A novel miRNA negatively regulates resistance to Glomerella leaf spot by suppressing expression of an NBS gene in apple

Glomerella leaf spot(GLS)of apple(Malus×domestica Borkh.),caused by Glomerella cingulata,is an emerging fungal epidemic threatening the apple industry.Little is known about the molecular mechanism underlying resistance to this devastating fungus.In this study,high-throughput sequencing technology was used to identify microRNAs(miRNAs)involved in GLS resistance in apple.We focused on miRNAs that target genes related to disease and found that expression of a novel miRNA,Md-miRln20,was higher in susceptible apple varieties than in resistant ones.Furthermore,its target gene Md-TN1-GLS exhibited the opposite expression pattern,which suggested that the expression levels of Md-miRln20 and its target gene are closely related to apple resistance to GLS.Furthermore,downregulation of MdmiRln20 in susceptible apple leaves resulted in upregulation of Md-TN1-GLS and reduced the disease incidence.Conversely,overexpression of Md-miRln20 in resistant apple leaves suppressed Md-TN1-GLS expression,with increased disease incidence.We demonstrated that Md-miRln20 negatively regulates resistance to GLS by suppressing Md-TN1-GLS expression and showed,for the first time,a crucial role for miRNA in response to GLS in apple.

Two pathogenesis-related proteins interact with leucine-rich repeat proteins to promote Alternaria leaf spot resistance in apple

Alternaria leaf spot in apple(Malus x domestica),caused by the fungal pathogen Alternaria alternata f.sp.mali(also called A.mali),is a devastating disease resulting in substantial economic losses.We previously established that the resistance(R)protein MdRNL2,containing a coiled-coil,nucleotide-binding,and leucine-rich repeat(CC R-NB-LRR)domain,interacts with another CC R-NB-LRR protein,MdRNL6,to form a MdRNL2–MdRNL6 complex that confers resistance to A.mali.Here,to investigate the function of the MdRNL2–MdRNL6 complex,we identified two novel pathogenesis-related(PR)proteins,MdPR10-1 and MdPR10-2,that interact with MdRNL2.Yeast two-hybrid(Y2H)assays and bimolecular fluorescence complementation(BiFC)assays confirmed that MdPR10-1 and MdPR10-2 interact with MdRNL2 and MdRNL6 at the leucine-rich repeat domain.Transient expression assays demonstrated that accumulation of MdPR10-1 and MdPR10-2 enhanced the resistance of apple to four strains of A.mali that we tested:ALT1,GBYB2,BXSB5,and BXSB7.In vitro antifungal activity assays demonstrated that both the proteins contribute to Alternaria leaf spot resistance by inhibiting fungal growth.Our data provide evidence for a novel regulatory mechanism in which MdRNL2 and MdRNL6 interact with MdPR10-1 and MdPR10-2 to inhibit fungal growth,thereby contributing to Alternaria leaf spot resistance in apple.The identification of these two novel PR proteins will facilitate breeding for fungal disease resistance in apple.

Damage Curves Derived from Hurricane Ike in the West of Galveston Bay Based on Insurance Claims and Hydrodynamic Simulations

Hurricane Ike,which struck the United States in September 2008,was the ninth most expensive hurricane in terms of damages.It caused nearly USD 30 billion in damage after making landfall on the Bolivar Peninsula,Texas.We used the Delft3dFM/SWAN hydrodynamic and spectral wave model to simulate the storm surge inundation around Galveston Bay during Hurricane Ike.Damage curves were established through the relationship between eight hydrodynamic parameters(water depth,flow velocity,unit discharge,flow momentum flux,significant wave height,wave energy flux,total water depth(flow depth plus wave height),and total(flow plus wave)force)simulated by the model and National Flood Insurance Program(NFIP)insurance damage data.The NFIP insurance database contains a large amount of building damage data,building stories,and elevation,as well as other information from the Ike event.We found that the damage curves are sensitive to the model grid resolution,building elevation,and the number of stories.We also found that the resulting damage functions are steeper than those developed for residential structures in many other locations.

Organoboron chemistry towards controlled and precise polymer synthesis

Organoboron reagents have garnered considerable attention due to their distinct properties. In recent years, boronic acids and boronate esters have been important intermediates for cross-coupling reactions and other functional group construction and are often used to synthesize small organic molecules, drugs, and bioactive substances. In this feature article, we encapsulate the strategy of harnessing the unique properties of organoboron reagents to overcome challenges encountered in conventional polymer synthesis. We delve into the synthesis of boron-containing monomers and polymer materials, unraveling the unique attributes of these newfound polymers while offering innovative insights into their application within recyclable or reprocessable materials. We develop organoboron-based photocatalysts, employing their inner-sphere electron transfer(ISET) mechanisms to initiate controlled radical polymerization. We utilize alkylborane to initiate controlled radical polymerization and further designed B-alkylcatecholboranes to prepare ultra-high molecular weight polymers. Notably, we also propose a liquid-phase synthesis method based on organoboron tags and apply it to the precise synthesis of sequence-controlled conjugated polymers.These advancements open up new frontiers in the realm of polymer science, and the versatility and potential of organoboron reagents in polymer synthesis continue to inspire exciting research endeavors.

Pharmacological Activation of RXR-a Promotes Hematoma Absorption via a PPAR-y-dependent Pathway After Intracerebral Hemorrhage

Endogenously eliminating the hematoma is a favorable strategy in addressing intracerebral hemorrhage(ICH).This study sought to determine the role of retinoid X receptor-ot(RXR-a)in the context of hematoma absorption after ICH.Our results showed that pharmacologically activating RXR-a with bexarotene significantly accelerated hematoma clearance and alleviated neurological dysfunction after ICH.RXR-ot was expressed in microglia/macro-phages,neurons,and astrocytes.Mechanistically,bexarotene promoted the nuclear translocation of RXR-a and PPAR-y,as well as reducing neuroinflammation by modulating microglia/macrophage reprograming from the Ml into the M2 phenotype.Furthermore,all the beneficial effects of RXR-a in ICH were reversed by the PPAR-y inhibitor GW9662.In conclusion,the pharmacological activation of RXR-a confers robust neuroprotection against ICH by accelerating hematoma clearance and repolarizing microglia/macrophages towards the M2 phenotype through PPAR-y-related mechanisms.Our data support the notion that RXR-ot might be a promising therapeutic target for ICH.