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Most land plant genomes carry genes that encode RPW8-NLR Resistance (R) proteins. Angiosperms carry two RPW8-NLR subclasses: ADR1 and NRG1. ADR1s act as ‘helper’ NLRs for multiple TIR- and CC-NLR R proteins in Arabidopsis. In angiosperm families, NRG1 cooccurs with TIR-NLR Resistance (R) genes. We tested whether NRG1 is required for signalling of multiple TIR-NLRs. Using CRISPR mutagenesis, we obtained an nrg1a-nrg1b double mutant in two Arabidopsis accessions, and an nrg1 mutant in Nicotiana benthamiana. These mutants are compromised in signalling of all TIR-NLRs tested, including WRR4A, WRR4B, RPP1, RPP2, RPP4 and the pairs RRS1/RPS4, RRS1B/RPS4B, CHS1/SOC3 and CHS3/CSA1. In Arabidopsis, NRG1 is required for the hypersensitive cell death response (HR) and full oomycete resistance, but not for salicylic acid induction or bacterial resistance. By contrast, nrg1 loss of function does not compromise the CC-NLR R proteins RPS5 and MLA. RPM1 and RPS2 (CC-NLRs) function is slightly compromised in an nrg1 mutant. Thus, NRG1 is required for full TIR-NLR function and contributes to the signalling of some CC-NLRs. Some NRG1-dependent R proteins also signal partially via the NRG1 sister clade, ADR1. We propose that some NLRs signal via NRG1 only, some via ADR1 only and some via both or neither.

This study demonstrates the photocatalytic degradation efficiency of doped NiZnO and co-doped CdNiZnO NPs. Initially, ZnO NPs with a unique mesoporous ellipsoidal morphology were synthesized by simple precipitation and calcination. Powder X-ray diffraction revealed the formation of a hexagonal phase of the wurtzite structure. The average crystallite size of pristine ZnO NPs is 48 nm. The NPs possess higher thermal stability with the surface area, pore volume, and pore size of 9.1302 m 2 /g, 0.028299 cm 3 /g, and 12.39819 nm, respectively. Furthermore, different mesoporous doped NiZnO and co-doped CdNiZnO NPs in the range of 34 and 29 nm were synthesized by co-precipitation method and characterized by XRD, EDX, SEM, TEM, PL, Raman, BET analyses and UV–Vis spectroscopy. The calculated optical bandgaps for pure ZnO, doped NiZnO and co-doped CdNiZnO NPs were found to be 3.1, 2.62 and 2.33 eV, respectively. The photocatalytic activity of co-doped CdNiZnO was significantly higher than that of pure ZnO. After 50 min of irradiation, approximately 98% of rhodamine B was degraded by CdNiZnO, compared to 65% with pure ZnO. This enhancement is attributed to the synergistic effects of Ni and Cd, which trap electrons and holes, reducing recombination and extending charge carrier lifetimes. The photocatalytic efficiency of the synthesized materials to decompose the RhB dye (30 mgL −1 ) in aqueous media was tested via Langmuir–Hinshelwood model under UV–visible light. The degradation process followed pseudo-first order kinetic model. The synthesized NPs were re-used for five cycles without any significant decrease in the photodegradation ability. The mechanistic concept of generating reactive oxygen species by electron and hole charge (e‾/h + ) carriers seems to be responsible for the photocatalytic degradation of the dye by CdNiZnO NPs. Zeta potential analysis revealed positive surface charges for all catalysts, with co-doping significantly increasing charge and colloidal stability, thereby supporting the pH-dependent photocatalytic performance.

To gain the fundamental understanding of deformation mechanisms in an aluminum-containing austenitic high-Mn steel (Fe-32Mn-8.9Al-0.78 C (wt.%)), in-situ straining transmission electron microscopy (TEM) analysis is conducted. The in-situ observation during the deformation demonstrates that the plastic deformation is accommodated by the pronounced planar dislocation gliding followed by the formation of slip bands (SBs) and highly dense dislocation walls (HDDWs). Experimental evidences of the glide plane softening can be obtained from the interaction between the gliding perfect dislocations and the L’1 2 ordered precipitates in the austenite matrix. Furthermore, the observation of the localized cross-slip of dislocations at the slip band intersections enables to understand why slip bands are extensively developed without mutual obstructions between the slip bands. The enhanced strain hardening rate of the aluminum-containing austenitic high-Mn steels can be attributed to the pronounced planar dislocation glides followed by formation of extensive slip band which prevent premature failure by suppressing strain localization.

To learn spatiotemporal representations and anomaly predictions from geophysical data, we propose STANet , a spatiotemporal neural network with a trainable attention mechanism, and apply it to El Niño predictions for long-lead forecasts. The STANet makes two critical architectural improvements: it learns spatial features globally by expanding the network’s receptive field and encodes long-term sequential features with visual attention using a stateful long-short term memory network. The STANet conducts multitask learning of Nino3.4 index prediction and calendar month classification for predicted indices. In a comparison of the proposed STANet performance with the state-of-the-art model, the accuracy of the 12-month forecast lead correlation coefficient was improved by 5.8% and 13% for Nino3.4 index prediction and corresponding temporal classification, respectively. Furthermore, the spatially attentive regions for the strong El Niño events displayed spatial relationships consistent with the revealed precursor for El Niño occurrence, indicating that the proposed STANet provides good understanding of the spatiotemporal behavior of global sea surface temperature and oceanic heat content for El Niño evolution.

The deformation behavior of a high-Mn austenitic steel was investigated using in-situ straining transmission electron microscopy (TEM), with emphasis on the dynamic interaction between stacking faults and partial dislocations during plastic deformation. Owing to the low stacking-fault energy of the alloy, plastic deformation is primarily governed by Shockley partial dislocations, leading to extensive stacking-fault formation on multiple {111} planes. As deformation proceeds, stacking faults generated on different slip variants frequently intersect within grain interiors. Real-time observations reveal that these intersections act as strong deformation-induced barriers that impede partial dislocation motion, resulting in dislocation pile-up and localized strain concentration. Such interactions are considered to contribute significantly to strain hardening in low stacking-fault energy austenitic alloys. Despite their strong blocking effect, stacking-fault intersections are not strictly impenetrable. Under conditions of significant dislocation accumulation, the separation distance between leading and trailing partial dislocations can locally decrease, allowing temporary recombination into a perfect dislocation segment. The recombined dislocation adopts screw character, enabling cross-slip onto a secondary {111} slip plane, followed by re-dissociation into Shockley partial dislocations.These findings demonstrate that stacking-fault intersections function as dynamic microstructural features that both impede and mediate dislocation motion. The present in-situ TEM observations provide direct mechanistic insight into stacking-fault intersection-controlled dislocation dynamics and their role in strain hardening and local plastic accommodation in low stacking-fault energy austenitic steels.

We investigated the effect of κ-carbide precipitates on the strain hardening behavior of aged Fe–Mn-Al-C alloys by microstructure analysis. The κ-carbides-strengthened Fe–Mn-Al-C alloys exhibited a superior strength-ductility balance enabled by the recovery of the strain hardening rate. To understand the relation between the κ-carbides and strain hardening recovery, dislocation gliding in the aged alloys during plastic deformation was analyzed through in situ tensile transmission electron microscopy (TEM). The in situ TEM results confirmed the particle shearing mechanism leads to planar dislocation gliding. During deformation of the 100 h-aged alloy, some gliding dislocations were strongly pinned by the large κ-carbide blocks and were prone to cross-slip, leading to the activation of multiple slip systems. The abrupt decline in the dislocation mean free path was attributed to the activation of multiple slip systems, resulting in the rapid saturation of the strain hardening recovery. It is concluded that the planar dislocation glide and sequential activation of slip systems are key to induce strain hardening recovery in polycrystalline metals. Thus, if a microstructure is designed such that dislocations glide in a planar manner, the strain hardening recovery could be utilized to obtain enhanced mechanical properties of the material.

Z-type hexagonal ferrites have recently received attention for their room-temperature magnetoelectric (ME), which is activated when the temperature at which the transverse-conical spin-state transitions to a ferrimagnetic state is increased. The changes in the magnetic domain structure at the transition have been well-documented; however, they are still not understood in detail. In the present study, Lorentz transmission electron microscopy (TEM) analysis combined with an in situ heating experiment was conducted to demonstrate the shift in magnetic domain structure during the transition from the transverse-conical spin arrangement to a ferrimagnetic spin order. The dynamics of the magnetic domain structure changes with the increasing temperature were acquired in real-time. At 490 K, the magnetization transition from the transverse-conical spin state to the ferromagnetic state was demonstrated. Cross-tie domain walls formed during the magnetic transition process. The increased effect of the demagnetizing field applied to the 180° magnetic domains was caused by a lower magnetocrystalline anisotropy (MCA) at the easy axis of magnetization.

Large-area graphene films are best synthesized via chemical vapour and/or solid deposition methods at elevated temperatures (~1,000 °C) on polycrystalline metal surfaces and later transferred onto other substrates for device applications. Here we report a new method for the synthesis of graphene films directly on SiO 2 /Si substrates, even plastics and glass at close to room temperature (25–160 °C). In contrast to other approaches, where graphene is deposited on top of a metal substrate, our method invokes diffusion of carbon through a diffusion couple made up of carbon-nickel/substrate to form graphene underneath the nickel film at the nickel–substrate interface. The resulting graphene layers exhibit tunable structural and optoelectronic properties by nickel grain boundary engineering and show micrometre-sized grains on SiO 2 surfaces and nanometre-sized grains on plastic and glass surfaces. The ability to synthesize graphene directly on non-conducting substrates at low temperatures opens up new possibilities for the fabrication of multiple nanoelectronic devices. Current methods for fabricating graphene rely on its transfer from metal surfaces to substrates suitable for device applications. This study demonstrates a transfer-free approach for growing graphene on substrates such as thermally oxidized silicon and plastic that forms the material underneath a nickel film, at the nickel–substrate interface.

Abstract Pseudomonas fluorescens group, such as Pseudomonas protegens and Pseudomonas chlororaphis, can be utilized as insect-killing agents. Most insecticidal Pseudomonas described so far have high toxicity for insects of the order Lepidoptera. In this study, Pseudomonas strain PcR3-3 was isolated from the willow root. It showed a high mortality for the coleopteran species Plagiodera versicolora (Coleoptera: Chrysomelidae), but not for the lepidopteran Helicoverpa armigera. Strain PcR3-3 displayed high colonization ability in the P. versicolora compared with P. chlororaphis PCL1391, indicating that the insecticidal activities correlated with the colonization ability of Pseudomonas strain in the host. Phylogenetic analysis of the genome revealed that PcR3-3 belonged to P. chlororaphis subsp. aureofaciens. Numerous insecticidal protein-encoding genes, typical biosynthetic gene clusters for some insecticidal metabolite and type VI secretion system, known to be involved in insect pathogenicity, were present in the P. chlororaphis PcR3-3 genome. However, the insecticidal toxin Fit-encoding gene which commonly presents in P. chlororaphis, was not found in the P. chlororaphis PcR3-3 genome. Furthermore, there are some divergent insecticidal genes between P. chlororaphis PcR3-3 and P. chlororaphis PCL1391. This finding implies that P. chlororaphis PcR3-3 is a promising biocontrol agent for pest management applications. The P. chlororaphis–P. versicolora association can be used as a model system to study the interaction between Pseudomonas and coleopteran insects.

To elucidate the complex interplay of undifferentiated cancer cells in malignancy, we focus on the crucial mechanisms that maintain the undifferentiated state of cancer stem-like cells, which drive tumor growth and therapy resistance. Here, we identify a protein called dehydrogenase/reductase 13 (DHRS13) that is abundant in undifferentiated glioblastoma cells. DHRS13 is primarily located in the mitochondria and functions as a retinaldehyde reductase, converting all- trans -retinaldehyde to all- trans -retinol with high affinity for NADPH. Mechanistically, DHRS13 prevents glioma stem-like cells from differentiating by blocking retinoic acid signaling, thereby maintaining their undifferentiated state. Remarkably, the depletion of DHRS13 results in mitochondrial reactive oxygen species-driven mitophagy and cell death. Consequently, loss of DHRS13 leads to a significant decrease in tumor initiation and progression. These findings hold promise for the development of strategies that target undifferentiated cancer cells, potentially leading to improved treatment outcomes. Cancer stem-like cells contribute to tumor growth and therapy resistance in glioblastoma. Here, authors identify that DHRS13 inhibition promotes differentiation of glioma stem-like cells by activating retinoic acid signaling and induces cell death through mitochondrial reactive oxygen species-driven mitophagy.