Establishing a unified paradigm of microwave absorption inspired by the merging of traditional microwave absorbing materials and metamaterials.

The merging of traditional microwave absorbing materials with metamaterials holds significant potential for enhancing microwave absorber performance. To unlock this potential, a unified paradigm is urgently required. We have successfully established such a paradigm, focusing on regulating effective electromagnetic parameters and interfacial forms across microscopic, mesoscopic, and macroscopic scales. Building upon this foundation, we introduce an active co-design methodology for jointly optimizing full-scale structures and the concept of "full-scale microwave absorbers" (FSMAs). Under this guidance, performance improvements can be achieved efficiently, leading to crucial breakthroughs. For demonstration, we present a case study designing ultra-thin miniaturized FSMAs capable of ultra-broadband and low-frequency absorption. Simulation results show absorptivity exceeding 90% in the 2-28 GHz range, with absorptivity surpassing 85% and 74% in the 1.5-2 GHz and 1-1.5 GHz ranges, respectively. Additionally, the total thickness and macro period are only 5 mm, roughly equivalent to 0.033 wavelengths of the lowest operating frequency. Most importantly, we have broken the Rozanov limit, with experimental results further validating this design. This work significantly enhances our understanding of microwave absorption and offers a shortcut for pursuing improved performances and breakthroughs.

A bacterial type III effector targets plant vesicle-associated membrane proteins.

The soilborne bacterial pathogen Ralstonia solanacearum is one of the most destructive plant pathogens worldwide, and its infection process involves the manipulation of numerous plant cellular functions. In this work, we found that the R. solanacearum effector protein RipD partially suppressed different levels of plant immunity triggered by R. solanacearum elicitors, including specific responses triggered by pathogen-associated molecular patterns and secreted effectors. RipD localized in different subcellular compartments in plant cells, including vesicles, and its vesicular localization was enriched in cells undergoing R. solanacearum infection, suggesting that this specific localization may be particularly relevant during infection. Among RipD-interacting proteins, we identified plant vesicle-associated membrane proteins (VAMPs). We also found that overexpression of Arabidopsis thaliana VAMP721 and VAMP722 in Nicotiana benthamiana leaves promoted resistance to R. solanacearum, and this was abolished by the simultaneous expression of RipD, suggesting that RipD targets VAMPs to contribute to R. solanacearum virulence. Among proteins secreted in VAMP721/722-containing vesicles, CCOAOMT1 is an enzyme required for lignin biosynthesis, and mutation of CCOAOMT1 enhanced plant susceptibility to R. solanacearum. Altogether our results reveal the contribution of VAMPs to plant resistance against R. solanacearum and their targeting by a bacterial effector as a pathogen virulence strategy.

m6A RNA methylation impairs gene expression variability and reproductive thermotolerance in Arabidopsis.

Heat-imposed crop failure is often attributed to reduced thermotolerance of floral tissues; however, the underlying mechanism remains unknown. Here, we demonstrate that m6A RNA methylation increases in Arabidopsis flowers and negatively regulates gene expression variability. Stochastic gene expression provides flexibility to cope with environmental stresses. We find that reduced transcriptional fluctuation is associated with compromised activation of heat-responsive genes. Moreover, disruption of an RNA demethylase AtALKBH10B leads to lower gene expression variability, suppression of heat-activated genes, and strong reduction of plant fertility. Our work proposes a novel role for RNA methylation in the bet-hedging strategy of heat stress response.

Heteroatom-free conjugated tetraphenylethylene polymers for selectively fluorescent detection of tetracycline.

The antibiotic tetracycline (Tc) is a major contaminant in food and water, with adverse effects on both ecosystems and human health. The development of novel sensors for tetracycline detection is of great importance. In this work, we develop a novel heteroatom-free conjugated tetraphenylethylene polymer (TPE-CMP) fluorescence sensor for the detection of tetracycline. In the presence of Tc, the emission fluorescence of TPE-CMP was quenched by the photoinduced electron transfer mechanism to achieve high sensitivity. The polymers can detect tetracycline at a concentration of 0-100 µg/mL with a good linear correlation (0.99), and the limit of detection (LOD) is 1.23 µg/mL. Furthermore, TPE-CMP has excellent selectivity in detecting Tc in the presence of various anti-interference analytes, including ions and antibiotics. In addition, the practical feasibilities of TPE-CMP for Tc sensing were further investigated in milk, urine and wastewater samples with satisfactory recoveries (from 94.96% to 112.53% for milk, from 96.41% to 99.31% for urine and from 98.54% to 100.52% for wastewater). We have designed and synthesized TPE-CMP based on heteroatom-free for the specific fluorescence detection of tetracycline, expanding the range of fluorescence detection sensors and offering great promise for practical applications.

SGT1 is not required for plant LRR-RLK-mediated immunity.

Plant immune signalling activated by the perception of pathogen-associated molecular patterns (PAMPs) or effector proteins is mediated by pattern-recognition receptors (PRRs) and nucleotide-binding and leucine-rich repeat domain-containing receptors (NLRs), which often share cellular components and downstream responses. Many PRRs are leucine-rich repeat receptor-like kinases (LRR-RLKs), which mostly perceive proteinaceous PAMPs. The suppressor of the G2 allele of skp1 (SGT1) is a core immune regulator required for the activation of NLR-mediated immunity. In this work, we examined the requirement of SGT1 for immune responses mediated by several LRR-RLKs in both Nicotiana benthamiana and Arabidopsis. Using complementary genetic approaches, we found that SGT1 is not limiting for early PRR-dependent responses or antibacterial immunity. We therefore conclude that SGT1 does not play a significant role in bacterial PAMP-triggered immunity.

Intra-strain Elicitation and Suppression of Plant Immunity by Ralstonia solanacearum Type-III Effectors in Nicotiana benthamiana.

Effector proteins delivered inside plant cells are powerful weapons for bacterial pathogens, but this exposes the pathogen to potential recognition by the plant immune system. Therefore, the effector repertoire of a given pathogen must be balanced for a successful infection. Ralstonia solanacearum is an aggressive pathogen with a large repertoire of secreted effectors. One of these effectors, RipE1, is conserved in most R. solanacearum strains sequenced to date. In this work, we found that RipE1 triggers immunity in N. benthamiana, which requires the immune regulator SGT1, but not EDS1 or NRCs. Interestingly, RipE1-triggered immunity induces the accumulation of salicylic acid (SA) and the overexpression of several genes encoding phenylalanine-ammonia lyases (PALs), suggesting that the unconventional PAL-mediated pathway is responsible for the observed SA biosynthesis. Surprisingly, RipE1 recognition also induces the expression of jasmonic acid (JA)-responsive genes and JA biosynthesis, suggesting that both SA and JA may act cooperatively in response to RipE1. We further found that RipE1 expression leads to the accumulation of glutathione in plant cells, which precedes the activation of immune responses. R. solanacearum secretes another effector, RipAY, which is known to inhibit immune responses by degrading cellular glutathione. Accordingly, RipAY inhibits RipE1-triggered immune responses. This work shows a strategy employed by R. solanacearum to counteract the perception of its effector proteins by plant immune system.

A Bacterial Effector Protein Hijacks Plant Metabolism to Support Pathogen Nutrition.

Many bacterial plant pathogens employ a type III secretion system to inject effector proteins within plant cells to suppress plant immunity. Whether and how effector proteins also co-opt plant metabolism to support extensive bacterial replication remains an open question. Here, we show that Ralstonia solanacearum, the causal agent of bacterial wilt disease, secretes the effector protein RipI, which interacts with plant glutamate decarboxylases (GADs) to alter plant metabolism and support bacterial growth. GADs are activated by calmodulin and catalyze the biosynthesis of gamma-aminobutyric acid (GABA), an important signaling molecule in plants and animals. RipI promotes the interaction of GADs with calmodulin, enhancing the production of GABA. R. solanacearum is able to replicate efficiently using GABA as a nutrient, and both RipI and plant GABA contribute to a successful infection. This work reveals a pathogenic strategy to hijack plant metabolism for the biosynthesis of nutrients that support microbial growth during plant colonization.