Regulatory Mechanisms of the Resistance to Common Bacterial Blight Revealed by Transcriptomic Analysis in Common Bean (Phaseolus vulgaris L.)

Common bean blight (CBB), primarily caused by Xanthomonas axonopodis pv. phaseoli (Xap), is one of the most destructive diseases of common bean (Phaseolus vulgaris L.). The tepary bean genotype PI 319443 displays high resistance to Xap, and the common bean genotypes HR45 and Bilu display high resistance and susceptibility to Xap, respectively. To identify candidate genes related to Xap resistance, transcriptomic analysis was performed to compare gene expression levels with Xap inoculation at 0, 24, and 48 h post inoculation (hpi) among the three genotypes. A total of 1,146,009,876 high-quality clean reads were obtained. Differentially expressed gene (DEG) analysis showed that 1,688 DEGs responded to pathogen infection in the three genotypes. Weighted gene coexpression network analysis (WGCNA) was also performed to identify three modules highly correlated with Xap resistance, in which 334 DEGs were likely involved in Xap resistance. By combining differential expression analysis and WGCNA, 139 DEGs were identified as core resistance-responsive genes, including 18 genes encoding resistance (R) proteins, 19 genes belonging to transcription factor families, 63 genes encoding proteins with oxidoreductase activity, and 33 plant hormone signal transduction-related genes, which play important roles in the resistance to pathogen infection. The expression patterns of 20 DEGs were determined by quantitative real-time PCR (qRT-PCR) and confirmed the reliability of the RNA-seq results.

Specific Strains of Honeybee Gut Lactobacillus Stimulate Host Immune System to Protect against Pathogenic Hafnia alvei

Honeybees are essential pollinators supporting global agricultural economies and food supplies. Recent honeybee decline has been linked to several factors, while pathogen infection is considered one of the most significant contributing factors.

Urbanization and plant pathogen infection interact to affect the outcome of ecological interactions in an experimental multitrophic system

Urbanization can change interactions in insect communities, and the few studies of tritrophic interactions in urban settings focus on interactions between plants, herbivorous insects and their mutualists and natural enemies. Plant pathogen infection is also widespread and common, and infection may also alter such interactions, but we have no understanding of whether the ecological consequences of pathogen infection vary with urbanization. Using replicated aphid colonies on experimental plants, we investigated how infection by the plant pathogen Botrytis cinerea influences interactions between plants, aphids and the aphid natural enemies and ant mutualists in highly urbanized, suburban and rural study sites. Aphid and natural enemy abundance were highest in the suburban site, while mutualist ants were most abundant in the urban site, reversing the usual positive density-dependent relationship between natural enemies and aphids. The effect of pathogen infection varied with trait and site, mediated by natural enemy preference for hosts or prey on uninfected plants. The effect of infection on aphid abundance was only seen in the suburban site, where natural enemies were most abundant on uninfected plants and aphid numbers were greatest on infected plants. In the urban site, there was no effect of infection, while in the rural site, aphid numbers were lower on infected plants. Uninfected plants were smaller than infected plants and differed between locations. This study suggests that the effects of urbanization on ecological interactions may become more complex and difficult to predict as we study ecological assemblages and communities at greater levels of structural complexity.

Crosstalk of DNA Methylation Triggered by Pathogen in Poplars With Different Resistances

DNA methylation plays crucial roles in responses to environmental stimuli. Modification of DNA methylation during development and abiotic stress responses has been confirmed in increasing numbers of plants, mainly annual plants. However, the epigenetic regulation mechanism underlying the immune response to pathogens remains largely unknown in plants, especially trees. To investigate whether DNA methylation is involved in the response to infection process or is related to the resistance differences among poplars, we performed comprehensive whole-genome bisulfite sequencing of the infected stem of the susceptible type Populus × euramerican ‘74/76’ and resistant type Populus tomentosa ‘henan’ upon Lonsdalea populi infection. The results revealed that DNA methylation changed dynamically in poplars during the infection process with a remarkable decrease seen in the DNA methylation ratio. Intriguingly, the resistant P. tomentosa ‘henan’ had a much lower basal DNA methylation ratio than the susceptible P. × euramerican ‘74/76’. Compared to mock-inoculation, both poplar types underwent post-inoculation CHH hypomethylation; however, significant decreases in mC and mCHH proportions were found in resistant poplar. In addition, most differentially CHH-hypomethylated regions were distributed in repeat and promoter regions. Based on comparison of DNA methylation modification with the expression profiles of genes, DNA methylation occurred in resistance genes, pathogenesis-related genes, and phytohormone genes in poplars during pathogen infection. Additionally, transcript levels of genes encoding methylation-related enzymes changed during pathogen infection. Interestingly, small-regulator miRNAs were subject to DNA methylation in poplars experiencing pathogen infection. This investigation highlights the critical role of DNA methylation in the poplar immune response to pathogen infection and provides new insights into epigenetic regulation in perennial plants in response to biotic stress.

Detection of Root Physiological Parameters and Potassium and Calcium Currents in the Rhizoplane of the Apple Rootstock Superior Line 12-2 With Improved Apple Replant Disease Resistance

The cultivation of resistant rootstocks is one of the more effective ways to mitigate apple replant disease (ARD). We performed an ion current test, a pot experiment, and a pathogen infection test on the apple rootstocks 12-2 (self-named), T337, and M26. The ion current test showed that exposure to ARD soil extract for 30 min had a significant effect on K+ ion currents at the meristem, elongation, and mature zones of the M26 rhizoplane and on Ca2+ currents in the meristem and elongation zones. ARD also had a significant effect on Ca2+ currents in the meristem, elongation, and mature zones of the T337 rhizoplane. Exposure to ARD soil extract for 5 min had a significant effect on K+ currents in the meristem, elongation, and mature zones of 12-2 and on the Ca2+ currents in the elongation and mature zones. Compared to a 5-min exposure, a 30-min exposure to ARD extract had a less pronounced effect on K+ and Ca2+ currents in the 12-2 rhizoplane. The pot experiment showed that ARD soil had no significant effect on any root architectural or physiological parameters of 12-2. By contrast, ARD soil significantly reduced some root growth indices and the dry and fresh weights of T337 and M26 compared with controls on sterilized soil. ARD also had a significant effect on root metabolic activity, root antioxidant enzyme activity (except superoxide dismutase for T337), and malondialdehyde content of T337 and M26. Pathogen infection tests showed that Fusarium proliferatum MR5 significantly affected the root structure and reduced the root metabolic activity of T337 and M26. It also reduced their root antioxidant enzyme activities (except catalase for T337) and significantly increased the root malondialdehyde content, reactive oxygen levels, and proline and soluble sugar contents. By contrast, MR5 had no such effects on 12-2. Based on these results, 12-2 has the potential to serve as an important ARD-resistant rootstock.

NITROGEN LIMITATION ADAPTATION functions as a negative regulator of Arabidopsis immunity

Background: Phosphorus is an important macronutrient required for plant growth and development. It is absorbed through the roots in the form of inorganic phosphate (Pi). To cope with Pi limitation, plants have evolved an array of adaptive mechanisms to facilitate Pi acquisition and protect them from stress caused by Pi starvation. The NITROGEN LIMITATION ADAPTION (NLA) gene plays a key role in the regulation of phosphate starvation responses (PSR), its expression being regulated by the microRNA miR827. Stress caused by Pi limiting conditions might also affect the plant response to pathogen infection. However, cross-talk between phosphate signaling pathways and immune responses remains unclear. Results: In this study, we investigated whether NLA plays a role in Arabidopsis immunity. We show that loss-of-function of NLA and MIR827 overexpression causes an increase in phosphate (Pi) content which results in resistance to infection by the fungal pathogen Plectosphaerella cucumerina. The nla mutant plants accumulated callose in their leaves, a response that is also observed in wild-type plants that have been treated with high Pi. We also show that pathogen infection and treatment with fungal elicitors is accompanied by transcriptional activation of MIR827 and down-regulation of NLA. Upon pathogen challenge, nla plants exhibited higher levels of the phytoalexin camalexin compared to wild type plants. Camalexin level also increases in wild type plants treated with high Pi. Furthermore, the nla mutant plants accumulated salicylic acid (SA) and jasmonic acid (JA) in the absence of pathogen infection whose levels further increased upon pathogen. Conclusions: This study shows that NLA acts as a negative regulator of Arabidopsis immunity. Overaccumulation of Pi in nla plants positively affects resistance to infection by fungal pathogens. This piece of information reinforces the idea of signaling convergence between Pi and immune responses for the regulation of disease resistance in Arabidopsis.

Iron treatment induces defense responses and disease resistance against Magnaporthe oryzae in rice

Background: Iron is an essential micronutrient required for plant growth and development. The impact of iron in plant-pathogen interactions is also well recognized. However, the molecular basis underlying the effect of plant iron status and immune function in plants is poorly understood. Here, we investigated the impact of treatment with high iron in rice immunity at the cellular and molecular level. Results: We show that treatment with high iron confers resistance to infection by the blast fungus M. oryzae in rice. Histochemical staining of M. oryzae-infected leaves revealed that iron and Reactive Oxygen Species (ROS) accumulate at high levels in cells in the vicinity of the infection site. During pathogen infection, a stronger induction of defense-related genes occurs in leaves of iron-treated plants. Notably, a superinduction of phytoalexin biosynthetic genes, both diterpene phytoalexins and sakuranetin, is observed in iron-treated plants during pathogen infection. As a consequence, phytoalexin accumulation was higher in iron-treated plants compared with control plants. Transcriptional alterations of iron homeostasis-related genes and a reduction in apoplastic iron content were observed in leaves of Fe-treated rice plants. Conclusions: These results illustrate that the iron status plays a key role in the response of rice plants to pathogen infection, while reinforcing the notion that iron signaling and defense signaling must operate in a coordinated manner in controlling disease resistance in plants. This information provides a basis to better understand the molecular mechanisms involved in rice immunity.

Phosphate-induced resistance to pathogen infection in Arabidopsis

In nature, plants are concurrently exposed to a number of abiotic and biotic stresses. Our understanding of convergence points between responses to combined biotic/abiotic stress pathways remains, however, rudimentary. Here we show that MIR399 overexpression, loss-of-function of PHO2 (PHOSPHATE2), or treatment with high Pi, is accompanied by an increase in phosphate (Pi) content and accumulation of reactive oxygen species (ROS) in Arabidopsis thaliana. High Pi plants (e.g. miR399 overexpressor, pho2 mutant, and plants grown under high Pi supply) exhibited resistance to infection by necrotrophic and hemibiotrophic fungal pathogens. In the absence of pathogen infection, the expression level of genes in the salicylic acid (SA)- and jasmonic acid (JA)-dependent signaling pathways was higher in high Pi plants compared to wild type plants, which is consistent with increased levels of SA and JA in non-infected high Pi plants. During infection, an opposite regulation in the two branches of the JA pathway (ERF1/PDF1.2 and MYC2/VSP2) occurs in high Pi plants. Thus, while the ERF1-PDF1 branch positively responds to fungal infection, the MYC2/VSP2 branch is negatively regulated during pathogen infection in high Pi plants. This study supports that Pi accumulation promotes resistance to infection by fungal pathogens in Arabidopsis, while providing a basis to better understand crosstalk between Pi signaling and hormonal signalling pathways for modulation of plant immune responses.