Explore the vast range of titles available.

The cold surges have frequently attacked North America (NA) in recent decades, which has been tied to the diminished sea‐ice over the Bering Sea. However, we find that the contribution of sea‐ice loss to NA winter coldness is state‐dependent on the Pacific Decadal Oscillation (PDO) phase. Using observations and CAM6 model simulations, we find that the phase regulates the atmospheric response to Bering ice loss. During the negative PDO phase (PDO−), there is an apparent eastward‐propagating wave train, accompanied by a strengthened Alaskan ridge and NA cold high, resulting in a robust cold over Central NA. Meanwhile, enhanced upward‐propagating planetary waves weaken the stratospheric polar vortex over the Pacific‐NA regions. During the positive phase (PDO+), the NA temperature response to Bering ice loss is quite weak or even warm. We speculate that more NA cold extremes will appear as the PDO− continues and less as the PDO− shifts to PDO+. Plain Language Summary Rapid Arctic warming has led to significant local changes in the Arctic and more uncertain remote changes in the Northern Hemisphere mid‐latitudes. However, the link between the Arctic and mid‐latitude North America is state‐dependent. Here, we show that the atmospheric responses to Bering sea ice (SIC) are significantly regulated by the Pacific Decadal Oscillation (PDO) phase. A significant Central North American cooling associated with Bering SIC loss during PDO− is due to the North American anticyclone and a weakened stratospheric polar vortex. While during PDO+, the North American temperature anomalies associated with reduced sea ice are weak and even warm. The contrasting impacts of Bering SIC loss between distinct PDO phases are because the circulation response to PDO− further strengthens the atmospheric response to the reduced Bering SIC. These new findings can help us improve the prediction of the North American cold extremes during distinct PDO phases. Key Points Central North American cooling in response to Bering Sea ice loss is greater during the negative Pacific Decadal Oscillation phase The Pacific Decadal Oscillation phase can modulate the impact of Bering Sea ice loss on North American temperature The response to Bering Sea ice loss is associated with a strengthened Alaskan ridge during the negative Pacific Decadal Oscillation

The rice NAC transcriptional factor family harbors 151 members, and some of them play important roles in rice immunity. Here, we report the function and molecular mechanism of a pathogen-inducible NAC transcription factor, ONAC096, in rice immunity against Magnaprothe oryzae and Xanthomonas oryzae pv. oryzae . Expression of ONAC096 was induced by M. oryzae and by abscisic acid and methyl jasmonate. ONAC096 had the DNA binding ability to NAC recognition sequence and was found to be a nucleus-localized transcriptional activator whose activity depended on its C-terminal. CRISPR/Cas9-mediated knockout of ONAC096 attenuated rice immunity against M. oryzae and X. oryzae pv. oryzae as well as suppressed chitin- and flg22-induced reactive oxygen species burst and expression of PTI marker genes OsWRKY45 and OsPAL4 ; by contrast, overexpression of ONAC096 enhanced rice immunity against these two pathogens and strengthened chitin- or flg22-induced PTI. RNA-seq transcriptomic profiling and qRT-PCR analysis identified a small set of defense and signaling genes that are putatively regulated by ONAC096, and further biochemical analysis validated that ONAC096 could directly bind to the promoters of OsRap2.6 , OsWRKY62 , and OsPAL1 , three known defense and signaling genes that regulate rice immunity. ONAC096 interacts with ONAC066, which is a positive regulator of rice immunity. These results demonstrate that ONAC096 positively contributes to rice immunity against M. oryzae and X. oryzae pv. oryzae through direct binding to the promoters of downstream target genes including OsRap2.6 , OsWRKY62 , and OsPAL1 .

Summary Tomato stress‐associated proteins (SAPs) belong to A20/AN1 zinc finger protein family, some of which have been shown to play important roles in plant stress responses. However, little is known about the functions and underlying molecular mechanisms of SAPs in plant immune responses. In the present study, we reported the function of tomato SlSAP3 in immunity to Pseudomonas syringae pv. tomato (Pst) DC3000. Silencing of SlSAP3 attenuated while overexpression of SlSAP3 in transgenic tomato increased immunity to Pst DC3000, accompanied with reduced and increased Pst DC3000‐induced expression of SA signalling and defence genes, respectively. Flg22‐induced reactive oxygen species (ROS) burst and expression of PAMP‐triggered immunity (PTI) marker genes SlPTI5 and SlLRR22 were strengthened in SlSAP3‐OE plants but were weakened in SlSAP3‐silenced plants. SlSAP3 interacted with two SlBOBs and the A20 domain in SlSAP3 is critical for the SlSAP3‐SlBOB1 interaction. Silencing of SlBOB1 and co‐silencing of all three SlBOB genes conferred increased resistance to Pst DC3000, accompanied with increased Pst DC3000‐induced expression of SA signalling and defence genes. These data demonstrate that SlSAP3 acts as a positive regulator of immunity against Pst DC3000 in tomato through the SA signalling and that SlSAP3 may exert its function in immunity by interacting with other proteins such as SlBOBs, which act as negative regulators of immunity against Pst DC3000 in tomato.

Fumarase plays a pivotal role in the tricarboxylic acid cycle, but its functions in plant pathogenic fungi are not well understood. We identified two fumarase genes in Fusarium proliferatum and generated individual deletion mutants. Loss of FpFumB led to defects in growth, sporulation, stress tolerance, and virulence. Exogenous malate supplementation restored growth defects. Site-directed mutagenesis of residues G452 and A463 reduced FpFumB enzyme activity. Transcriptomic analysis identified significant changes in gene expression related to different metabolic pathways. Protein interaction assays showed that FpFumB interacts with the DNA repair protein FpSae2. Both ΔFpFumB and ΔFpSae2 mutants displayed altered sensitivity to DNA-damaging agents and reduced virulence, indicating that FpFumB modulates DNA repair and pathogenicity through its interaction with FpSae2. Together, these findings highlight FpFumB as a key regulator of basic biological processes, DNA damage repair, and virulence in Fusarium proliferatum.

Cepharanthine (CEP) is a natural bisbenzylisoquinoline alkaloid known for its antibacterial, antiviral, and anti-inflammatory activities. Its antifungal effect, however, has not been well studied. In this work, we used machine learning-based virtual screening with Random Forest, Neural Network, and Support Vector Machine models to identify potential inhibitors of Fusarium solani. CEP was selected as a candidate and tested experimentally. The results showed that it inhibited the growth of Fusarium solani, Fusarium proliferatum, Fusarium oxysporum, Alternaria alternata, and Botrytis cinerea. It also reduced the sporulation and spore germination of Fusarium solani and disrupted its redox balance. Transcriptome analysis showed changes in gene expression related to basic metabolic pathways. Molecular docking suggested that CEP binds to the FsCFEM1 protein, and molecular dynamics simulations confirmed stable binding, with key roles for residues THR748 and LEU950. These results suggest that CEP is a potential bio-based antifungal agent and provide novel insights into its mechanism against Fusarium solani.

Fusarium oxysporum is a devastating plant-pathogenic fungus that causes vascular wilt disease in many economically important crops, including watermelon, worldwide. F. oxysporum f. sp. nievum ( Fon ) causes serious yield loss in watermelon production. However, the molecular mechanism of Fusarium wilt development by Fon remains largely unknown. Fusarium oxysporum f. sp. niveum ( Fon ), a soilborne phytopathogenic fungus, causes watermelon Fusarium wilt, resulting in serious yield losses worldwide. However, the underlying molecular mechanism of Fon virulence is largely unknown. The present study investigated the biological functions of six FonPUFs , encoding RNA binding Pumilio proteins, and especially explored the molecular mechanism of FonPUF1 in Fon virulence. A series of phenotypic analyses indicated that FonPUFs have distinct but diverse functions in vegetative growth, asexual reproduction, macroconidia morphology, spore germination, cell wall, or abiotic stress response of Fon . Notably, the deletion of FonPUF1 attenuates Fon virulence by impairing the invasive growth and colonization ability inside the watermelon plants. FonPUF1 possesses RNA binding activity, and its biochemical activity and virulence function depend on the RNA recognition motif or Pumilio domains. FonPUF1 associates with the actin-related protein 2/3 (ARP2/3) complex by interacting with FonARC18, which is also required for Fon virulence and plays an important role in regulating mitochondrial functions, such as ATP generation and reactive oxygen species production. Transcriptomic profiling of ΔFonPUF1 identified a set of putative FonPUF1-dependent virulence-related genes in Fon , possessing a novel A-rich binding motif in the 3′ untranslated region (UTR), indicating that FonPUF1 participates in additional mechanisms critical for Fon virulence. These findings highlight the functions and molecular mechanism of FonPUFs in Fon virulence. IMPORTANCE Fusarium oxysporum is a devastating plant-pathogenic fungus that causes vascular wilt disease in many economically important crops, including watermelon, worldwide. F. oxysporum f. sp. nievum ( Fon ) causes serious yield loss in watermelon production. However, the molecular mechanism of Fusarium wilt development by Fon remains largely unknown. Here, we demonstrate that six putative Pumilio proteins-encoding genes ( FonPUFs ) differentially operate diverse basic biological processes, including stress response, and that FonPUF1 is required for Fon virulence. Notably, FonPUF1 possesses RNA binding activity and associates with the actin-related protein 2/3 complex to control mitochondrial functions. Furthermore, FonPUF1 coordinates the expression of a set of putative virulence-related genes in Fon by binding to a novel A-rich motif present in the 3′ UTR of a diverse set of target mRNAs. Our study disentangles the previously unexplored molecular mechanism involved in regulating Fon virulence, providing a possibility for the development of novel strategies for disease management.

NAC transcriptional factors constitute a large family in rice and some of them have been demonstrated to play crucial roles in rice immunity. The present study investigated the function and mechanism of ONAC066 in rice immunity. ONAC066 shows transcription activator activity that depends on its C-terminal region in rice cells. ONAC066 -OE plants exhibited enhanced resistance while ONAC066 -Ri and onac066-1 plants showed attenuated resistance to Magnaporthe oryzae . A total of 81 genes were found to be up-regulated in ONAC066 -OE plants, and 26 of them were predicted to be induced by M. oryzae . Four OsWRKY genes, including OsWRKY45 and OsWRKY62 , were up-regulated in ONAC066 -OE plants but down-regulated in ONAC066 -Ri plants. ONAC066 bound to NAC core-binding site in OsWRKY62 promoter and activated OsWRKY62 expression, indicating that OsWRKY62 is a ONAC066 target. A set of cytochrome P450 genes were found to be co-expressed with ONAC066 and 5 of them were up-regulated in ONAC066 -OE plants but down-regulated in ONAC066 -Ri plants. ONAC066 bound to promoters of cytochrome P450 genes LOC_Os02g30110 , LOC_Os06g37300 , and LOC_Os02g36150 and activated their transcription, indicating that these three cytochrome P450 genes are ONAC066 targets. These results suggest that ONAC066, as a transcription activator, positively contributes to rice immunity through modulating the expression of OsWRKY62 and a set of cytochrome P450 genes to activate defense response.

O-GlcNAcylation, an important post-translational modification catalyzed by O-GlcNAc transferase (OGT), plays critical roles in several biological processes. In this study, we present our findings on the function of FpOGT in regulating physiological processes and pathogenicity of Fusarium proliferatum ( Fp ), the alfalfa root rot fungus. The deletion of FpOGT impaired mycelial growth and altered macroconidia morphology in Fp . Furthermore, Δ FpOGT mutant displayed altered tolerance to various stressors, including cell wall perturbing agents, osmotic stressors, metal ionic stressors, and fungicides. Deletion of FpOGT significantly decreased Fp virulence toward alfalfa. The transcriptome analysis demonstrated that FpOGT plays a regulatory role in glucose metabolic pathways, including glycolysis, tricarboxylic acid (TCA) cycle, and hexosamine biosynthesis pathway (HBP), by influencing the expression of relevant genes. The downregulation of the glucokinase gene, FpGCK , was observed in Δ FpOGT , and the disruption of FpGCK led to a decrease in Fp virulence. Additionally, FpOGT affected the expression levels of the FpGCK -AS1 isoform, thereby impacting glucokinase function. The molecular docking analysis elucidated the plausible physical interaction between FpOGT and FpGCK, thereby offering valuable insights into their interrelationship. These findings underscore the indispensable involvement of FpOGT, the sole O-GlcNAc transferase in Fp , in various biological processes and the pathogenicity through its regulation of fundamental metabolic processes. Consequently, this study emphasizes the significance and elucidates the molecular mechanism underlying the role of O-GlcNAc transferase in diverse fundamental biological processes and the pathogenicity of phytopathogenic fungi.

SUMOylation is an essential protein modification process that regulates numerous crucial cellular and biochemical processes in phytopathogenic fungi, and thus plays important roles in multiple biological functions. The present study characterizes the SUMOylation pathway components, including SMT3 (SUMO), AOS1 (an E1 enzyme), UBC9 (an E2 enzyme), and MMS21 (an E3 ligase), in Fusarium oxysporum f. sp. niveum (Fon), the causative agent of watermelon Fusarium wilt, in terms of the phylogenetic relationship, gene/protein structures, and basic biological functions. The SUMOylation components FonSMT3, FonAOS1, FonUBC9, and FonMMS21 are predominantly located in the nucleus. FonSMT3, FonAOS1, FonUBC9, and FonMMS21 are highly expressed in the germinating macroconidia, but their expression is downregulated gradually in infected watermelon roots with the disease progression. The disruption of FonUBA2 and FonSIZ1 seems to be lethal in Fon. The deletion mutant strains for FonSMT3, FonAOS1, FonUBC9, and FonMMS21 are viable, but exhibit significant defects in vegetative growth, asexual reproduction, conidial morphology, spore germination, responses to metal ions and DNA-damaging agents, and apoptosis. The disruption of FonSMT3, FonAOS1, FonUBC9, and FonMMS21 enhances sensitivity to cell wall-perturbing agents, but confers tolerance to digestion by cell wall-degrading enzymes. Furthermore, the disruption of FonSMT3, FonAOS1, and FonUBC9 negatively regulates autophagy in Fon. Overall, these results demonstrate that the SUMOylation pathway plays vital roles in regulating multiple basic biological processes in Fon, and, thus, can serve as a potential target for developing a disease management approach to control Fusarium wilt in watermelon.

Bronchoalveolar lavage fluid (BALF) exosomes possess different properties in different diseases, which are mediated through microRNAs (miRNAs) and long noncoding RNAs (lncRNAs), among others. By sequencing the differentially expressed lncRNAs in BALF exosomes, we seek potential targets for the diagnosis and treatment of acute lung injury (ALI). Considering that human and rat genes are about 80% similar, ALI was induced using lipopolysaccharide in six male Wistar rats, with six rats as control (all weighing 200 ± 20 g and aged 6-8 weeks). BALF exosomes were obtained 24 h after ALI. The exosomes in BALF were extracted by ultracentrifugation. The differential expression of BALF exosomal lncRNAs in BALF was analyzed by RNA sequencing. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed to predict the functions of differentially expressed lncRNAs, which were confirmed by reverse transcription-polymerase chain reaction. Compared with the control group, the ALI group displayed a higher wet/dry ratio, tumor necrosis factor-α levels, and interleukin-6 levels (all < 0.001). The airway injection of exosomes in rats led to significant infiltration by neutrophils. A total of 2,958 differentially expressed exosomal lncRNAs were identified, including 2,524 upregulated and 434 downregulated ones. Five lncRNAs confirmed the reliability of the sequencing data. The top three GO functions were phagocytic vesicle membrane, regulation of receptor biosynthesis process, and I-SMAD binding. Salmonella infection, Toll-like receptor signaling pathway, and osteoclast differentiation were the most enriched KEGG pathways. The lncRNA-miRNA interaction network of the five confirmed lncRNAs could be predicted using miRDB. BALF-derived exosomes play an important role in ALI development and help identify potential therapeutic targets related to ALI.