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Biology subjects

Bar, M.

Publications and source records attributed to Bar, M..

17 recordsLinked to original sources

Tomato brown rugose fruit virus and pepino mosaic virus differentially modulate disease severity of bacterial pith necrosis and bacterial canker in tomato

Tomato worldwide production is increasingly challenged by complex disease outbreaks involving multiple interacting pathogens. In Israel, recent years have seen a marked rise in vascular collapse symptoms in greenhouse-grown tomatoes, coinciding with the widespread emergence of tomato brown rugose fruit virus (ToBRFV) and pepino mosaic virus (PepMV). Here, we investigated the bacterial and viral agents associated with these outbreaks and examined how viral infection influences the development and severity of bacterial diseases that cause vascular collapse. Surveys conducted between 2021 and 2026 revealed that tomato pith necrosis outbreaks were associated with a diverse bacterial community dominated by members of the Pseudomonadales and Enterobacterales, while bacterial canker outbreaks were exclusively linked to Clavibacter michiganensis. Multilocus sequence analysis showed that pith necrosis-associated Pseudomonas isolates clustered primarily within the P. syringae, and P. corrugata phylogroups. Pathogenicity assays demonstrated that only a subset of pith necrosis-associated bacteria, P. mediterranea, P. capsici, P. viridiflava, and Xanthomonas euvesicatoria pv. perforans, induced pith necrosis under controlled conditions, with high variability in symptom severity. Co-inoculation experiments showed that ToBRFV- and PepMV-infected plants exhibited a 40-100% increase in lesion size following inoculation with pith necrosis-associated bacteria, without a corresponding increase in bacterial colonization, whereas the same viral infections attenuated wilt symptoms caused by C. michiganensis. Together, our findings demonstrate that endemic viral infections differentially modulate bacterial disease outcomes, either exacerbating or attenuating symptoms depending on the pathogen. These results highlight the importance of multi-pathogen interactions in disease severity and have important implications for tomato disease management.

plant biology↗

A tonoplast cytokinin riboside transporter gates intracellular hormone availability at the plant-microbe interface

Cytokinin ribosides are major mobile and precursor forms of cytokinins, plant hormones whose transport and subcellular distribution shape developmental and stress responses. Here, we identify Arabidopsis thaliana EQUILIBRATIVE NUCLEOSIDE TRANSPORTER1 (ENT1) as a tonoplast-localized cytokinin riboside transporter. Tissue-specific subcellular analysis under native regulatory elements localized ENT1 predominantly to the tonoplast of root epidermal and lateral root cap cells, where it gates intracellular cytokinin riboside availability. Accordingly, ENT1 overexpression enhanced cytokinin riboside sensitivity and signalling, whereas loss of ENT1 altered adenosine metabolism and disrupted cytokinin homeostasis, leading to the accumulation of multiple zeatin-type cytokinins. ENT1-dependent cytokinin riboside compartmentalization was required for beneficial microbe-induced protection, as ent1 mutants failed to acquire protection against the fungal pathogen Botrytis cinerea and the bacterial pathogen Pseudomonas syringae pv. tomato DC3000. These findings reveal a vacuolar gatekeeping mechanism that controls intracellular cytokinin riboside availability and links hormone compartmentalization to beneficial microbe-dependent plant defence.

plant biology↗

Differential effects of two common GVHD prophylaxis regimens on the gut microbiome: Results from the BMT CTN 1801 study

Allogeneic hematopoietic cell transplantation (allo-HCT) is a potentially curative treatment for many hematological malignancies, but graft-versus-host disease (GVHD) is a common complication. Low gut microbiome diversity is associated with higher GVHD risk and shorter survival in multiple studies. Recently, the BMT CTN 1703 clinical trial demonstrated superiority of a GVHD-prophylaxis regimen including post-transplant cyclophosphamide (PTCy) compared to the standard prophylaxis (tacrolimus and methotrexate, Tac/MTX) in terms of GVHD-free, relapse-free survival at one year among reduced intensity conditioning allo-HCT recipients. However, the effect of PTCy on the gut microbiome and its association with clinical outcome have not been described. Here, we report on a companion randomized clinical controlled trial (BMT CTN 1801), which collected 2575 longitudinal stool samples from 304 study participants. Samples were obtained up to weekly up to day 84 post allo-HCT and at less frequent intervals thereafter, up to 2 years. Microbiome diversity and absolute microbial load were lower in the PTCy group compared to the Tac/MTX group on days 14-28 post-HCT. However, diversity at the timepoint closest to neutrophil engraftment was not significantly associated with non-relapse mortality after one year or other clinical outcomes, contrary to expectations from previous studies. Microbial domination events, when a single species exceeds 30% relative abundance, were comparable across treatment arms and reflected both pathogen blooms as well as less severe disruptions of the microbial community. Clostridium scindens and secondary bile acid metabolism pathways were less prevalent in the PTCy arm than in the Tac/MTX arm post-HCT, yet presence of secondary bile acid metabolism pathways was associated with a lower risk of chronic GVHD. Given that PTCy was associated with a greater disruption of the microbiome as measured by diversity, absolute microbial abundance, and bile acid metabolism capability, but better clinical outcomes overall, these data suggest that the importance of the microbiome in modulating the host immune systems after allo-HCT is specific to different types of GVHD prophylaxis.

microbiology↗

Tissue-Specific Experimental Evolution Reveals Adaptive Trade-Offs in the Plant Vascular Pathogen Clavibacter michiganensis

The plant pathogenic bacterium Clavibacter michiganensis (Cm) is a systemic vascular pathogen that colonizes both xylem vessels and the intracellular apoplast during different stages of infection. To identify traits and loci associated with adaptation to these distinct host microenvironments, we conducted tissue-specific experimental evolution. Twenty independent Cm lineages were repeatedly passaged in either tomato stems or leaves to promote adaptation to vascular or apoplastic lifestyles, respectively. After fifteen passages, adapted clones were characterized for virulence and virulence-related traits. These characterizations demonstrated clear differential associations of virulence-associated traits with the adapted tissue. The majority of vascular-adapted clones displayed enhanced surface attachment, reduced cellulase activity, reduced exopolysaccharide (EPS) production, and attenuated virulence on tomato compared to the parent clone. On the other hand, apoplast-adapted clones displayed reduced biofilm formation and enhanced EPS production while maintaining their virulence on tomato. Whole-genome sequencing of all adapted clones revealed candidate loci linked to tissue adaptation. Notably, six of ten vascular-adapted clones carried two independent mutations in CMM_1284, a putative HipB/XRE-type transcriptional regulator. A CMM_1284 marker exchange mutant displayed phenotypes similar to vascular-adapted clones, suggesting a role for this regulator in vascular colonization. Together, these findings highlight the role of phenotypic plasticity in tissue adaptation of plant pathogens, showing that tissue-specific adaptation involves modulation of surface attachment, EPS production, and cell wall-degrading enzymes. They further reveal a regulated trade-off between vascular persistence, supported by strong surface attachment, and systemic virulence, which depends on bacterial dispersal and migration.

microbiology↗

PDCD1 expression increases at elevated temperatures.

PDCD1 (Programmed cell death protein 1) is an immune checkpoint that inhibits the excessive response of antigen-activated T cells to prevent autoimmune tissue damage. In chronic infections or cancers, lasting antigen exposure leads to permanent PDCD1 expression that can limit immune-mediated clearance of pathogens or degenerated cells. Consequently, blocking PDCD1 can enhance T cell function, which is the basis of cancer immune checkpoint therapy. We found that PDCD1 expression can increase within hours of temperature elevation in human leukemic and lymphoblastoid cell lines (such as Jurkat, THP1, HL-60, GM07062, and NK-92) and mouse lymphoid organs (e.g., thymus, spleen, and lymph nodes). Transcriptional upregulation of the PDCD1 gene was associated with the binding of heat shock factor 1 (HSF1) to the promoter, and HSF1 knockout in HL-60 cells resulted in reduced PDCD1 activation. Furthermore, a heat shock-dependent increase in glycosylated (and therefore active) PDCD1 protein levels was associated with PDCD1 exposure on the cell membrane and a reduction in the cytotoxic properties of NK-92 cells. Our observations suggest that the immune response could be attenuated in various physiological conditions accompanied by increased temperatures (infection, heat stroke, etc.). This observation may have clinical implications, and therefore, further research is warranted to understand the importance of fever and PDCD1 in various disease states, as well as their interaction with treatment.

immunology↗

Immunity priming uncouples the growth-defense tradeoff in tomato

Plants have developed an array of mechanisms to protect themselves against pathogen invasion. The deployment of defense mechanisms is imperative for plant survival, but can come at the expense of plant growth, leading to the "growth- defense trade-off" phenomenon. Following pathogen exposure, plants can develop resistance to further attack. This is known as induced resistance, or priming. Here, we investigated the growth-defense trade-off, examining how defense priming via Systemic Acquired Resistance (SAR), or Induced Systemic Resistance (ISR), affects tomato development and growth. We found that defense priming can promote, rather than inhibit, plant development, and that defense priming and growth tradeoffs can be uncoupled. Cytokinin response was activated during induced resistance, and found to be required for the observed growth and disease resistance resulting from ISR activation. ISR was found to have a stronger effect on plant development than SAR. Our results suggest that growth promotion and induced resistance can be co-dependent, and that in certain cases, defense priming can drive developmental processes and promote plant yield. Summary statementGrowth-defense tradeoffs in plants result in loss of yield. Here, we demonstrate that immunity priming in different pathways uncouples this tradeoff and allows for disease resistant plants with robust growth.

plant biology↗

TOR mediates cytokinin-driven development and defense cues

Plants constantly perceive and process environmental signals and balance between the energetic demands of growth and defense. Growth arrest upon pathogen attack was previously suggested to result from a redirection of the plants metabolic resources towards the activation of plant defense. The energy sensor Target of Rapamycin (TOR) kinase is a conserved master coordinator of growth and development in all eukaryotes. Although TOR is positioned at the interface between development and defense, little is known about the mechanisms in which TOR may potentially regulate the relationship between these two modalities. The plant hormones cytokinin (CK) and gibberellin (GA) execute various aspects of plant development and defense. The ratio between CK and GA was reported to determine the outcome of developmental programs. Here, investigating the interplay between TOR-mediated development and TOR-mediated defense in tomato, we found that TOR silencing resulted in rescue of several different aberrant developmental phenotypes, demonstrating that TOR is required for the execution of developmental cues. In parallel, TOR inhibition enhanced immunity in genotypes with a low CK/GA ratio but not in genotypes with a high CK/GA ratio. TOR-inhibition mediated disease resistance was found to depend on developmental status, and was abolished in strongly morphogenetic leaves, while being strongest in mature, differentiated leaves. CK repressed TOR activity, suggesting that CK-mediated immunity may rely on TOR downregulation. At the same time, TOR activity was promoted by GA, and TOR silencing reduced GA sensitivity, indicating that GA signaling requires normal TOR activity. Our results demonstrate that TOR likely acts in concert with CK and GA signaling, executing signaling cues in both defense and development. Thus, differential regulation of TOR or TOR-mediated processes could regulate the required outcome of development-defense prioritization.

plant biology↗

Cytokinin regulates energy utilization in Botrytis cinerea

The plant hormone cytokinin (CK) is an important developmental regulator, promoting morphogenesis and delaying senescence. Previous work by us and others has demonstrated that CKs also mediate plant immunity and disease resistance. Some phytopathogens have been reported to secrete CKs, and may manipulate CK signaling to regulate the host cell cycle and nutrient allocation, to improve their pathogenic abilities. In a recent work, we demonstrated that CK directly inhibits the growth, development, and virulence of fungal phytopathogens, by down regulating the cell cycle and reducing cytoskeleton organization and cellular trafficking in the fungus. Here, focusing on Botrytis cinerea (Bc), we report that the effect of CK on Bc is tied to nutrient availability; CK strongly inhibits Bc growth and de-regulated cytoskeleton organization in a nutrient rich environment, but has a diminished effect when nutrients are scarce. Using biochemical assays and transgenic redox sensitive botrytis lines, we examined the effect of CK on energy consumption in the fungus, and demonstrate that CK promotes glycolysis and energy consumption in Bc, both in vitro and in planta. Here, glycolysis and increased oxidation were stronger with waning nutrient availability. Transcriptomic data further supports our findings, demonstrating significant upregulation to glycolysis, oxidative phosphorylation, and sucrose metabolism, upon CK treatment. The metabolic effects of CK on the fungus likely reflect the role of plant CK during early infection by necrotrophic pathogens, which are known to have an initial, short biotrophic phase. In addition to the plant producing CK during its interaction with the pathogen for defense priming and pathogen inhibition, the pathogen may take advantage of this increased CK to boost its metabolism and energy production, in preparation for the necrotrophic phase of the infection. Thus, the role of CK in controlling senescence can be exploited by diverse phytopathogens to their advantage. Author summaryCytokinin (CK) is one of the primary plant developmental hormones, regulating many developmental processes. Several works have highlighted the involvement of CK in plant defense. We recently reported that CK can directly inhibit fungal plant pathogens. CK inhibits Botrytis cinerea growth by arresting the cell cycle and de-regulating cytoskeleton organization and cellular trafficking. Here, we report that CK positively regulates B. cinerea energy consumption, causing an increase in glycolytic rates and energy consumption. The effect of CK on B. cinerea was dependent on nutrient availability, with CK causing stronger increases in glycolysis and lower growth inhibition when nutrient availably was low, and weaker glycolytic increases coupled with stronger growth inhibition in a high nutrient environment. We propose that CK can be viewed as a bidirectional signaling molecule in plant pathogen interactions: CK acts as a signal to the fungus that plant tissue is present, causing it to activate sugar and energy metabolism pathways to take advantage of the available food source, while at the same time, CK is employed by the plant to inhibit the attacking pathogen.

microbiology↗

Cytokinin- microbiome interactions regulate developmental functions

The interaction of plants with the complex microbial networks that inhabit them is important for plant health. While the reliance of plants on their microbial inhabitants for defense against invading pathogens is well documented, the acquisition of data concerning the relationships between plant developmental stage or aging, and microbiome assembly, is still underway. In this work, we observed developmental-age dependent changes in the phyllopshere microbiome of tomato. The plant hormone cytokinin (CK) regulates various plant growth and developmental processes. Here, we show that age-related shifts in microbiome content vary based on content of, or sensitivity to, CK. We observed a developmental age associated decline in microbial richness and diversity, accompanied by a decline in the presence of growth promoting and resistance inducing bacilli in the phyllosphere. This decline was absent from CK-rich or CK-hypersensitive genotypes. Bacillus isolates we obtained from CK rich genotypes were found to re-program the transcriptome to support morphogenesis and alter the leaf developmental program when applied to seedlings, and enhance yield and agricultural productivity when applied to mature plants. Our results support the notion that CK-dependent effects on microbiome content support developmental functions, suggesting that these are mediated by CK in part via the bacterial community.

plant biology↗

The VIL gene CRAWLING ELEPHANT controls maturation and differentiation in tomato via polycomb silencing

VERNALIZATION INSENSITIVE 3-LIKE (VIL) proteins are PHD-finger proteins that recruit the repressor complex Polycomb Repressive Complex 2 (PRC2) to the promoters of target genes. Most known VIL targets are flowering repressor genes. Here, we show that the tomato VIL gene CRAWLING ELEPHANT (CREL) promotes differentiation throughout plant development by facilitating the trimethylation of Histone H3 on lysine 27 (H3K27me3). We identified the crel mutant in a screen for suppressors of the simple-leaf phenotype of entire (e), a mutant in the AUX/IAA gene ENTIRE/SlIAA9, involved in compound-leaf development in tomato. crel mutants have increased leaf complexity, and suppress the ectopic blade growth of e mutants. In addition, crel mutants are late flowering, and have delayed and aberrant stem, root and flower development. Consistent with a role for CREL in recruiting PRC2, crel mutants present altered H3K27me3 modifications at a subset of PRC2 targets throughout the genome. Our results uncover a wide role for CREL in plant and organ differentiation in tomato and suggest that CREL is required for targeting PRC2 activity to, and thus silencing, a specific subset of polycomb targets. Author summaryPlants form organs continuously throughout their lives, and the number and shape of their organs is determined in a flexible manner according to the internal and external circumstances. Alongside this flexibility, plants maintain basic developmental programs to ensure proper functioning. Among the ways by which plants achieve flexible development is by tuning the pace of their maturation and differentiation, at both the plant and organ levels. One of the ways plants regulate the rate of maturation and differentiation is by changing gene expression. Here, we identified a gene that promotes plant and organ maturation and differentiation. This gene, CRAWLING ELEPHANT (CREL) acts by bringing a repressing complex to target genes. We show the importance of CREL in multiple developmental processes and in the expression of multiple genes throughout the tomato genome.

plant biology↗

Coordinating the morphogenesis-differentiation balance by tweaking the cytokinin-gibberellin equilibrium

Morphogenesis and differentiation are important stages in organ development and shape determination. However, how they are balanced and tuned during development is not fully understood. In the compound leaved tomato, an extended morphogenesis phase allows for the initiation of leaflets, resulting in the compound form. Maintaining a prolonged morphogenetic phase in early stages of compound-leaf development is dependent on delayed activity of several factors that promote differentiation, including CIN-TCP transcription factor (TF) LA, the MYB TF CLAU and the plant hormone Gibberellin (GA). Here, we investigated the genetic regulation of the morphogenesis-differentiation balance by studying the relationship between LA, CLAU and GA. Our genetic and molecular examination suggest that LA is expressed more broadly than CLAU and determines the spatio-temporal context of CLAU activity. We demonstrate that both LA and CLAU affect the Cytokinin/Gibberellin (CK/GA) balance. LA reduces the sensitivity of the leaf margin to CK, shown before to be also affected by CLAU. CLAU affects leaf active GA content and sensitivity, shown previously to be also influenced by LA. Therefore, LA and CLAU likely function in parallel pathways to promote leaf differentiation by converging on common downstream processes, including the CK/GA balance.

plant biology↗

Cytokinin inhibits fungal development and virulence by targeting cellular trafficking

Cytokinin (CK) is an important plant developmental regulator, having activities in many aspects of plant life and its response to the environment. CKs are involved in diverse processes in the plant, including stem-cell maintenance, vascular differentiation, growth and branching of roots and shoots, leaf senescence, nutrient balance and stress tolerance. In some cases, phytopathogens secrete CKs. It has been suggested that to achieve pathogenesis in the host, CK-secreting biotrophs manipulate CK signaling to regulate the host cell cycle and nutrient allocation. CK is known to induce host plant resistance to several classes of phytopathogens from a handful of works, with induced host immunity via salicylic acid signaling suggested to be the prevalent mechanism for this host resistance. Here, we show that CK directly inhibits the growth, development, and virulence of fungal phytopathogens. Focusing on Botrytis cinerea (Bc), we demonstrate that various aspects of fungal development can be reversibly inhibited by CK. We also found that CK affects both budding and fission yeast in a similar manner. Investigating the mechanism by which CK influences fungal development, we conducted RNA-NGS on mock and CK treated B. cinerea samples, finding that CK inhibits the cell cycle, cytoskeleton, and endocytosis. Cell biology experiments demonstrated that CK affects cytoskeleton structure and cellular trafficking in Bc, lowering endocytic rates and endomembrane compartment sizes, likely leading to reduced growth rates and arrested developmental programs. Mutant analyses in yeast confirmed that the endocytic pathway is altered by CK. Our work uncovers a remarkably conserved role for a plant growth hormone in fungal biology, suggesting that pathogen-host interactions resulted in fascinating molecular adaptations on fundamental processes in eukaryotic biology. ImportanceCytokinins (CKs), important plant growth/ developmental hormones, have previously been associated with host disease resistance. Here, we demonstrate that CK directly inhibits the growth, development, and virulence of B. cinerea (Bc) and many additional phytopathogenic fungi. Molecular and cellular analyses revealed that CK is not toxic to Bc, but rather, Bc likely recognizes CK and responds to it, resulting in cell cycle and individual cell growth retardation, via downregulation of cytoskeletal components and endocytic trafficking. Mutant analyses in yeast confirmed that the endocytic pathway is a CK target. Our work demonstrates a conserved role for CK in yeast and fungal biology, suggesting that suggesting that pathogen-host interactions may cause molecular adaptations on fundamental processes in eukaryotic biology.

microbiology↗

Collaboration of multiple pathways in making a compound leaf

O_LIThe variability in leaf form in nature is immense. Leaf patterning occurs by differential growth that occurs during a limited window of morphogenetic activity at the leaf marginal meristem. While many regulators have been implicated in the designation of the morphogenetic window and in leaf patterning, how these effectors interact to generate a particular form is still not well understood. C_LIO_LIWe addressed the interaction among different effectors of tomato compound leaf development, using genetic and molecular analyses. C_LIO_LIMutations in the tomato auxin response factor SlARF5/SlMP, which promotes leaflet formation, suppressed the increased leaf complexity of mutants with extended morphogenetic window. Impaired activity of the NAC/CUC transcription factor GOBLET (GOB), which specifies leaflet boundaries, also reduced leaf complexity in these backgrounds. Analysis of genetic interactions showed that the patterning factors SlMP, GOB and the MYB transcription factor LYRATE (LYR) act in parallel to promote leaflet formation. C_LIO_LIThis work places an array of developmental regulators in a morphogenetic context. It reveals how organ-level differentiation rate and local growth are coordinated to sculpture an organ. These concepts and findings are applicable to other plant species and developmental processes that are regulated by patterning and differentiation. C_LI

plant biology↗

Cytokinin response induces immunity and fungal pathogen resistance in tomato by modulating cellular trafficking of PRRs

Plant immunity is often defined by the "immunity hormones": salicylic acid (SA), jasmonic acid (JA), and ethylene (ET). These hormones are well known for differentially regulating defense responses against pathogens. In recent years, the involvement of other plant growth hormones such as auxin, gibberellic acid, abscisic acid, and cytokinins (CKs) in biotic stresses has been recognized. Previous reports have indicated that endogenous and exogenous CK treatment can result in pathogen resistance. We show here that CK induces systemic tomato immunity, modulating cellular trafficking of the PRR LeEIX2 and promoting biotrophic and necrotrophic pathogen resistance in an SA and ET dependent mechanism. CK perception within the host underlies its protective effect. Our results support the notion that CK acts as a priming agent, promoting pathogen resistance by inducing immunity in the host.

plant biology↗

Perceptual decisions are biased toward relevant prior choices

Perceptual decisions are biased by recent perceptual history, a phenomenon termed 'serial dependence.' Using a visual location discrimination task, we investigated what aspects of perceptual decisions lead to serial dependence, and disambiguated the influences of low-level sensory information, prior choices and motor actions on subsequent perceptual decisions. Following several biased (prior) location discriminations, subsequent (test) discriminations were biased toward the prior choices, even when reported via different motor actions, and when prior and test stimuli differed in color. By contrast, biased discriminations about an irrelevant stimulus feature did not substantially influence subsequent location discriminations. Additionally, biased stimulus locations, when color was discriminated, no longer substantially influenced subsequent location decisions. Hence, the degree of relevance between prior and subsequent perceptual decisions is a key factor for serial dependence. This suggests that serial-dependence reflects a high-level mechanism by which the brain predicts and interprets incoming sensory information in accordance with relevant prior choices.

neuroscience↗

Show me your secret(ed) weapons: a multifaceted approach reveals novel type III-secreted effectors of a plant pathogenic bacterium

Many Gram-negative plant and animal pathogenic bacteria employ a type III secretion system (T3SS) to secrete protein effectors into the cells of their hosts and promote disease. The plant pathogen Acidovorax citrulli requires a functional T3SS for pathogenicity. As with Xanthomonas and Ralstonia spp., an AraC-type transcriptional regulator, HrpX, regulates expression of genes encoding T3SS components and type III-secreted effectors (T3Es) in A. citrulli. A previous study reported eleven T3E genes in this pathogen, based on the annotation of a sequenced strain. We hypothesized that this was an underestimation. Guided by this hypothesis, we aimed at uncovering the T3E arsenal of the A. citrulli model strain, M6. We carried out a thorough sequence analysis searching for similarity to known T3Es from other bacteria. This analysis revealed 51 A. citrulli genes whose products are similar to known T3Es. Further, we combined machine learning and transcriptomics to identify novel T3Es. The machine learning approach ranked all A. citrulli M6 genes according to their propensity to encode T3Es. RNA-Seq revealed differential gene expression between wild-type M6 and a mutant defective in HrpX. Data combined from these approaches led to the identification of seven novel T3E candidates, that were further validated using a T3SS-dependent translocation assay. These T3E genes encode hypothetical proteins, do not show any similarity to known effectors from other bacteria, and seem to be restricted to plant pathogenic Acidovorax species. Transient expression in Nicotiana benthamiana revealed that two of these T3Es localize to the cell nucleus and one interacts with the endoplasmic reticulum. This study not only uncovered the arsenal of T3Es of an important pathogen, but it also places A. citrulli among the \"richest\" bacterial pathogens in terms of T3E cargo. It also revealed novel T3Es that appear to be involved in the pathoadaptive evolution of plant pathogenic Acidovorax species.\n\nAuthor summaryAcidovorax citrulli is a Gram-negative bacterium that causes bacterial fruit blotch (BFB) disease of cucurbits. This disease represents a serious threat to cucurbit crop production worldwide. Despite the agricultural importance of BFB, the knowledge about basic aspects of A. citrulli-plant interactions is rather limited. As many Gram-negative plant and animal pathogenic bacteria, A. citrulli employs a complex secretion system, named type III secretion system, to deliver protein virulence effectors into the host cells. In this work we aimed at uncovering the arsenal of type III-secreted effectors (T3Es) of this pathogen by combination of bioinformatics and experimental approaches. We found that this bacterium possesses at least 51 genes that are similar to T3E genes from other pathogenic bacteria. In addition, our study revealed seven novel T3Es that seem to occur only in A. citrulli strains and in other plant pathogenic Acidovorax species. We found that two of these T3Es localize to the plant cell nucleus while one partially interacts with the endoplasmic reticulum. Further characterization of the novel T3Es identified in this study may uncover new host targets of pathogen effectors and new mechanisms by which pathogenic bacteria manipulate their hosts.

microbiology↗

Inferior parietal lobule and early visual areas support elicitation of individualized meanings during narrative listening

When listening to a narrative, the verbal expressions translate into meanings and flow of mental imagery, at best vividly immersing the keen listener into the sights, sounds, scents, objects, actions, and events in the story. However, the same narrative can be heard quite differently based on differences in listeners previous experiences and knowledge, as the semantics and mental imagery elicited by words and phrases in the story vary extensively between any given two individuals. Here, we capitalized on such inter-individual differences to disclose brain regions that support transformation of narrative into individualized propositional meanings and associated mental imagery by analyzing brain activity associated with behaviorally-assessed individual meanings elicited by a narrative. Sixteen subjects listed words best describing what had come to their minds during each 3-5 sec segment of an eight-minute narrative that they listened during fMRI of brain hemodynamic activity. Similarities in these word listings between subjects, estimated using latent-semantic analysis combined with WordNet knowledge, predicted similarities in brain hemodynamic activity in supramarginal and angular gyri as well as in cuneus. Our results demonstrate how inter-individual differences in semantic representations can be measured and utilized to identify specific brain regions that support the elicitation of individual propositional meanings and the associated mental imagery when one listens to a narrative.

neuroscience↗