Strangulated Gastric Hernia Following a Missed Traumatic Diaphragmatic Injury: A Case Report.

Traumatic diaphragmatic injuries (TDIs) are rare and can be life-threatening, depending on the size of the injury and the contents herniating through it. They usually result from blunt or penetrating trauma to the thoracoabdominal area, with an incidence of 0.8-5% and up to 30% presenting late. A high index of suspicion should be maintained when evaluating patients with a history of trauma (severe blunt or thoracoabdominal penetrating trauma) and upper abdominal symptoms. We present a case of a missed TDI after a left posterior thoracoabdominal stab injury, which was evaluated with a diagnostic laparoscopy at an outside hospital. He presented to our emergency department (ED) with sudden onset left-sided chest pain and uncontrollable vomiting. A CT scan was obtained and showed a distended stomach herniating through a defect in the left hemidiaphragm. The patient was immediately taken for laparoscopic exploration and repair. There was a 5 cm defect in the left posterolateral diaphragm containing a strangulated stomach (approximately ⅔) and necrotic omentum. Complete reduction was achieved and the diaphragmatic defect was repaired primarily. His postoperative course was uncomplicated. This case illustrates the importance of maintaining a high index of suspicion for TDI, despite reports of previous exploration. Missed TDI can present with herniated intra-abdominal organs, which can become strangulated and increase morbidity and mortality.

Prevalencia y caracterización de las neoplasias malignas en personas viviendo con VIH en Colombia

Introducción: En el síndrome de inmunodeficiencia adquirida las neoplasias han jugado un papel preponderante, y con el advenimiento del tratamiento antirretroviral (TAR), la infección por VIH se ha transformado en una enfermedad crónica, siendo los tumores malignos una causa importante de morbilidad y mortalidad. Objetivo: Describir las características demográficas, clínicas y de laboratorio de las personas que viven con VIH (PVVIH) y han sido diagnosticadas con cáncer en Colombia y comparar los grupos de neoplasias definitorias y no definitorias de Sida. Métodos: Revisión multicéntrica retrospectiva, en la que se recolectó y analizó datos relacionados con la infección por VIH y de diagnóstico de cáncer y tipo. Incluyó PVVIH diagnosticadas con neoplasias malignas atendidas en 23 centros de atención de pacientes con VIH en 11 ciudades de Colombia desde 1986 hasta 2018. Resultados: En 23.189 pacientes, se identificaron 650 casos de malignidad (prevalencia de 2,8 % [IC de 95%: 2,6-2,9]). La neoplasia definitoria de Sida (NDS) sigue siendo el tipo de cáncer prevalente (71,1%), las neoplasias malignas más frecuentes fueron sarcoma de Kaposi (n: 330; 50,8%), linfoma no Hodgkin (n: 110; 16,9%), cáncer de piel (n: 48; 7,4%) y linfoma de Hodgkin (n: 25; 3,8%). Los pacientes con NDS tenían más probabilidades de ser HSH y estar en un estadio CDC 3, un recuento de linfocitos T CD4 < 200/μL y una carga viral del VIH ≥ 50 copias/mL al momento del diagnóstico de malignidad. Las personas con neoplasias no definitorias de Sida (NNDS) eran significativamente mayores y tenían más probabilidades de ser fumadores. Conclusiones: Estos hallazgos son relevantes considerando la creciente carga de cáncer en las PVVIH que envejecen y las causas cambiantes de morbilidad y mortalidad. La presentación tardía a la atención del VIH y el retraso en el inicio del TAR son probablemente factores que contribuyen al cambio más lento hacia NNDS en comparación con las regiones de altos ingresos donde hay un acceso más rápido y temprano al TAR. El conocimiento de las tendencias epidemiológicas actuales y el perfil del cáncer en las PVVIH es fundamental para mejorar los esfuerzos de prevención y tratamiento del cáncer en el contexto de la atención integral del VIH.

Background: In the acquired immunodeficiency syndrome, neoplasms have played a preponderant role, and with the advent of antiretroviral treatment (ART), HIV has become a chronic disease, with malignant tumors being an important cause of morbidity and mortality. Aim: To describe the demographic, clinical, and laboratory characteristics of people living with HIV (PLHIV) who have been diagnosed with cancer in Colombia and to compare the groups of AIDS-defining (ADC) and non-AIDS-defining neoplasms (NADC). Methods: Retrospective, multicenter study that included people living with HIV/AIDS (PLHIV) diagnosed with malignancies treated at 23 HIV care centers located in 11 Colombian cities from 1986 to 2018. Data related to HIV infection and cancer diagnosis were collected and analyzed. Results: Among 23,189 patients, 650 malignancy cases were identified (prevalence of 2.8% [95% CI 2.6-2.9]). AIDS-defining neoplasm remains the most prevalent type of cancer (71.1%), The most frequent individual malignancies were Kaposi sarcoma (n: 330; 50.8%), non-Hodgkin lymphoma (n: 110; 16.9%), skin cancer (n: 48; 7.4%), and Hodgkin lymphoma (n: 25; 3.8%). Compared people with NADC, with ADC were more likely to be MSM and have a CDC HIV stage 3, CD4 T cell count < 200/μL, and HIV viral load ≥ 50 copies/mL at the time of malignancy diagnosis. PLHIV and with NADC were significantly older and were more likely to be smokers. Conclusions: These findings are relevant considering the increasing burden of cancer in the aging PLHIV and the changing causes of morbidity and mortality. Late presentation to HIV care and delayed ART initiation are likely factors contributing to the slower shift toward NADCs compared with high-income regions where access to ART is better. Knowledge of the current epidemiological trends and profile of cancer in PLWHA is critical to improve cancer prevention and treatment efforts in the context of comprehensive HIV care.

Reasons for antiretroviral switching in Colombia: A retrospective cohort study.

INTRODUCTION: Long-term use of antiretroviral therapy (ART) for HIV infection might lead to the necessity of switching regimens. We aimed to analyze the reasons for the ART switch, the time-to-switch of ART, and its associated factors in a Colombian cohort. METHODS: We conducted a retrospective cohort in 20 HIV clinics, including participants ≥18 years old with confirmed HIV infection who underwent an ART switch from January 2017 to December 2019 with at least 6 months of follow-up. A time-to-event analysis and an exploratory Cox model were performed. RESULTS: 796 participants switched ART during the study period. The leading cause of ART switch was drug intolerance (n = 449; 56.4%) with a median time-to-switch of 12.2 months. The longest median time-to-switch was due to regimen simplification (42.4 months). People ≥50 years old (HR = 0.6; 95% CI (0.5-0.7) and CDC stage 3 at diagnosis (HR = 0.8; 95% CI (0.6-0.9) had less hazard for switching ART over time. CONCLUSIONS: In this Colombian cohort, drug intolerance was the main cause of the ART switch, and the time-to-switch is shorter than reports from other countries. In Colombia, it is crucial to apply current recommendations for ART initiation to choose regimens with a better tolerability profile.

Laparoscopic Janeway gastrostomy as preferred enteral access in specific patient populations: A systematic review and case series.

BACKGROUND: Nutrition is one of the fundamental needs of both patient and non-patient populations. General trends promote enteral feeding as a superior route, with the most common enteral access being the percutaneous endoscopic gastrostomy (PEG) as the first-line procedure, with surgical access including Witzel gastrostomy, Stamm Gastrostomy, Janeway gastrostomy (JG) as secondary means. AIM: To describe cases and technique of laparoscopic Janeway gastrostomy (LJG) and perform a systematic review of the data. METHODS: We successfully performed two LJG procedures, after which we conducted a literature review of all documented cases of LJG from 1991 to 2022. We surveyed these cases to show the efficacy of LJG and provide comparisons to other existing procedures with primary outcomes of operative time, complications, duration of gastrostomy use, and application settings. The data were then extracted and assessed on the basis of the Reference Citation Analysis (https://www.referencecitationanalysis.com/). RESULTS: We presented two cases of LJG, detailing the simplicity and benefits of this technique. We subsequently identified 26 articles and 56 cases of LJG and extrapolated the data relating to our outcome measures. We could show the potential of LJG as a viable and preferred option in certain patient populations requiring enteral access, drawing reference to its favorable outcome profile and low complication rate. CONCLUSION: The LJG is a simple, reproducible procedure with a favorable complication profile. By its technical ease and benefits relating to the gastric tube formed, we propose this procedure as a viable, favorable enteral access in patients with the need for permanent or palliative gastrostomy, those with neurologic disease, agitation or at high risk of gastrostomy dislodgement, or where PEG may be infeasible.

A Novel Simulation Model for Training Emergency Medicine Residents in the Ultrasound Identification of Landmarks for Cricothyrotomy.

Objectives The objective of this study is to describe a simple, replicable method to create neck models for the purpose of education and practice of ultrasound (US) identification of anatomic landmarks for cricothyrotomy. The second objective is to assess the model's capability in training emergency medicine (EM) residents in the US identification of anatomic landmarks for cricothyrotomy. Methods This is a cross-sectional study using a convenience sample of EM residents. Participants were taught to identify the thyroid cartilage, the cricothyroid membrane (CTM), and the cricoid cartilage using US. After an instructional period, participants performed a US examination on gel models designed to overly a live, human neck simulating various scenarios: thin neck, thick neck, anterior neck hematoma, and subcutaneous emphysema. Residents were asked to identify the thyroid cartilage, the CTM, and the cricoid cartilage as quickly as possible. The mean time to successful identification was reported in seconds. Following the scanning session, participants were asked to complete a post-survey. After the session, the video recordings were reviewed by an emergency US fellowship-trained physician to assess the visuomotor skills of each participant. Results A total of 42 residents participated in the study. Ninety-three percent (32/42; 95% CI 80.3% - 98.2%) of residents were able to obtain an optimal sagittal or parasagittal sonographic view of the anterior airway landmarks. Of these residents, 21.4% (9/42; 95% CI 11.5% - 36.2%) required minimal assistance with the initial probe placement. The visuomotor scores were recorded for each participant. Results of the pearson correlation indicated that there was a significant positive relationship between the residents' year in training with their visuomotor score (r(40) = .41, p = .007). When scanning the thin neck, 90.5% (38/42; 95% CI 77.4% - 96.8%) of residents were able to successfully identify the landmarks. The median time to completion was 27 seconds. When scanning the subcutaneous air model, 88.1% (37/42; 95% CI 74.5% - 95.3%) of residents were able to successfully identify the landmarks. The median time to completion was 26 seconds. When scanning the neck with the fluid collection 95.2% (40/42; 95% CI 83.4% - 99.5%) of residents were able to successfully identify the landmarks with a median time of 20 seconds for identification. When scanning the thick neck model, 73.8% (31/42; 95% CI 58.8% - 84.8%) of residents were able to successfully identify the landmarks taking a median time of 26 seconds. After the training session, 76.2% of residents reported that they felt either "confident" or "extremely confident" in identifying the CTM using US. Conclusion The novel anterior neck gel models used in this study were found to be adequate for training EM residents in the US identification of anterior neck anatomy. Residents were successfully trained in identifying the important anterior neck landmarks that are useful when predicting a difficult anterior airway and planning for surgical cricothyrotomy. Residents overall felt that the models simulated the appropriate anatomic scenarios. The majority felt confident in identifying the CTM using US.

Opposing roles of plant laticifer cells in the resistance to insect herbivores and fungal pathogens.

More than 12,000 plant species (ca. 10% of flowering plants) exude latex when their tissues are injured. Latex is produced and stored in specialized cells named "laticifers". Laticifers form a tubing system composed of rows of elongated cells that branch and create an internal network encompassing the entire plant. Laticifers constitute a recent evolutionary achievement in ecophysiological adaptation to specific natural environments; however, their fitness benefit to the plant still remains to be proven. The identification of Euphorbia lathyris mutants (pil mutants) deficient in laticifer cells or latex metabolism, and therefore compromised in latex production, allowed us to test the importance of laticifers in pest resistance. We provided genetic evidence indicating that laticifers represent a cellular adaptation for an essential defense strategy to fend off arthropod herbivores with different feeding habits, such as Spodoptera exigua and Tetranychus urticae. In marked contrast, we also discovered that a lack of laticifer cells causes complete resistance to the fungal pathogen Botrytis cinerea. Thereafter, a latex-derived factor required for conidia germination on the leaf surface was identified. This factor promoted disease susceptibility enhancement even in the non-latex-bearing plant Arabidopsis. We speculate on the role of laticifers in the co-evolutionary arms race between plants and their enemies.

The Role of ABA in Plant Immunity is Mediated through the PYR1 Receptor.

ABA is involved in plant responses to a broad range of pathogens and exhibits complex antagonistic and synergistic relationships with salicylic acid (SA) and ethylene (ET) signaling pathways, respectively. However, the specific receptor of ABA that triggers the positive and negative responses of ABA during immune responses remains unknown. Through a reverse genetic analysis, we identified that PYR1, a member of the family of PYR/PYL/RCAR ABA receptors, is transcriptionally upregulated and specifically perceives ABA during biotic stress, initiating downstream signaling mediated by ABA-activated SnRK2 protein kinases. This exerts a damping effect on SA-mediated signaling, required for resistance to biotrophic pathogens, and simultaneously a positive control over the resistance to necrotrophic pathogens controlled by ET. We demonstrated that PYR1-mediated signaling exerted control on a priori established hormonal cross-talk between SA and ET, thereby redirecting defense outputs. Defects in ABA/PYR1 signaling activated SA biosynthesis and sensitized plants for immune priming by poising SA-responsive genes for enhanced expression. As a trade-off effect, pyr1-mediated activation of the SA pathway blunted ET perception, which is pivotal for the activation of resistance towards fungal necrotrophs. The specific perception of ABA by PYR1 represented a regulatory node, modulating different outcomes in disease resistance.

Starch degradation, abscisic acid and vesicular trafficking are important elements in callose priming by indole-3-carboxylic acid in response to Plectosphaerella cucumerina infection.

A fast callose accumulation has been shown to mediate defence priming in certain plant-pathogen interactions, but the events upstream of callose assembly following chemical priming are poorly understood, mainly because those steps comprise sugar transfer to the infection site. ß-Amino butyric acid (BABA)-induced resistance in Arabidopsis against Plectosphaerella cucumerina is known to be mediated by callose priming. Indole-3-carboxylic acid (ICOOH, also known as I3CA) mediates BABA-induced resistance in Arabidopsis against P. cucumerina. This indolic compound is found in a common fingerprint of primed metabolites following treatments with various priming stimuli. In the present study, we show that I3CA induces resistance in Arabidopsis against P. cucumerina and primes enhancement of callose accumulation. I3CA treatment increased abscisic acid (ABA) levels before infection with P. cucumerina. An intact ABA synthesis pathway is needed to activate a starch amylase (BAM1) to trigger augmented callose deposition against P. cucumerina during I3CA-IR. To verify the relevance of the BAM1 amylase in I3CA-IR, knockdown mutants and overexpressors of the BAM1 gene were tested. The mutant bam1 was impaired to express I3CA-IR, but complemented 35S::BAM1-YFP lines in the background of bam1 restored an intact I3CA-IR and callose priming. Therefore, a more active starch metabolism is a committed step for I3CA-IR, inducing callose priming in adult plants. Additionally, I3CA treatments induced expression of the ubiquitin ligase ATL31 and syntaxin SYP131, suggesting that vesicular trafficking is relevant for callose priming. As a final element in the callose priming, an intact Powdery Mildew resistant4 (PMR4) gene is also essential to fully express I3CA-IR.

Endoscopic Management of Foreign Bodies in the Gastrointestinal Tract: A Review of the Literature.

Foreign body ingestion is a common diagnosis that presents in emergency departments throughout the world. Distinct foreign bodies predispose to particular locations of impaction in the gastrointestinal tract, commonly meat boluses in the esophagus above a preexisting esophageal stricture or ring in adults and coins in children. Several other groups are at high risk of foreign body impaction, mentally handicapped individuals or those with psychiatric illness, abusers of drugs or alcohol, and the geriatric population. Patients with foreign body ingestion typically present with odynophagia, dysphagia, sensation of having an object stuck, chest pain, and nausea/vomiting. The majority of foreign bodies pass through the digestive system spontaneously without causing any harm, symptoms, or necessitating any further intervention. A well-documented clinical history and thorough physical exam is critical in making the diagnosis, if additional modalities are needed, a CT scan and diagnostic endoscopy are generally the preferred modalities. Various tools can be used to remove foreign bodies, and endoscopic treatment is safe and effective if performed by a skilled endoscopist.

Novel disease susceptibility factors for fungal necrotrophic pathogens in Arabidopsis.

Host cells use an intricate signaling system to respond to invasions by pathogenic microorganisms. Although several signaling components of disease resistance against necrotrophic fungal pathogens have been identified, our understanding for how molecular components and host processes contribute to plant disease susceptibility is rather sparse. Here, we identified four transcription factors (TFs) from Arabidopsis that limit pathogen spread. Arabidopsis mutants defective in any of these TFs displayed increased disease susceptibility to Botrytis cinerea and Plectosphaerella cucumerina, and a general activation of non-immune host processes that contribute to plant disease susceptibility. Transcriptome analyses revealed that the mutants share a common transcriptional signature of 77 up-regulated genes. We characterized several of the up-regulated genes that encode peptides with a secretion signal, which we named PROVIR (for provirulence) factors. Forward and reverse genetic analyses revealed that many of the PROVIRs are important for disease susceptibility of the host to fungal necrotrophs. The TFs and PROVIRs identified in our work thus represent novel genetic determinants for plant disease susceptibility to necrotrophic fungal pathogens.

Mediated plastid RNA editing in plant immunity.

Plant regulatory circuits coordinating nuclear and plastid gene expression have evolved in response to external stimuli. RNA editing is one of such control mechanisms. We determined the Arabidopsis nuclear-encoded homeodomain-containing protein OCP3 is incorporated into the chloroplast, and contributes to control over the extent of ndhB transcript editing. ndhB encodes the B subunit of the chloroplast NADH dehydrogenase-like complex (NDH) involved in cyclic electron flow (CEF) around photosystem I. In ocp3 mutant strains, ndhB editing efficiency decays, CEF is impaired and disease resistance to fungal pathogens substantially enhanced, a process recapitulated in plants defective in editing plastid RNAs encoding NDH complex subunits due to mutations in previously described nuclear-encoded pentatricopeptide-related proteins (i.e. CRR21, CRR2). Furthermore, we observed that following a pathogenic challenge, wild type plants respond with editing inhibition of ndhB transcript. In parallel, rapid destabilization of the plastidial NDH complex is also observed in the plant following perception of a pathogenic cue. Therefore, NDH complex activity and plant immunity appear as interlinked processes.

Reciprocal regulation between AtNRT2.1 and AtAMT1.1 expression and the kinetics of NH(4)(+) and NO(3)(-) influxes.

Our results show that AtNRT2.1 expression has a positive effect on the NH(4)(+) ion influx, mediated by the HATS, as also occurs with AtAMT1.1 expression on the NO(3)(-) ion influx. AtNRT2.1 expression plays a key role in the regulation of AtAMT1.1 expression and in the NH(4)(+) ion influx, differentiating the nitrogen source, and particularly, the lack of it. Nitrogen starvation produces a compensatory effect by AtAMT1.1 when there is an absence of the AtNRT2.1 gene. Our results also show that, in the atnrt2 mutant lacking both AtNRT2.1 and AtNRT2.2, gene functions present different kinetic parameters on the NH(4)(+) ion influx mediated by the HATS, according to the source and availability of nitrogen. Finally, the absence of AMT1.1 also produces changes in the kinetic parameters of the NO(3)(-) influx, showing different V(max) values depending on the source of nitrogen available.

A deletion in NRT2.1 attenuates Pseudomonas syringae-induced hormonal perturbation, resulting in primed plant defenses.

For an efficient defense response against pathogens, plants must coordinate rapid genetic reprogramming to produce an incompatible interaction. Nitrate Trasnporter2 (NRT2) gene family members are sentinels of nitrate availability. In this study, we present an additional role for NRT2.1 linked to plant resistance against pathogens. This gene antagonizes the priming of plant defenses against the bacterial pathogen Pseudomonas syringae pv tomato DC3000 (Pst). The nrt2 mutant (which is deficient in two genes, NRT2.1 and NRT2.2) displays reduced susceptibility to this bacterium. We demonstrate that modifying environmental conditions that stimulate the derepression of the NRT2.1 gene influences resistance to Pst independently of the total level of endogenous nitrogen. Additionally, hormonal homeostasis seemed to be affected in nrt2, which displays priming of salicylic acid signaling and concomitant irregular functioning of the jasmonic acid and abscisic acid pathways upon infection. Effector-triggered susceptibility and hormonal perturbation by the bacterium seem to be altered in nrt2, probably due to reduced sensitivity to the bacterial phytotoxin coronatine. The main genetic and metabolic targets of coronatine in Arabidopsis (Arabidopsis thaliana) remain largely unstimulated in nrt2 mutants. In addition, a P. syringae strain defective in coronatine synthesis showed the same virulence toward nrt2 as the coronatine-producing strain. Taken together, the reduced susceptibility of nrt2 mutants seems to be a combination of priming of salicylic acid-dependent defenses and reduced sensitivity to the bacterial effector coronatine. These results suggest additional functions for NRT2.1 that may influence plant disease resistance by down-regulating biotic stress defense mechanisms and favoring abiotic stress responses.

Arabidopsis ocp3 mutant reveals a mechanism linking ABA and JA to pathogen-induced callose deposition.

In the present study, we evaluated the role of the defense-related gene OCP3 in callose deposition as a response to two necrotrophic fungal pathogens, Botrytis cinerea and Plectosphaerella cucumerina. ocp3 plants exhibited accelerated and intensified callose deposition in response to fungal infection associated with enhanced disease resistance to the two pathogens. A series of double mutant analyses showed potentiation of callose deposition and the heightened disease resistance phenotype in ocp3 plants required the plant hormone abscisic acid (ABA) and the PMR4 gene encoding a callose synthase. This finding was congruent with an observation that ocp3 plants exhibited increased ABA accumulation, and ABA was rapidly synthesized following fungal infection in wild-type plants. Furthermore, we determined that potentiation of callose deposition in ocp3 plants, including enhanced disease resistance, also required jasmonic acid (JA) recognition though a COI1 receptor, however JA was not required for basal callose deposition following fungal infection. In addition, potentiation of callose deposition in ocp3 plants appeared to follow a different mechanism than that proposed for callose ß-amino-butyric acid (BABA)-induced resistance and priming, because ocp3 plants responded to BABA-induced priming for callose deposition and induced resistance of a magnitude similar to that observed in wild-type plants. Our results point to a model in which OCP3 represents a specific control point for callose deposition regulated by JA yet ultimately requiring ABA. These results provide new insights into the mechanism of callose deposition regulation in response to pathogen attack; however the complexities of the processes remain poorly understood.

Enhanced disease resistance to Botrytis cinerea in myb46 Arabidopsis plants is associated to an early down-regulation of CesA genes.

The cell wall is a protective barrier of paramount importance for the survival of plant cells. Monitoring the integrity of cell wall allows plants to quickly activate defence pathways to minimize pathogen entry and reduce the spread of disease. Counterintuitively, however, pharmacological effects as well as genetic lesions that affect cellulose biosynthesis and content confer plants with enhanced resistance against necrotrophic fungi. This kind of pathogens target cellulose for degradation to facilitate penetration and to generate glucose units as a food source. Our results points towards the existence of a transcriptional reprogramming mechanism in genes encoding cellulose synthases (CesAs) that occurs very soon after Botrytis cinerea attack and that results in a temporarily shut down of some CesA genes. Interestingly, the observed coordinated down-regulation of CesA genes is more pronounced, and occurs earlier, in myb46 mutant plants. In the resistant myb46 plants, pathogen infection induces transient down-regulation of CesA genes that concurs with a selective transcriptional reprogramming in a set of genes encoding structural cell wall proteins and extracellular remodelling enzymes. Together with previous indications, our results favour the hypothesis that CesAs are part of a surveillance system of the cell wall integrity that senses the presence of a pathogen and transduces that signal into a rapid transcriptional reprogramming of the affected cell.

MYB46 modulates disease susceptibility to Botrytis cinerea in Arabidopsis.

In this study, we show that the Arabidopsis (Arabidopsis thaliana) transcription factor MYB46, previously described to regulate secondary cell wall biosynthesis in the vascular tissue of the stem, is pivotal for mediating disease susceptibility to the fungal pathogen Botrytis cinerea. We identified MYB46 by its ability to bind to a new cis-element located in the 5' promoter region of the pathogen-induced Ep5C gene, which encodes a type III cell wall-bound peroxidase. We present genetic and molecular evidence indicating that MYB46 modulates the magnitude of Ep5C gene induction following pathogenic insults. Moreover, we demonstrate that different myb46 knockdown mutant plants exhibit increased disease resistance to B. cinerea, a phenotype that is accompanied by selective transcriptional reprogramming of a set of genes encoding cell wall proteins and enzymes, of which extracellular type III peroxidases are conspicuous. In essence, our results substantiate that defense-related signaling pathways and cell wall integrity are interconnected and that MYB46 likely functions as a disease susceptibility modulator to B. cinerea through the integration of cell wall remodeling and downstream activation of secondary lines of defense.

The RNA silencing enzyme RNA polymerase v is required for plant immunity.

RNA-directed DNA methylation (RdDM) is an epigenetic control mechanism driven by small interfering RNAs (siRNAs) that influence gene function. In plants, little is known of the involvement of the RdDM pathway in regulating traits related to immune responses. In a genetic screen designed to reveal factors regulating immunity in Arabidopsis thaliana, we identified NRPD2 as the OVEREXPRESSOR OF CATIONIC PEROXIDASE 1 (OCP1). NRPD2 encodes the second largest subunit of the plant-specific RNA Polymerases IV and V (Pol IV and Pol V), which are crucial for the RdDM pathway. The ocp1 and nrpd2 mutants showed increases in disease susceptibility when confronted with the necrotrophic fungal pathogens Botrytis cinerea and Plectosphaerella cucumerina. Studies were extended to other mutants affected in different steps of the RdDM pathway, such as nrpd1, nrpe1, ago4, drd1, rdr2, and drm1drm2 mutants. Our results indicate that all the mutants studied, with the exception of nrpd1, phenocopy the nrpd2 mutants; and they suggest that, while Pol V complex is required for plant immunity, Pol IV appears dispensable. Moreover, Pol V defective mutants, but not Pol IV mutants, show enhanced disease resistance towards the bacterial pathogen Pseudomonas syringae DC3000. Interestingly, salicylic acid (SA)-mediated defenses effective against PsDC3000 are enhanced in Pol V defective mutants, whereas jasmonic acid (JA)-mediated defenses that protect against fungi are reduced. Chromatin immunoprecipitation analysis revealed that, through differential histone modifications, SA-related defense genes are poised for enhanced activation in Pol V defective mutants and provide clues for understanding the regulation of gene priming during defense. Our results highlight the importance of epigenetic control as an additional layer of complexity in the regulation of plant immunity and point towards multiple components of the RdDM pathway being involved in plant immunity based on genetic evidence, but whether this is a direct or indirect effect on disease-related genes is unclear.

OCP3 is an important modulator of NPR1-mediated jasmonic acid-dependent induced defenses in Arabidopsis.

BACKGROUND: Upon appropriate stimulation, plants increase their level of resistance against future pathogen attack. This phenomenon, known as induced resistance, presents an adaptive advantage due to its reduced fitness costs and its systemic and broad-spectrum nature. In Arabidopsis, different types of induced resistance have been defined based on the signaling pathways involved, particularly those dependent on salicylic acid (SA) and/or jasmonic acid (JA). RESULTS: Here, we have assessed the implication of the transcriptional regulator OCP3 in SA- and JA-dependent induced defenses. Through a series of double mutant analyses, we conclude that SA-dependent defense signaling does not require OCP3. However, we found that ocp3 plants are impaired in a Pseudomonas fluorescens WCS417r-triggered induced systemic resistance (ISR) against both Pseudomonas syrinagae DC3000 and Hyaloperonospora arabidopsidis, and we show that this impairment is not due to a defect in JA-perception. Likewise, exogenous application of JA failed to induce defenses in ocp3 plants. In addition, we provide evidence showing that the over-expression of an engineered cytosolic isoform of the disease resistance regulator NPR1 restores the impaired JA-induced disease resistance in ocp3 plants. CONCLUSIONS: Our findings point to a model in which OCP3 may modulate the nucleocytosolic function of NPR1 in the regulation of JA-dependent induced defense responses.