defense response at low temperatures.Here, we identified and characterized two suppressors of rpp4-1d from a genetic screen, hsp90.2 and hsp90.3, which carry point mutations in the cytosolic heat shock proteins HSP90.2 and HSP90.3, respectively.The hsp90 mutants suppressed the chilling sensitivity of rpp4-1d, including seedling lethality, activation of the defense responses and cell death under chilling stress. The hsp90 mutants exhibited compromised RPM1 (RESISTANCE TO PSEUDOMONAS MACULICOLA 1)-, RPS4 (RIBOSOMAL PROTEIN S4)- and RPP4-mediated pathogen resistance. The wild-type RPP4 and the mutated form rpp4 could interact with HSP90 to form a protein complex. Furthermore, RPP4 and rpp4 proteins accumulated in the cytoplasm and nucleus at normal temperatures, whereas the nuclear accumulation of the mutated rpp4 was decreased at low temperatures. Genetic analysis of the intragenic suppressors of rpp4-1d revealed the important functions of the NB-ARC and LRR domains of RPP4 in temperature-dependent defense signaling. In addition, the rpp4-1d-induced chilling sensitivity was largely independent of the WRKY70 or MOS (modifier of snc1) genes.This study reveals that Arabidopsis HSP90 regulates RPP4-mediated temperature-dependent cell death and defense responses.


Via Christophe Jacquet, Suayib Üstün
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Rescooped by tianxing84 from Plant-Microbe Interaction
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TFBMs of NBS-LRR Genes of Rice and Arabidopsis - Genome-wide Identification and Characterization of Transcription Factor Binding Motifs of NBS-LRR Genes in Rice and Arabidopsis

TFBMs of NBS-LRR Genes of Rice and Arabidopsis - Genome-wide Identification and Characterization of Transcription Factor Binding Motifs of NBS-LRR Genes in Rice and Arabidopsis | research on plant resistance gene for disease | Scoop.it

Upstream sequences of 206 entire NBS-LRR genes of Arabidopsis and 120 genes of rice were analyzed with three highly reliable motif prediction tools for enhanced accuracy of prediction and characterization of potential transcription factor binding motifs (TFBMs).  The analysis revealed that rice sequences have many unique TFBMs and are more evolved in gene expression mechanisms. 


Via Elsa Ballini, Guogen Yang
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Rescooped by tianxing84 from Effectors and Plant Immunity
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New Phytol.: SWEET sugar transporters for phloem transport and pathogen nutrition (2013)

New Phytol.: SWEET sugar transporters for phloem transport and pathogen nutrition (2013) | research on plant resistance gene for disease | Scoop.it

Many intercellular solute transport processes require an apoplasmic step, that is, efflux from one cell and subsequent uptake by an adjacent cell. Cellular uptake transporters have been identified for many solutes, including sucrose; however, efflux transporters have remained elusive for a long time. Cellular efflux of sugars plays essential roles in many processes, such as sugar efflux as the first step in phloem loading, sugar efflux for nectar secretion, and sugar efflux for supplying symbionts such as mycorrhiza, and maternal efflux for filial tissue development. Furthermore, sugar efflux systems can be hijacked by pathogens for access to nutrition from hosts. Mutations that block recruitment of the efflux mechanism by the pathogen thus cause pathogen resistance. Until recently, little was known regarding the underlying mechanism of sugar efflux. The identification of sugar efflux carriers, SWEETs (Sugars Will Eventually be Exported Transporters), has shed light on cellular sugar efflux. SWEETs appear to function as uniporters, facilitating diffusion of sugars across cell membranes. Indeed, SWEETs probably mediate sucrose efflux from putative phloem parenchyma into the phloem apoplasm, a key step proceeding phloem loading. Engineering of SWEET mutants using transcriptional activator-like effector nuclease (TALEN)-based genomic editing allowed the engineering of pathogen resistance. The widespread expression of the SWEET family promises to provide insights into many other cellular efflux mechanisms.

 

Li-Qing Chen


Via Nicolas Denancé
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Rescooped by tianxing84 from plant cell genetics
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PLOS ONE: System for Stable β-Estradiol-Inducible Gene Expression in the Moss Physcomitrella patens

PLOS ONE: System for Stable β-Estradiol-Inducible Gene Expression in the Moss Physcomitrella patens | research on plant resistance gene for disease | Scoop.it

Inducible transgene expression provides a useful tool to analyze gene function. The mossPhyscomitrella patens is a model basal land plant with well-developed research tools, including a high efficiency of gene targeting and substantial genomics resources. However, current systems for controlled transgene expression remain limited. Here we report the development of an estrogen receptor mediated inducible gene expression system, based on the system used in flowering plants. After identifying the appropriate promoters to drive the chimeric transducer, we succeeded in inducing transcription over 1,000-fold after 24 h incubation with β-estradiol. The P. patens system was also effective for high-level long-term induction of gene expression; transcript levels of the activated gene were maintained for at least seven days on medium containing β-estradiol. We also established two potentially neutral targeting sites and a set of vectors for reproducible expression of two transgenes. This β-estradiol-dependent system will be useful to test genes individually or in combination, allowing stable, inducible transgenic expression in P.patens.


Via Jean-Pierre Zryd
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Rescooped by tianxing84 from Plants and Microbes
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Curr Opin Plant Biol: Genetic and cellular mechanisms regulating plant responses to necrotrophic pathogens (2013)

Curr Opin Plant Biol: Genetic and cellular mechanisms regulating plant responses to necrotrophic pathogens (2013) | research on plant resistance gene for disease | Scoop.it

Necrotrophs are plant pathogens that kill host cells and proliferate on nutrients from dead or dying tissues causing devastating diseases of horticultural and agronomic crops. Their interactions with plants involve a complex network of pathogen disease factors and corresponding plant immune response regulators. Mechanisms of quantitative resistance and the major regulators intersect regardless of pathogen life style. By contrast, some plant immune responses, such as effector-triggered immunity (ETI), a major source of qualitative resistance to biotrophs, are co-opted by necrotrophs to promote disease, which highlights the disparate plant immunity systems. Advances towards understanding mechanisms and processes underlying host responses to necrotrophs are summarized.


Via Kamoun Lab @ TSL
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Rescooped by tianxing84 from Trends in MPMI
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J Experimental Botany: Pathogen-associated molecular pattern-triggered immunity and resistance to the root pathogen Phytophthora parasitica in Arabidopsis (2013)

J Experimental Botany: Pathogen-associated molecular pattern-triggered immunity and resistance to the root pathogen Phytophthora parasitica in Arabidopsis (2013) | research on plant resistance gene for disease | Scoop.it

The cellulose binding elicitor lectin (CBEL) of the genus Phytophthora induces necrosis and immune responses in several plant species, including Arabidopsis thaliana. However, the role of CBEL-induced responses in the outcome of the interaction is still unclear. This study shows that some of CBEL-induced defence responses, but not necrosis, required the receptor-like kinase BAK1, a general regulator of basal immunity in Arabidopsis, and the production of a reactive oxygen burst mediated by respiratory burst oxidases homologues (RBOH). Screening of a core collection of 48 Arabidopsis ecotypes using CBEL uncovered a large variability in CBEL-induced necrotic responses. Analysis of non-responsive CBEL lines Ws-4, Oy-0, and Bla-1 revealed that Ws-4 and Oy-0 were also impaired in the production of the oxidative burst and expression of defence genes, whereas Bla-1 was partially affected in these responses. Infection tests using two Phytophthora parasitica strains, Pp310 and Ppn0, virulent and avirulent, respectively, on the Col-0 line showed that BAK1 and RBOH mutants were susceptible to Ppn0, suggesting that some immune responses controlled by these genes, but not CBEL-induced cell death, are required for Phytophthora parasitica resistance. However, Ws-4, Oy-0, and Bla-1 lines were not affected in Ppn0 resistance, showing that natural variability in CBEL responsiveness is not correlated to Phytophthora susceptibility. Overall, the results uncover a BAK1- and RBOH-dependent CBEL-triggered immunity essential for Phytophthora resistance and suggest that natural quantitative variation of basal immunity triggered by conserved general elicitors such as CBEL does not correlate to Phytophthora susceptibility.


Via Nicolas Denancé, Kamoun Lab @ TSL, CP
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Rescooped by tianxing84 from Plant-microbe interaction
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Perception of conserved pathogen elicitors at the plasma membrane leads to relocalization of the Arabidopsis PEN3 transporter

Perception of conserved pathogen elicitors at the plasma membrane leads to relocalization of the Arabidopsis PEN3 transporter | research on plant resistance gene for disease | Scoop.it

Abstract

The Arabidopsis PENETRATION RESISTANCE 3 (PEN3) ATP binding cassette transporter participates in nonhost resistance to fungal and oomycete pathogens and is required for full penetration resistance to the barley powdery mildew Blumeria graminis f. sp. hordei. PEN3 resides in the plasma membrane and is recruited to sites of attempted penetration by invading fungal appressoria, where the transporter shows strong focal accumulation. We report that recruitment of PEN3 to sites of pathogen detection is triggered by perception of pathogen-associated molecular patterns, such as flagellin and chitin. PEN3 recruitment requires the corresponding pattern recognition receptors but does not require the BAK1 coreceptor. Pathogen- and pathogen-associated molecular pattern-induced focal accumulation of PEN3 and the PENETRATION RESISTANCE 1 (PEN1) syntaxin show differential sensitivity to specific pharmacological inhibitors, indicating distinct mechanisms for recruitment of these defense-associated proteins to the host–pathogen interface. Focal accumulation of PEN3 requires actin but is not affected by inhibitors of microtubule polymerization, secretory trafficking, or protein synthesis, and plasmolysis experiments indicate that accumulation of PEN3 occurs outside of the plasma membrane within papillae. Our results implicate pattern recognition receptors in the recruitment of defense-related proteins to sites of pathogen detection. Additionally, the process through which PEN3 is recruited to the host–pathogen interface is independent of new protein synthesis and BFA-sensitive secretory trafficking events, suggesting that existing PEN3 is redirected through an unknown trafficking pathway to sites of pathogen detection for export into papillae.


Via Suayib Üstün
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Rescooped by tianxing84 from Plants and Microbes
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PLOS Pathogens: The Salmonella Type III Effector SspH2 Specifically Exploits the NLR Co-chaperone Activity of SGT1 to Subvert Immunity (2013)

PLOS Pathogens: The Salmonella Type III Effector SspH2 Specifically Exploits the NLR Co-chaperone Activity of SGT1 to Subvert Immunity (2013) | research on plant resistance gene for disease | Scoop.it

To further its pathogenesis, S. Typhimurium delivers effector proteins into host cells, including the novel E3 ubiquitin ligase (NEL) effector SspH2. Using model systems in a cross-kingdom approach we gained further insight into the molecular function of this effector. Here, we show that SspH2 modulates innate immunity in both mammalian and plant cells. In mammalian cell culture, SspH2 significantly enhanced Nod1-mediated IL-8 secretion when transiently expressed or bacterially delivered. In addition, SspH2 also enhanced an Rx-dependent hypersensitive response in planta. In both of these nucleotide-binding leucine rich repeat receptor (NLR) model systems, SspH2-mediated phenotypes required its catalytic E3 ubiquitin ligase activity and interaction with the conserved host protein SGT1. SGT1 has an essential cell cycle function and an additional function as an NLR co-chaperone in animal and plant cells. Interaction between SspH2 and SGT1 was restricted to SGT1 proteins that have NLR co-chaperone function and accordingly, SspH2 did not affect SGT1 cell cycle functions. Mechanistic studies revealed that SspH2 interacted with, and ubiquitinated Nod1 and could induce Nod1 activity in an agonist-independent manner if catalytically active. Interestingly, SspH2 in vitro ubiquitination activity and protein stability were enhanced by SGT1. Overall, this work adds to our understanding of the sophisticated mechanisms used by bacterial effectors to co-opt host pathways by demonstrating that SspH2 can subvert immune responses by selectively exploiting the functions of a conserved host co-chaperone.


Via Kamoun Lab @ TSL
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Rescooped by tianxing84 from Plant-microbe interaction
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Pseudomonas syringae pv. tomato DC3000: A Model Pathogen for Probing Disease Susceptibility and Hormone Signaling in Plants

Pseudomonas syringae pv. tomato DC3000: A Model Pathogen for Probing Disease Susceptibility and Hormone Signaling in Plants | research on plant resistance gene for disease | Scoop.it

Scooped from: Annual Review of Phytopathology, 2013
Authors: Xiu-Fang Xin and Sheng Yang He

Summary: Since the early 1980s, various strains of the gram-negative bacterial pathogen Pseudomonas syringae have been used as models for understanding plant-bacterial interactions. In 1991, a P. syringae pathovar tomato (Pst) strain, DC3000, was reported to infect not only its natural host tomato but also Arabidopsis in the laboratory, a finding that spurred intensive efforts in the subsequent two decades to characterize the molecular mechanisms by which this strain causes disease in plants. Genomic analysis shows that Pst DC3000 carries a large repertoire of potential virulence factors, including proteinaceous effectors that are secreted through the type III secretion system and a polyketide phytotoxin called coronatine, which structurally mimics the plant hormone jasmonate ( JA). Study of Pst DC3000 pathogenesis has not only provided several conceptual advances in understanding how a bacterial pathogen employs type III effectors to suppress plant immune responses and promote disease susceptibility but has also facilitated the discovery of the immune function of stomata and key components of JA signaling in plants. The concepts derived from the study of Pst DC3000 pathogenesis may prove useful in understanding pathogenesis mechanisms of other plant pathogens.


Via Freddy Monteiro, Suayib Üstün
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Damien Meyer's curator insight, June 19, 2013 3:25 PM

remarkable review

Rescooped by tianxing84 from Plant Pathogenomics
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PLOS Genetics: Plant-Symbiotic Fungi as Chemical Engineers: Multi-Genome Analysis of the Clavicipitaceae Reveals Dynamics of Alkaloid Loci (2013)

PLOS Genetics: Plant-Symbiotic Fungi as Chemical Engineers: Multi-Genome Analysis of the Clavicipitaceae Reveals Dynamics of Alkaloid Loci (2013) | research on plant resistance gene for disease | Scoop.it

The fungal family Clavicipitaceae includes plant symbionts and parasites that produce several psychoactive and bioprotective alkaloids. The family includes grass symbionts in the epichloae clade (Epichloë and Neotyphodium species), which are extraordinarily diverse both in their host interactions and in their alkaloid profiles. Epichloae produce alkaloids of four distinct classes, all of which deter insects, and some—including the infamous ergot alkaloids—have potent effects on mammals. The exceptional chemotypic diversity of the epichloae may relate to their broad range of host interactions, whereby some are pathogenic and contagious, others are mutualistic and vertically transmitted (seed-borne), and still others vary in pathogenic or mutualistic behavior. We profiled the alkaloids and sequenced the genomes of 10 epichloae, three ergot fungi (Claviceps species), a morning-glory symbiont (Periglandula ipomoeae), and a bamboo pathogen (Aciculosporium take), and compared the gene clusters for four classes of alkaloids. Results indicated a strong tendency for alkaloid loci to have conserved cores that specify the skeleton structures and peripheral genes that determine chemical variations that are known to affect their pharmacological specificities. Generally, gene locations in cluster peripheries positioned them near to transposon-derived, AT-rich repeat blocks, which were probably involved in gene losses, duplications, and neofunctionalizations. The alkaloid loci in the epichloae had unusual structures riddled with large, complex, and dynamic repeat blocks. This feature was not reflective of overall differences in repeat contents in the genomes, nor was it characteristic of most other specialized metabolism loci. The organization and dynamics of alkaloid loci and abundant repeat blocks in the epichloae suggested that these fungi are under selection for alkaloid diversification. We suggest that such selection is related to the variable life histories of the epichloae, their protective roles as symbionts, and their associations with the highly speciose and ecologically diverse cool-season grasses.

 


Via Kamoun Lab @ TSL
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Rescooped by tianxing84 from Plant Pathogenomics
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BMC Genomics: MITEs in the promoters of effector genes allow prediction of novel virulence genes in Fusarium oxysporum (2013)

BMC Genomics: MITEs in the promoters of effector genes allow prediction of novel virulence genes in Fusarium oxysporum (2013) | research on plant resistance gene for disease | Scoop.it

Background - The plant-pathogenic fungus Fusarium oxysporum f.sp.lycopersici (Fol) has accessory, lineage-specific (LS) chromosomes that can be transferred horizontally between strains. A single LS chromosome in the Fol4287 reference strain harbors all known Fol effector genes. Transfer of this pathogenicity chromosome confers virulence to a previously non-pathogenic recipient strain. We hypothesize that expression and evolution of effector genes is influenced by their genomic context.

 

Results - To gain a better understanding of the genomic context of the effector genes, we manually curated the annotated genes on the pathogenicity chromosome and identified and classified transposable elements. Both retro- and DNA transposons are present with no particular overrepresented class. Retrotransposons appear evenly distributed over the chromosome, while DNA transposons tend to concentrate in large chromosomal subregions. In general, genes on the pathogenicity chromosome are dispersed within the repeat landscape. Effector genes are present within subregions enriched for DNA transposons. A miniature Impala (mimp) is always present in their promoters. Although promoter deletion studies of two effector gene loci did not reveal a direct function of the mimp for gene expression, we were able to use proximity to a mimp as a criterion to identify new effector gene candidates. Through xylem sap proteomics we confirmed that several of these candidates encode proteins secreted during plant infection.

 

Conclusions - Effector genes in Fol reside in characteristic subregions on a pathogenicity chromosome. Their genomic context allowed us to develop a method for the successful identification of novel effector genes. Since our approach is not based on effector gene similarity, but on unique genomic features, it can easily be extended to identify effector genes in Fo strains with different host specificities.


Via Kamoun Lab @ TSL
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Rescooped by tianxing84 from TAL effector science
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Breaking the DNA-binding code of Ralstonia solanacearum TAL effectors provides new possibilities to generate plant resistance genes against bacterial wilt disease - New Phytologist

(Via T. Lahaye & T. Schreiber) De Lange et al 2013 Ralstonia solanacearum is a devastating bacterial phytopathogen with a broad host range. Ralstonia solanacearum injected effector proteins (Rips) are key to the successful invasion of host plants. We have characterized Brg11(hrpB-regulated 11), the first identified member of a class of Rips with high sequence similarity to the transcription activator-like (TAL) effectors of Xanthomonas spp., collectively termed RipTALs. Fluorescence microscopy of in planta expressed RipTALs showed nuclear localization. Domain swaps between Brg11 and Xanthomonas TAL effector (TALE) AvrBs3 (avirulence protein triggering Bs3 resistance) showed the functional interchangeability of DNA-binding and transcriptional activation domains. PCR was used to determine the sequence of brg11 homologs from strains infecting phylogenetically diverse host plants. Brg11 localizes to the nucleus and activates promoters containing a matching effector-binding element (EBE). Brg11 and homologs preferentially activate promoters containing EBEs with a 5′ terminal guanine, contrasting with the TALE preference for a 5′ thymine. Brg11 and other RipTALs probably promote disease through the transcriptional activation of host genes. Brg11 and the majority of homologs identified in this study were shown to activate similar or identical target sequences, in contrast to TALEs, which generally show highly diverse target preferences. This information provides new options for the engineering of plants resistant to R. solanacearum.


Via dromius
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Rescooped by tianxing84 from Plants and Microbes
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Plant Physiology: The leucine-rich repeat receptor-like kinase BAK1 and the cytochrome P450 PAD3 contribute to innate immunity to aphids in Arabidopsis (2014)

Plant Physiology: The leucine-rich repeat receptor-like kinase BAK1 and the cytochrome P450 PAD3 contribute to innate immunity to aphids in Arabidopsis (2014) | research on plant resistance gene for disease | Scoop.it

The importance of pathogen-associated molecular patterns (PAMPs)-triggered immunity (PTI) against microbial pathogens has been recently demonstrated. However, it is currently unclear if this layer of immunity mediated by surface-localized pattern recognition receptors (PRRs) also plays a role in basal resistance to insects, such as aphids. Here we show that PTI is an important component of plant innate immunity to insects. Extract of the green peach aphid (GPA) Myzus persicae triggers responses characteristic of PTI in Arabidopsis. Two separate eliciting GPA-derived fractions trigger induced-resistance to GPA that is dependent on the leucine-rich repeat receptor like kinase (LRR-RLK) BRASSINOSTEROID INSENSITIVE1-ASSOCIATED KINASE1/ SOMATIC-EMBRYOGENESIS RECEPTOR-LIKE KINASE3 (BAK1/AtSERK3), which is a key regulator of several LRR-containing PRRs. BAK1 is required for GPA elicitor-mediated induction of reactive oxygen species (ROS) and callose deposition. Arabidopsis bak1 mutant plants are also compromised in immunity to Acyrthosiphon pisum (pea aphid) for which Arabidopsis is normally a non-host. Aphid-derived elicitors induce expression of PHYTOALEXIN DEFICIENT 3 (PAD3), a key cytochrome P450 involved in the biosynthesis of camalexin, which is a major Arabidopsis phytoalexin that is toxic to GPA. PAD3 is also required for induced-resistance to GPA, independently of BAK1 and ROS production. Our results reveal that plant innate immunity to insects may involve early perception of elicitors by cell surface-localized PRRs leading to subsequent downstream immune signaling.


Via Kamoun Lab @ TSL
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Rescooped by tianxing84 from Effectors and Plant Immunity
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Plant–microbe interactions as drivers of ecosystem functions relevant for the biodegradation of organic contaminants

Plant–microbe interactions as drivers of ecosystem functions relevant for the biodegradation of organic contaminants | research on plant resistance gene for disease | Scoop.it

Highlights• Biotransformation is an ecosystem property.• Microbes are the main drivers in biotransformation.• Dispersal of chemicals and bacteria drives degradation effectiveness.• Ecosystem stability is increased by plant–microbe interactions


Via Francis Martin, Jean-Michel Ané, Nicolas Denancé
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An E4 Ligase Facilitates Polyubiquitination of Plant Immune Receptor Resistance Proteins in Arabidopsis

An E4 Ligase Facilitates Polyubiquitination of Plant Immune Receptor Resistance Proteins in Arabidopsis | research on plant resistance gene for disease | Scoop.it

Proteins with nucleotide binding and leucine-rich repeat domains (NLRs) serve as immune receptors in animals and plants that recognize pathogens and activate downstream defense responses. As high accumulation of NLRs can result in unwarranted autoimmune responses, their cellular concentrations must be tightly regulated. However, the molecular mechanisms of this process are poorly detailed. The F-box protein Constitutive expressor of PR genes 1 (CPR1) was previously identified as a component of a Skp1, Cullin1, F-box protein E3 complex that targets NLRs, including Suppressor of NPR1, Constitutive 1 (SNC1) and Resistance to Pseudomonas syringae 2 (RPS2), for ubiquitination and further protein degradation. From a forward genetic screen, we identified Mutant, snc1-enhancing 3 (MUSE3), an E4 ubiquitin ligase involved in polyubiquitination of its protein targets. Knocking out MUSE3 in Arabidopsis thaliana results in increased levels of NLRs, including SNC1 and RPS2, whereas overexpressing MUSE3 together with CPR1 enhances polyubiquitination and protein degradation of these immune receptors. This report on the functional role of an E4 ligase in plants provides insight into the scarcely understood NLR degradation pathway.


Via Suayib Üstün
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Dinesh Dhurvas's curator insight, March 15, 2014 5:49 PM

E4 Ligase(MUSE3) adds up more Ub-Ub-Ub-Ub-Ub-Ubs to its target following E3 Ligase ! 

Rescooped by tianxing84 from Plant genetics
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PLOS Genetics: An Atypical Kinase under Balancing Selection Confers Broad-Spectrum Disease Resistance in Arabidopsis

PLOS Genetics: An Atypical Kinase under Balancing Selection Confers Broad-Spectrum Disease Resistance in Arabidopsis | research on plant resistance gene for disease | Scoop.it

The failure of gene-for-gene resistance traits to provide durable and broad-spectrum resistance in an agricultural context has led to the search for genes underlying quantitative resistance in plants. Such genes have been identified in only a few cases, all for fungal or nematode resistance, and encode diverse molecular functions. However, an understanding of the molecular mechanisms of quantitative resistance variation to other enemies and the associated evolutionary forces shaping this variation remain largely unknown. We report the identification, map-based cloning and functional validation of QRX3 (RKS1, Resistance related KinaSe 1), conferring broad-spectrum resistance to Xanthomonas campestris (Xc), a devastating worldwide bacterial vascular pathogen of crucifers. RKS1 encodes an atypical kinase that mediates a quantitative resistance mechanism in plants by restricting bacterial spread from the infection site. Nested Genome-Wide Association mapping revealed a major locus corresponding to an allelic series at RKS1 at the species level. An association between variation in resistance and RKS1 transcription was found using various transgenic lines as well as in natural accessions, suggesting that regulation of RKS1 expression is a major component of quantitative resistance to Xc. The co-existence of long lived RKS1 haplotypes in A. thalianais shared with a variety of genes involved in pathogen recognition, suggesting common selective pressures. The identification of RKS1 constitutes a starting point for deciphering the mechanisms underlying broad spectrum quantitative disease resistance that is effective against a devastating and vascular crop pathogen. Because putative RKS1 orthologous have been found in other Brassica species, RKS1 provides an exciting opportunity for plant breeders to improve resistance to black rot in crops.


Via Suayib Üstün, Nicolas Denancé, Guogen Yang
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Rescooped by tianxing84 from Trends in MPMI
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Trends in Plant Science: Susceptibility to plant disease: more than a failure of host immunity (2013)

Trends in Plant Science: Susceptibility to plant disease: more than a failure of host immunity (2013) | research on plant resistance gene for disease | Scoop.it

Susceptibility to infectious diseases caused by pathogens affects most plants in their natural habitat and leads to yield losses in agriculture. However, plants are not helpless because their immune system can deal with the vast majority of attackers. Nevertheless, adapted pathogens are able to circumvent or avert host immunity making plants susceptible to these uninvited guests. In addition to the failure of the plant immune system, there are other host processes that contribute to plant disease susceptibility. In this review, we discuss recent studies that show the active role played by the host in supporting disease, focusing mainly on biotrophic stages of infection. Plants attract pathogens, enable their entry and accommodation, and facilitate nutrient provision.


Via Kamoun Lab @ TSL, CP
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Rescooped by tianxing84 from Plant Pathogenomics
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Genome Announcements: Several plant pathogen genomes published in the issue of May/June 2013

Draft Genome Sequence of Botrytis cinerea BcDW1, Inoculum for Noble Rot of Grape Berries

Barbara Blanco-Ulate, Greg Allen, Ann L. T. Powell, and Dario CantuGenome Announc. May/June 2013 1:e00252-13; doi:10.1128/genomeA.00252-13http://genomea.asm.org/content/1/3/e00252-13.abstract.html

 

Draft Genome Sequence of the Grapevine Dieback Fungus Eutypa lata UCR-EL1

Barbara Blanco-Ulate, Philippe E. Rolshausen, and Dario CantuGenome Announc. May/June 2013 1:e00228-13; doi:10.1128/genomeA.00228-13http://genomea.asm.org/content/1/3/e00228-13.abstract.html

 

Draft Genome Sequence of Neofusicoccum parvum Isolate UCR-NP2, a Fungal Vascular Pathogen Associated with Grapevine Cankers

Barbara Blanco-Ulate, Philippe Rolshausen, and Dario CantuGenome Announc. May/June 2013 1:e00339-13; doi:10.1128/genomeA.00339-13http://genomea.asm.org/content/1/3/e00339-13.abstract.html

 

Draft Genome Sequence of the Ascomycete Phaeoacremonium aleophilum Strain UCR-PA7, a Causal Agent of the Esca Disease Complex in Grapevines

Barbara Blanco-Ulate, Philippe Rolshausen, and Dario CantuGenome Announc. May/June 2013 1:e00390-13; doi:10.1128/genomeA.00390-13http://genomea.asm.org/content/1/3/e00390-13.abstract.html

 

Genome Sequencing of Ralstonia solanacearum FQY_4, Isolated from a Bacterial Wilt Nursery Used for Breeding Crop Resistance

Yi Cao, Baoyu Tian, Yanxia Liu, Liuti Cai, Hancheng Wang, Ning Lu, Maosheng Wang, Shenghua Shang, Zhengyou Luo, and Junxiong ShiGenome Announc. May/June 2013 1:e00125-13; doi:10.1128/genomeA.00125-13http://genomea.asm.org/content/1/3/e00125-13.abstract.html

 

Draft Genome Sequence of Erwinia toletana, a Bacterium Associated with Olive Knots Caused by Pseudomonas savastanoi pv. Savastanoi

Daniel Passos da Silva, Giulia Devescovi, Konrad Paszkiewicz, Chiaraluce Moretti, Roberto Buonaurio, David J. Studholme, and Vittorio VenturiGenome Announc. May/June 2013 1:e00205-13; doi:10.1128/genomeA.00205-13http://genomea.asm.org/content/1/3/e00205-13.abstract.html

 

Genome Sequences of Pseudomonas spp. Isolated from Cereal CropsDonald M. Gardiner, Jiri Stiller, Lorenzo Covarelli, Magdalen Lindeberg, Roger G. Shivas, and John M. MannersGenome Announc. May/June 2013 1:e00209-13; doi:10.1128/genomeA.00209-13http://genomea.asm.org/content/1/3/e00209-13.abstract.html

 

Complete Genome Sequence of Xanthomonas citri subsp. citri Strain Aw12879, a Restricted-Host-Range Citrus Canker-Causing Bacterium

Neha Jalan, Dibyendu Kumar, Fahong Yu, Jeffrey B. Jones, James H. Graham, and Nian WangGenome Announc. May/June 2013 1:e00235-13; doi:10.1128/genomeA.00235-13http://genomea.asm.org/content/1/3/e00235-13.abstract.html

 

Genome Sequence of Xanthomonas arboricola pv. Corylina, Isolated from Turkish Filbert in Colorado

Jorge Ibarra Caballero, Marcelo M. Zerillo, Jacob Snelling, Christina Boucher, and Ned TisseratGenome Announc. May/June 2013 1:e00246-13; doi:10.1128/genomeA.00246-13http://genomea.asm.org/content/1/3/e00246-13.abstract.html

 

Genome Sequence of the Banana Pathogen Dickeya zeae Strain MS1, Which Causes Bacterial Soft Rot

Jing-Xin Zhang, Bi-Run Lin, Hui-Fang Shen, and Xiao-Ming PuGenome Announc. May/June 2013 1:e00317-13; doi:10.1128/genomeA.00317-13http://genomea.asm.org/content/1/3/e00317-13.abstract.html

 

Genome Sequence of the Pectobacterium atrosepticum Strain CFBP6276, Causing Blackleg and Soft Rot Diseases on Potato Plants and Tubers

Anthony Kwasiborski, Samuel Mondy, Amélie Beury-Cirou, and Denis FaureGenome Announc. May/June 2013 1:e00374-13; doi:10.1128/genomeA.00374-13http://genomea.asm.org/content/1/3/e00374-13.abstract.html

 

Complete Genome Sequences of Two Sweet Potato Chlorotic Stunt Virus Isolates from China

Yanhong Qin, Zhenchen Zhang, Qi Qiao, Desheng Zhang, Yuting Tian, Yongjiang Wang, and Shuang WangGenome Announc. May/June 2013 1:e00218-13; doi:10.1128/genomeA.00218-13http://genomea.asm.org/content/1/3/e00218-13.abstract.html


Via Nicolas Denancé, Kamoun Lab @ TSL
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The Receptor-Like Protein ReMAX of Arabidopsis Detects the Microbe-Associated Molecular Pattern eMax from Xanthomonas

The Receptor-Like Protein ReMAX of Arabidopsis Detects the Microbe-Associated Molecular Pattern eMax from Xanthomonas | research on plant resistance gene for disease | Scoop.it

As part of their immune system, plants have pattern recognition receptors (PRRs) that can detect a broad range of microbe-associated molecular patterns (MAMPs). Here, we identified a PRR of Arabidopsis thaliana with specificity for the bacterialMAMP eMax from xanthomonads. Response to eMax seems to be restricted to theBrassicaceae family and also varied among different accessions of Arabidopsis. In crosses between sensitive accessions and the insensitive accession Shakhdara, eMax perception mapped to RECEPTOR-LIKE PROTEIN1 (RLP1). Functional complementation of rlp1 mutants required gene constructs that code for a longer version of RLP1 that we termed ReMAX (for receptor of eMax). ReMAX/RLP1 is a typical RLP with structural similarity to the tomato (Solanum lycopersicum) RLP Eix2, which detects fungal xylanase as a MAMP. Attempts to demonstrate receptor function by interfamily transfer of ReMAX to Nicotiana benthamiana were successful after using hybrid receptors with the C-terminal part of ReMAX replaced by that of Eix2. These results show that ReMAX determines specificity for eMax. They also demonstrate hybrid receptor technology as a promising tool to overcome problems that impede interfamily transfer of PRRs to enhance pathogen detection in crop plants.


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PLOS Pathogens: Genomic Analysis of the Kiwifruit Pathogen Pseudomonas syringae pv. actinidiae Provides Insight into the Origins of an Emergent Plant Disease (2013)

PLOS Pathogens: Genomic Analysis of the Kiwifruit Pathogen Pseudomonas syringae pv. actinidiae Provides Insight into the Origins of an Emergent Plant Disease (2013) | research on plant resistance gene for disease | Scoop.it

The origins of crop diseases are linked to domestication of plants. Most crops were domesticated centuries – even millennia – ago, thus limiting opportunity to understand the concomitant emergence of disease. Kiwifruit (Actinidia spp.) is an exception: domestication began in the 1930s with outbreaks of canker disease caused by P. syringae pv. actinidiae(Psa) first recorded in the 1980s. Based on SNP analyses of two circularized and 34 draft genomes, we show that Psa is comprised of distinct clades exhibiting negligible within-clade diversity, consistent with disease arising by independent samplings from a source population. Three clades correspond to their geographical source of isolation; a fourth, encompassing thePsa-V lineage responsible for the 2008 outbreak, is now globally distributed. Psa has an overall clonal population structure, however, genomes carry a marked signature of within-pathovar recombination. SNP analysis of Psa-V reveals hundreds of polymorphisms; however, most reside within PPHGI-1-like conjugative elements whose evolution is unlinked to the core genome. Removal of SNPs due to recombination yields an uninformative (star-like) phylogeny consistent with diversification of Psa-V from a single clone within the last ten years. Growth assays provide evidence of cultivar specificity, with rapid systemic movement of Psa-V inActinidia chinensis. Genomic comparisons show a dynamic genome with evidence of positive selection on type III effectors and other candidate virulence genes. Each clade has highly varied complements of accessory genes encoding effectors and toxins with evidence of gain and loss via multiple genetic routes. Genes with orthologs in vascular pathogens were found exclusively within Psa-V. Our analyses capture a pathogen in the early stages of emergence from a predicted source population associated with wild Actinidia species. In addition to candidate genes as targets for resistance breeding programs, our findings highlight the importance of the source population as a reservoir of new disease.


Via Kamoun Lab @ TSL, Guogen Yang
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PNAS: The syntaxin SYP132 contributes to plant resistance against bacteria and secretion of pathogenesis-related protein 1 (2007)

PNAS: The syntaxin SYP132 contributes to plant resistance against bacteria and secretion of pathogenesis-related protein 1 (2007) | research on plant resistance gene for disease | Scoop.it

In contrast to many mammalian pathogens, potential bacterial pathogens of plants remain outside the host cell. The plant must, therefore, promote an active resistance mechanism to combat the extracellular infection. How this resistance against bacteria is manifested and whether similar processes mediate basal, gene-for-gene, and salicylate-associated defense, however, are poorly understood. Here, we identify a specific plasma membrane syntaxin, NbSYP132, as a component contributing to gene-for-gene resistance in Nicotiana benthamiana. Silencing NbSYP132 but not NbSYP121, the apparent orthologue of a syntaxin required for resistance to powdery mildew fungus, compromised AvrPto-Pto resistance. Because syntaxins may play a role in secretion of proteins to the extracellular space, we performed a limited proteomic analysis of the apoplastic fluid. We found that NbSYP132-silenced plants were impaired in the accumulation of at least a subset of pathogenesis-related (PR) proteins in the cell wall. These results were confirmed by both immunoblot analysis and imunolocalization of a PR protein, PR1a. These results implicate NbSYP132 as the cognate target soluble N-ethylmaleimide-sensitive factor attachment protein receptor for exocytosis of vesicles containing antimicrobial PR proteins. NbSYP132 also contributes to basal and salicylate-associated defense, indicating that SYP132-dependent secretion is a component of multiple forms of defense against bacterial pathogens in plants.


Via Kamoun Lab @ TSL, Freddy Monteiro
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PLOS Pathogens: The Xanthomonas campestris Type III Effector XopJ Targets the Host Cell Proteasome to Suppress Salicylic-Acid Mediated Plant Defence

PLOS Pathogens: The Xanthomonas campestris Type III Effector XopJ Targets the Host Cell Proteasome to Suppress Salicylic-Acid Mediated Plant Defence | research on plant resistance gene for disease | Scoop.it

The phytopathogenic bacterium Xanthomonas campestris pv. vesicatoria (Xcv) requires type III effector proteins (T3Es) for virulence. After translocation into the host cell, T3Es are thought to interact with components of host immunity to suppress defence responses. XopJ is a T3E protein from Xcv that interferes with plant immune responses; however, its host cellular target is unknown. Here we show that XopJ interacts with the proteasomal subunit RPT6 in yeast andin planta to inhibit proteasome activity. A C235A mutation within the catalytic triad of XopJ as well as a G2A exchange within the N-terminal myristoylation motif abolishes the ability of XopJ to inhibit the proteasome. Xcv ΔxopJ mutants are impaired in growth and display accelerated symptom development including tissue necrosis on susceptible pepper leaves. Application of the proteasome inhibitor MG132 restored the ability of the Xcv ΔxopJ to attenuate the development of leaf necrosis. The XopJ dependent delay of tissue degeneration correlates with reduced levels of salicylic acid (SA) and changes in defence- and senescence-associated gene expression. Necrosis upon infection with Xcv ΔxopJ was greatly reduced in pepper plants with reduced expression of NPR1, a central regulator of SA responses, demonstrating the involvement of SA-signalling in the development of XopJ dependent phenotypes. Our results suggest that XopJ-mediated inhibition of the proteasome interferes with SA-dependent defence response to attenuate onset of necrosis and to alter host transcription. A central role of the proteasome in plant defence is discussed.


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CP's comment, June 14, 2013 9:14 AM
Congrats again!!
Freddy Monteiro's comment, February 20, 2014 2:32 PM
Jim, I agree: another great publication to go side by side with this one: <br> Gimenez-Ibanez et al. The Bacterial Effector HopX1 Targets JAZ Transcriptional Repressors to Activate Jasmonate Signaling and Promote Infection in Arabidopsis. PLOS Biology 2014.<br>http://dx.plos.org/10.1371/journal.pbio.1001792
Freddy Monteiro's curator insight, February 20, 2014 2:33 PM

Another great publication to go side by side with this one:

Gimenez-Ibanez et al. The Bacterial Effector HopX1 Targets JAZ Transcriptional Repressors to Activate Jasmonate Signaling and Promote Infection in Arabidopsis. PLOS Biology 2014.

http://dx.plos.org/10.1371/journal.pbio.1001792

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PLOS Genetics: Genetic Requirements for Signaling from an Autoactive Plant NB-LRR Intracellular Innate Immune Receptor

PLOS Genetics: Genetic Requirements for Signaling from an Autoactive Plant NB-LRR Intracellular Innate Immune Receptor | research on plant resistance gene for disease | Scoop.it

Plants react to pathogen attack via recognition of, and response to, pathogen-specific molecules at the cell surface and inside the cell. Pathogen effectors (virulence factors) are monitored by intracellular nucleotide-binding leucine-rich repeat (NB-LRR) sensor proteins in plants and mammals. Here, we study the genetic requirements for defense responses of an autoactive mutant of ADR1-L2, an Arabidopsis coiled-coil (CC)-NB-LRR protein. ADR1-L2 functions upstream of salicylic acid (SA) accumulation in several defense contexts, and it can act in this context as a “helper” to transduce specific microbial activation signals from “sensor” NB-LRRs. This helper activity does not require an intact P-loop. ADR1-L2 and another of two closely related members of this small NB-LRR family are also required for propagation of unregulated runaway cell death (rcd) in an lsd1 mutant. We demonstrate here that, in this particular context, ADR1-L2 function is P-loop dependent. We generated an autoactive missense mutation, ADR1-L2D484V, in a small homology motif termed MHD. Expression of ADR1-L2D848V leads to dwarfed plants that exhibit increased disease resistance and constitutively high SA levels. The morphological phenotype also requires an intact P-loop, suggesting that these ADR1-L2D484V phenotypes reflect canonical activation of this NB-LRR protein. We used ADR1-L2D484V to define genetic requirements for signaling. Signaling from ADR1-L2D484V does not require NADPH oxidase and is negatively regulated by EDS1 andAtMC1. Transcriptional regulation of ADR1-L2D484V is correlated with its phenotypic outputs; these outputs are both SA–dependent and –independent. The genetic requirements for ADR1-L2D484V activity resemble those that regulate an SA–gradient-dependent signal amplification of defense and cell death signaling initially observed in the absence of LSD1. Importantly, ADR1-L2D484V autoactivation signaling is controlled by both EDS1 and SA in separable, but linked pathways. These data allows us to propose a genetic model that provides insight into an SA–dependent feedback regulation loop, which, surprisingly, includes ADR1-L2.


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