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The accurate ab-initio simulation of molecules and periodic solids with diagrammatic perturbation theory is an important task in quantum chemistry, condensed matter physics, and materials science. In this article, we present the WeakCoupling module of the open-source software package Green, which implements fully self-consistent diagrammatic weak coupling simulations, capable of dealing with real materials in the finite-temperature formalism. The code is licensed under the permissive MIT license. We provide self-consistent GW (scGW) and self-consistent second-order Green's function perturbation theory (GF2) solvers, analysis tools, and post-processing methods. This paper summarizes the theoretical methods implemented and provides background, tutorials and practical instructions for running simulations. 

Abstract Powdery mildew fungi are obligate biotrophic pathogens that only invade plant epidermal cells. There are two epidermal surfaces in every plant leaf: the adaxial (upper) side and the abaxial (lower) side. While both leaf surfaces can be susceptible to adapted powdery mildew fungi in many plant species, there have been observations of leaf abaxial immunity in some plant species including Arabidopsis. The genetic basis of such leaf abaxial immunity remains unknown. In this study, we tested a series of Arabidopsis mutants defective in one or more known defense pathways with the adapted powdery mildew isolate Golovinomyces cichoracearum UCSC1. We found that leaf abaxial immunity was significantly compromised in mutants impaired for both the EDS1/PAD4- and PEN2/PEN3-dependent defenses. Consistently, expression of EDS1–yellow fluorescent protein and PEN2–green fluorescent protein fusions from their respective native promoters in the respective eds1-2 and pen2-1 mutant backgrounds was higher in the abaxial epidermal cells than in the adaxial epidermal cells. Altogether, our results indicate that leaf abaxial immunity against powdery mildew in Arabidopsis is at least partially due to enhanced EDS1/PAD4- and PEN2/PEN3-dependent defenses. Such transcriptionally pre-programmed defense mechanisms may underlie leaf abaxial immunity in other plant species such as hemp and may be exploited for engineering adaxial immunity against powdery mildew fungi in crop plants. 

Neural markers of attention, including those frequently linked to the event-related potential P3 (P300) or P3b component, vary widely within and across participants. Understanding the neural mechanisms of attention that contribute to the P3 is crucial for better understanding attention-related brain disorders. All ten participants were scanned twice with a resting-state PCASL perfusion MRI and an ERP with a visual oddball task to measure brain resting-state functional connectivity (rsFC) and P3 parameters (P3 amplitudes and P3 latencies). Global rsFC (average rsFC across the entire brain) was associated with both P3 amplitudes (r = 0.57, p = 0.011) and P3 onset latencies (r = −0.56, p = 0.012). The observed P3 parameters were correlated with predicted P3 amplitude from the global rsFC (amplitude: r = +0.48, p = 0.037; latency: r = +0.40, p = 0.088) but not correlated with the rsFC over the most significant individual edge. P3 onset latency was primarily related to long-range connections between the prefrontal and parietal/limbic regions, while P3 amplitudes were related to connections between prefrontal and parietal/occipital, between sensorimotor and subcortical, and between limbic/subcortical and parietal/occipital regions. These results demonstrated the power of resting-state PCASL and P3 correlation with brain global functional connectivity. 

Arabidopsis RESISTANCE TO POWDERY MILDEW 8.2 (RPW8.2) is specifically induced by the powdery mildew (PM) fungus (Golovinomyces cichoracearum) in the infected epidermal cells to activate immunity. However, the mechanism of RPW8.2-induction is not well understood. Here, we identify a G. cichoracearum effector that interacts with RPW8.2, named Gc-RPW8.2 interacting protein 1 (GcR8IP1), by a yeast two-hybrid screen of an Arabidopsis cDNA library. GcR8IP1 physically associated with RPW8.2 with its RING finger domain that is essential and sufficient for the association. GcR8IP1 was secreted and translocated into the nucleus of host cell infected with PM. Association of GcR8IP1 with RPW8.2 led to an increase of RPW8.2 in the nucleus. In turn, the nucleus-localised RPW8.2 promoted the activity of the RPW8.2 promoter, resulting in transcriptional self-amplification of RPW8.2 to boost immunity at infection sites. Additionally, ectopic expression or host-induced gene silencing of GcR8IP1 supported its role as a virulence factor in PM. Altogether, our results reveal a mechanism of RPW8.2-dependent defense strengthening via altered partitioning of RPW8.2 and transcriptional self-amplification triggered by a PM fungal effector, which exemplifies an atypical form of effector-triggered immunity. 

Abstract Study on the regulation of broad‐spectrum resistance is an active area in plant biology.RESISTANCE TO POWDERY MILDEW 8.1(RPW8.1) is one of a few broad‐spectrum resistance genes triggering the hypersensitive response (HR) to restrict multiple pathogenic infections. To address the question how RPW8.1 signaling is regulated, we performed a genetic screen and tried to identify mutations enhancing RPW8.1‐mediated HR. Here, we provided evidence to connect an annexin protein with RPW8.1‐mediated resistance inArabidopsisagainst powdery mildew. We isolated and characterizedArabidopsis b7‐6mutant. A point mutation inb7‐6at theAt5g12380locus resulted in an amino acid substitution in ANNEXIN 8 (AtANN8). Loss‐of‐function or RNA‐silencing ofAtANN8led to enhanced expression ofRPW8.1, RPW8.1‐dependent necrotic lesions in leaves, and defense against powdery mildew. Conversely, over‐expression ofAtANN8compromised RPW8.1‐mediated disease resistance and cell death. Interestingly, the mutation in AtANN8 enhanced RPW8.1‐triggered H₂O₂. In addition, mutation in AtANN8 led to hypersensitivity to salt stress. Together, our data indicate that AtANN8 is involved in multiple stress signaling pathways and negatively regulates RPW8.1‐mediated resistance against powdery mildew and cell death, thus linking ANNEXIN's function with plant immunity.