Rice false smut virulence protein subverts host chitin perception and signaling at lemma and palea for floral infection.

The flower-infecting fungus Ustilaginoidea virens causes rice false smut, which is a severe emerging disease threatening rice (Oryza sativa) production worldwide. False smut not only reduces yield, but more importantly produces toxins on grains, posing a great threat to food safety. U. virens invades spikelets via the gap between the 2 bracts (lemma and palea) enclosing the floret and specifically infects the stamen and pistil. Molecular mechanisms for the U. virens-rice interaction are largely unknown. Here, we demonstrate that rice flowers predominantly employ chitin-triggered immunity against U. virens in the lemma and palea, rather than in the stamen and pistil. We identify a crucial U. virens virulence factor, named UvGH18.1, which carries glycoside hydrolase activity. Mechanistically, UvGH18.1 functions by binding to and hydrolyzing immune elicitor chitin and interacting with the chitin receptor CHITIN ELICITOR BINDING PROTEIN (OsCEBiP) and co-receptor CHITIN ELICITOR RECEPTOR KINASE1 (OsCERK1) to impair their chitin-induced dimerization, suppressing host immunity exerted at the lemma and palea for gaining access to the stamen and pistil. Conversely, pretreatment on spikelets with chitin induces a defense response in the lemma and palea, promoting resistance against U. virens. Collectively, our data uncover a mechanism for a U. virens virulence factor and the critical location of the host-pathogen interaction in flowers and provide a potential strategy to control rice false smut disease.

Structured Catalysts and Catalytic Processes: Transport and Reaction Perspectives.

The structure of catalysts determines the performance of catalytic processes. Intrinsically, the electronic and geometric structures influence the interaction between active species and the surface of the catalyst, which subsequently regulates the adsorption, reaction, and desorption behaviors. In recent decades, the development of catalysts with complex structures, including bulk, interfacial, encapsulated, and atomically dispersed structures, can potentially affect the electronic and geometric structures of catalysts and lead to further control of the transport and reaction of molecules. This review describes comprehensive understandings on the influence of electronic and geometric properties and complex catalyst structures on the performance of relevant heterogeneous catalytic processes, especially for the transport and reaction over structured catalysts for the conversions of light alkanes and small molecules. The recent research progress of the electronic and geometric properties over the active sites, specifically for theoretical descriptors developed in the recent decades, is discussed at the atomic level. The designs and properties of catalysts with specific structures are summarized. The transport phenomena and reactions over structured catalysts for the conversions of light alkanes and small molecules are analyzed. At the end of this review, we present our perspectives on the challenges for the further development of structured catalysts and heterogeneous catalytic processes.

Highly selective NH3 synthesis from N2 on electron-rich Bi0 in a pressurized electrolyzer.

Electrochemical conversion of N2 into ammonia presents a sustainable pathway to produce hydrogen storage carrier but yet requires further advancement in electrocatalyst design and electrolyzer integration. This technology suffers from low selectivity and yield owing to the extremely strong N≡N bond and the exceptionally low solubility of N2 in aqueous systems. A high NH3 synthesis performance is restricted by the high activation energy of N≡N bond and the supply insufficiency of N2 to active sites. This paper describes the introduction of electron-rich Bi0 sites into Ag catalysts with a high-pressure electrolyzer that enables a dramatically enhanced Faradaic efficiency of 44.0% and yield of 28.43 µg cm-2 h-1 at 4.0 MPa. Combined with density functional theory results, in situ attenuated total reflectance surface-enhanced infrared absorption spectroscopy demonstrates that N2 reduction reaction follows an associative mechanism, in which a high coverage of N-N bond and -NH2 intermediates suggest electron-rich Bi0 boosts sound activation of N2 molecules and low hydrogenation barrier. The proposed strategy of engineering electrochemical catalysts and devices provides powerful guidelines for achieving industrial-level green ammonia production.

Tutorial on survival modeling with applications to omics data.

MOTIVATION: Identification of genomic, molecular and clinical markers prognostic of patient survival is important for developing personalized disease prevention, diagnostic and treatment approaches. Modern omics technologies have made it possible to investigate the prognostic impact of markers at multiple molecular levels, including genomics, epigenomics, transcriptomics, proteomics and metabolomics, and how these potential risk factors complement clinical characterization of patient outcomes for survival prognosis. However, the massive sizes of the omics datasets, along with their correlation structures, pose challenges for studying relationships between the molecular information and patients' survival outcomes. RESULTS: We present a general workflow for survival analysis that is applicable to high-dimensional omics data as inputs when identifying survival-associated features and validating survival models. In particular, we focus on the commonly used Cox-type penalized regressions and hierarchical Bayesian models for feature selection in survival analysis, which are especially useful for high-dimensional data, but the framework is applicable more generally. AVAILABILITY AND IMPLEMENTATION: A step-by-step R tutorial using The Cancer Genome Atlas survival and omics data for the execution and evaluation of survival models has been made available at https://ocbe-uio.github.io/survomics.

TNFAIP3 Derived from Skeletal Stem Cells Alleviated Rat Osteoarthritis by Inhibiting the Necroptosis of Subchondral Osteoblasts.

Recent investigations have shown that the necroptosis of tissue cells in joints is important in the development of osteoarthritis (OA). This study aimed to investigate the potential effects of exogenous skeletal stem cells (SSCs) on the necroptosis of subchondral osteoblasts in OA. Human SSCs and subchondral osteoblasts isolated from human tibia plateaus were used for Western blotting, real-time PCR, RNA sequencing, gene editing, and necroptosis detection assays. In addition, the rat anterior cruciate ligament transection OA model was used to evaluate the effects of SSCs on osteoblast necroptosis in vivo. The micro-CT and pathological data showed that intra-articular injections of SSCs significantly improved the microarchitecture of subchondral trabecular bones in OA rats. Additionally, SSCs inhibited the necroptosis of subchondral osteoblasts in OA rats and necroptotic cell models. The results of bulk RNA sequencing of SSCs stimulated or not by tumor necrosis factor α suggested a correlation of SSCs-derived tumor necrosis factor α-induced protein 3 (TNFAIP3) and cell necroptosis. Furthermore, TNFAIP3-derived from SSCs contributed to the inhibition of the subchondral osteoblast necroptosis in vivo and in vitro. Moreover, the intra-articular injections of TNFAIP3-overexpressing SSCs further improved the subchondral trabecular bone remodeling of OA rats. Thus, we report that TNFAIP3 from SSCs contributed to the suppression of the subchondral osteoblast necroptosis, which suggests that necroptotic subchondral osteoblasts in joints may be possible targets to treat OA by stem cell therapy.

Interior Exciton Extraction by Spatial-Controlled Iodine Doping in BiOBr Photocatalysts.

Extracting interior photoinduced species to the surface before their recombination is of great importance in pursuing high-efficiency semiconductor-based photocatalysis. Traditional strategies toward charge-carrier extraction, mostly relying on the construction of an electric field gradient, would be invalid toward the neutral-exciton counterpart in low-dimensional systems. In this work, by taking bismuth oxybromide (BiOBr) as an example, we manipulate interior exciton extraction to the surface by implementing iodine doping at the edges of BiOBr plates. Spatial- and time-resolved spectroscopic analyses verified the accumulation of excitons and charge carriers at the edges of iodine-doped BiOBr (BiOBr-I) plates. This phenomenon could be associated with interior exciton extraction, driven by an energy-level gradient between interior and edge exciton states, and the following exciton dissociation processes. As such, BiOBr-I shows remarkable performance in photocatalytic C-H fluorination, mediated by both energy- and charge-transfer processes. This work uncovers the importance of spatial regulation of excitonic properties in low-dimensional semiconductor-based photocatalysis.

Atomic Defects Engineering Boosts Urea Synthesis toward Carbon Dioxide and Nitrate Coelectroreduction.

The atomic defect engineering could feasibly decorate the chemical behaviors of reaction intermediates to regulate catalytic performance. Herein, we created oxygen vacancies on the surface of In(OH)3 nanobelts for efficient urea electrosynthesis. When the oxygen vacancies were constructed on the surface of the In(OH)3 nanobelts, the faradaic efficiency for urea reached 80.1%, which is 2.9 times higher than that (20.7%) of the pristine In(OH)3 nanobelts. At -0.8 V versus reversible hydrogen electrode, In(OH)3 nanobelts with abundant oxygen vacancies exhibited partial current density for urea of -18.8 mA cm-2. Such a value represents the highest activity for urea electrosynthesis among recent reports. Density functional theory calculations suggested that the unsaturated In sites adjacent to oxygen defects helped to optimize the adsorbed configurations of key intermediates, promoting both the C-N coupling and the activation of the adsorbed CO2NH2 intermediate. In-situ spectroscopy measurements further validated the promotional effect of the oxygen vacancies on urea electrosynthesis.

Dimensional and Doping Engineering of Chiral Perovskites with Enhanced Spin Selectivity for Green Emissive Spin Light-Emitting Diodes.

Chiral perovskites play a pivotal role in spintronics and optoelectronic systems attributed to their chiral-induced spin selectivity (CISS) effect. Specifically, they allow for spin-polarized charge transport in spin light-emitting diodes (LEDs), yielding circularly polarized electroluminescence at room temperature without external magnetic fields. However, chiral lead bromide-based perovskites have yet to achieve high-performance green emissive spin-LEDs, owing to limited CISS effects and charge transport. Herein, we employ dimensional regulation and Sn2+-doping to optimize chiral bromide-based perovskite architecture for green emissive spin-LEDs. The optimized (PEA)x(S/R-PRDA)2-xSn0.1Pb0.9Br4 chiral perovskite film exhibits an enhanced CISS effect, higher hole mobility, and better energy level alignment with the emissive layer. These improvements allow us to fabricate green emissive spin-LEDs with an external quantum efficiency (EQE) of 5.7% and an asymmetry factor |gCP-EL| of 1.1 × 10-3. This work highlights the importance of tailored perovskite architectures and doping strategies in advancing spintronics for optoelectronic applications.

Nickel-Catalyzed Asymmetric (3 + 2) Annulations of Propargylic Carbonates and Vinylogous Donors via an Alkenylation Pathway.

The transition-metal-catalyzed alkenylation strategy of propargylic alcohol derivatives provides an efficient protocol to access multifunctional products in a double-nucleophilic attack pattern. While limited relevant asymmetric examples have been reported via palladium catalysis, here we first demonstrate that a nonprecious Ni(0)-based chiral complex can efficiently promote the tandem substitution process between propargylic carbonates and N-trifluoroethyl ketimines via consecutive aza-vinylogous activations, finally accomplishing a (3 + 2) annulation reaction to afford products embedding a 4-methylene-3,4-dihydro-2H-pyrrole framework with high regio-, diastereo-, and enantiocontrol. Their assemblies with a few all-carbon-based vinylogous precursors are also successful, and enantioenriched adducts containing a 3-methylenecyclopentene scaffold are furnished effectively. The substitution patterns for both types of substrates are substantial, and an array of synthetic elaborations is conducted to deliver more versatile architectures with high application potential. In addition, density functional theory calculations and control experiments have been conducted to rationalize the catalytic pathways and regio- and enantioselectivity control.

Photocatalytic Acetylene Hydrochlorination by Pairing Proton Reduction and Chlorine Oxidation over g-C3N4/BiOCl Catalysts.

Acetylene hydrochlorination is a vital industrial process for the manufacture of vinyl chloride monomer (VCM). Current thermocatalytic acetylene hydrochlorination requires toxic mercury-based or costly noble metal-based catalysts, high temperatures (≥180 °C) and excessive gaseous HCl. Here, we report a room-temperature photocatalytic acetylene hydrochlorination strategy involving concurrent coupling of electron-driven proton reduction (*H) and hole-driven chloride oxidation (*Cl) on photocatalyst surfaces. Under simulated solar light illumination, the developed noble-metal-free g-C3N4/BiOCl photocatalysts show a considerably high VCM production rate of 1198.6 µmol g-1 h-1 and a high VCM selectivity of 95% in a 0.1 M HCl aqueous solution. Even in chloride-rich natural seawater and acidified natural seawater, the VCM production rates of g-C3N4/BiOCl photocatalysts are up to 170.3 µmol g-1 h-1 with a VCM selectivity of 80.4% and 1247.7 µmol g-1 h-1 with a VCM selectivity of 94.7%, respectively. Moreover, with sunlight irradiation and acidified natural seawater, the g-C3N4/BiOCl photocatalysts in a large-scale photosystem retain outstanding acetylene hydrochlorination performance over 10 days of operation. The radical scavenging, in situ photochemical Fourier transform infrared spectroscopy, theoretical simulations, and control experiments reveal that active *Cl and *H play key roles in photocatalytic acetylene hydrochlorination via a possible reaction pathway of C2H2 → *C2H2 → *C2H2Cl → *C2H3Cl → C2H3Cl. With respect to sustainability and low cost, this photocatalytic acetylene hydrochlorination offers excellent advantages over conventional thermocatalytic hydrochlorination technologies.

Atomically Isolated Pd Sites Promote Electrochemical CO Reduction to Acetate through a Protonation-Regulated Mechanism.

Electrochemical CO reduction reaction (CORR) offers a promising approach for sustainable acetate production, the promotion of which requires the control of multiple protonation steps. This paper describes the synthesis of atomically isolated Pd sites onto Cu nanoflakes to regulate the protonation of key intermediates. The Pd sites with moderate water activation capability are found to enhance the protonation of *CO at the neighboring Cu site to *COH, which is confirmed to be the rate-determining step through kinetic isotope effect studies. The formation of *COH-*CO is therefore promoted. Additionally, the Pd sites would preferentially protonate the C-OH group in *COH-*CO due to the spatial approximability and electronic modulation effects, generating *CCO for the selective formation of acetate. An acetate Faradaic efficiency of 59.5% is achieved at -0.78 V vs reversible hydrogen electrode (RHE), with a maximum partial current density of 286 mA cm-2 at -0.86 V vs RHE. The optimized catalyst also exhibits long-term stability for 500 h at 100 mA cm-2 in a membrane electrode assembly. This work reveals a new promoting mechanism for selective CORR with simultaneous tuning of the structural and electronic properties of the proton-supplying sites.

DRD4 promotes chemo-resistance and cancer stem cell-like phenotypes by mediating the activation of the Akt/ß-catenin signaling axis in liver cancer.

BACKGROUND: Liver cancer stem cells (LCSCs) significantly impact chemo-resistance and recurrence in liver cancer. Dopamine receptor D4 (DRD4) is known to enhance the cancer stem cell (CSC) phenotype in glioblastoma and correlates with poor prognosis in some non-central nervous system tumors; however, its influence on LCSCs remains uncertain. METHODS: To investigate the gene and protein expression profiles of DRD4 in LCSCs and non-LCSCs, we utilized transcriptome sequencing and Western blotting analysis. Bioinformatics analysis and immunohistochemistry were employed to assess the correlation between DRD4 expression levels and the pathological characteristics of liver cancer patients. The impact of DRD4 on LCSC phenotypes and signaling pathways were explored using pharmacological or gene-editing techniques. Additionally, the effect of DRD4 on the protein expression and intracellular localization of ß-catenin were examined using Western blotting and immunofluorescence. RESULTS: DRD4 expression is significantly elevated in LCSCs and correlates with short survival in liver cancer. The expression and activity of DRD4 are positive to resistance, self renewal and tumorigenicity in HCC. Mechanistically, DRD4 stabilizes ß-catenin and promotes its entry into the nucleus via activating the PI3K/Akt/GSK-3ß pathway, thereby enhancing LCSC phenotypes. CONCLUSIONS: Inhibiting DRD4 expression and activation offers a promising targeted therapy for eradicating LCSCs and relieve chemo-resistance.

Targeting OXCT1-mediated ketone metabolism reprograms macrophages to promote antitumor immunity via CD8+ T cells in hepatocellular carcinoma.

BACKGROUND & AIMS: The liver is the main organ of ketogenesis, while ketones are mainly metabolized in peripheral tissues via the critical enzyme 3-oxoacid CoA-transferase 1 (OXCT1). We previously found that ketolysis is reactivated in hepatocellular carcinoma (HCC) cells through OXCT1 expression to promote tumor progression; however, whether OXCT1 regulates antitumor immunity remains unclear. METHODS: To investigate the expression pattern of OXCT1 in HCC in vivo, we conducted multiplex immunohistochemistry experiments on human HCC specimens. To explore the role of OXCT1 in mouse HCC tumor-associated macrophages (TAMs), we generated LysMcreOXCT1f/f (OXCT1 conditional knockout in macrophages) mice. RESULTS: Here, we found that inhibiting OXCT1 expression in tumor-associated macrophages reduced CD8+ T-cell exhaustion through the succinate-H3K4me3-Arg1 axis. Initially, we found that OXCT1 was highly expressed in liver macrophages under steady state and that OXCT expression was further increased in TAMs. OXCT1 deficiency in macrophages suppressed tumor growth by reprogramming TAMs toward an antitumor phenotype, reducing CD8+ T-cell exhaustion and increasing CD8+ T-cell cytotoxicity. Mechanistically, high OXCT1 expression induced the accumulation of succinate, a byproduct of ketolysis, in TAMs, which promoted Arg1 transcription by increasing the H3K4me3 level in the Arg1 promoter. In addition, pimozide, an inhibitor of OXCT1, suppressed Arg1 expression as well as TAM polarization toward the protumor phenotype, leading to decreased CD8+ T-cell exhaustion and slower tumor growth. Finally, high expression of OXCT1 in macrophages was positively associated with poor survival in patients with HCC. CONCLUSIONS: In conclusion, our results demonstrate that OXCT1 epigenetically suppresses antitumor immunity, suggesting that suppressing OXCT1 activity in TAMs could be an effective approach for treating liver cancer. IMPACT AND IMPLICATIONS: The intricate metabolism of liver macrophages plays a critical role in shaping hepatocellular carcinoma progression and immune modulation. Targeting macrophage metabolism to counteract immune suppression presents a promising avenue for hepatocellular carcinoma treatment. Herein, we found that the ketogenesis gene OXCT1 was highly expressed in tumor-associated macrophages (TAMs) and promoted tumor growth by reprogramming TAMs toward a protumor phenotype. Pharmacological targeting or genetic downregulation of OXCT1 in TAMs enhances antitumor immunity and slows tumor growth. Our results suggest that suppressing OXCT1 activity in TAMs could be an effective approach for treating liver cancer.

Antibiotic-induced gut microbiota disruption promotes vascular calcification by reducing short-chain fatty acid acetate.

BACKGROUND: Vascular calcification is a common vascular lesion associated with high morbidity and mortality from cardiovascular events. Antibiotics can disrupt the gut microbiota (GM) and have been shown to exacerbate or attenuate several human diseases. However, whether antibiotic-induced GM disruption affects vascular calcification remains unclear. METHODS: Antibiotic cocktail (ABX) treatment was utilized to test the potential effects of antibiotics on vascular calcification. The effects of antibiotics on GM and serum short-chain fatty acids (SCFAs) in vascular calcification mice were analyzed using 16 S rRNA gene sequencing and targeted metabolomics, respectively. Further, the effects of acetate, propionate and butyrate on vascular calcification were evaluated. Finally, the potential mechanism by which acetate inhibits osteogenic transformation of VSMCs was explored by proteomics. RESULTS: ABX and vancomycin exacerbated vascular calcification. 16 S rRNA gene sequencing and targeted metabolomics analyses showed that ABX and vancomycin treatments resulted in decreased abundance of Bacteroidetes in the fecal microbiota of the mice and decreased serum levels of SCFAs. In addition, supplementation with acetate was found to reduce calcium salt deposition in the aorta of mice and inhibit osteogenic transformation in VSMCs. Finally, using proteomics, we found that the inhibition of osteogenic transformation of VSMCs by acetate may be related to glutathione metabolism and ubiquitin-mediated proteolysis. After adding the glutathione inhibitor Buthionine sulfoximine (BSO) and the ubiquitination inhibitor MG132, we found that the inhibitory effect of acetate on VSMC osteogenic differentiation was weakened by the intervention of BSO, but MG132 had no effect. CONCLUSION: ABX exacerbates vascular calcification, possibly by depleting the abundance of Bacteroidetes and SCFAs in the intestine. Supplementation with acetate has the potential to alleviate vascular calcification, which may be an important target for future treatment of vascular calcification.

High-Precision Printing of Cermets by Collapsable Matrix Assisted Digital Light Processing.

Shaping hard and brittle materials, e.g. cermets, at micrometer resolution has long been known challenging for both mechanical machining and high energy beam based additive manufacturing. Digital light processing (DLP), which features great printing quality and decent precision, unfortunately lacks capability to deal with the popular slurry-typed cermet precursor due to the tremendous optical absorption by its particles. Here, an innovative protocol based on a versatile collapsable matrix is devised to allow high-precision printing of WC-Co cermets on DLP platform. By tuning the external environment, this matrix attenuates composite powders to facilitate photopolymerization at the printing stage, and shrinks to condense green parts prior to thermal sintering. The as-obtained samples by collapsable matrix assisted DLP can reach a relative density of ≈90%, a record-breaking resolution of ≈10 µm, and a microhardness of up to 14.5 GPa. Complex delicate structures, including school emblem, honeycomb, and micro-drill can be directly fabricated, which has never been achieved before. Impressively, the as-obtained micro-drill is able to be directly used in drilling tasks. The above strategy represents a great progress in DLP by enabling shaping strong light attenuating materials at high resolution. Such advantages are ideal for the next generation ceramic-metal composite additive manufacturing.

Broad-spectrum resistance gene RPW8.1 balances immunity and growth via feedback regulation of WRKYs.

Arabidopsis RESISTANCE TO POWDERY MILDEW 8.1 (RPW8.1) is an important tool for engineering broad-spectrum disease resistance against multiple pathogens. Ectopic expression of RPW8.1 leads to enhanced disease resistance with cell death at leaves and compromised plant growth, implying a regulatory mechanism balancing RPW8.1-mediated resistance and growth. Here, we show that RPW8.1 constitutively enhances the expression of transcription factor WRKY51 and activates salicylic acid and ethylene signalling pathways; WRKY51 in turn suppresses RPW8.1 expression, forming a feedback regulation loop. RPW8.1 and WRKY51 are both induced by pathogen infection and pathogen-/microbe-associated molecular patterns. In ectopic expression of RPW8.1 background (R1Y4), overexpression of WRKY51 not only rescues the growth suppression and cell death caused by RPW8.1, but also suppresses RPW8.1-mediated broad-spectrum disease resistance and pattern-triggered immunity. Mechanistically, WRKY51 directly binds to and represses RPW8.1 promoter, thus limiting the expression amplitude of RPW8.1. Moreover, WRKY6, WRKY28 and WRKY41 play a role redundant to WRKY51 in the suppression of RPW8.1 expression and are constitutively upregulated in R1Y4 plants with WRKY51 being knocked out (wrky51 R1Y4) plants. Notably, WRKY51 has no significant effects on disease resistance or plant growth in wild type without RPW8.1, indicating a specific role in RPW8.1-mediated disease resistance. Altogether, our results reveal a regulatory circuit controlling the accumulation of RPW8.1 to an appropriate level to precisely balance growth and disease resistance during pathogen invasion.

Bulk RNA sequencing for analysis of post COVID-19 condition in adolescents and young adults.

BACKGROUND: Post COVID-19 condition (PCC) is a complication of SARS-COV-2 infection and can lead to long-term disability. METHODS: The present study was designed to analyse the gene expression patterns of PCC through bulk RNA sequencing of whole blood and to explore the potential molecular mechanisms of PCC. Whole blood was collected from 80 participants enrolled in a prospective cohort study following SARS-CoV-2 infected and non-infected individuals for 6 months after recruitment and was used for bulk RNA sequencing. Identification of differentially expressed genes (DEG), pathway enrichment and immune cell deconvolution was performed to explore potential biological pathways involved in PCC. RESULTS: We have found 13 differentially expressed genes associated with PCC. Enriched pathways were related to interferon-signalling and anti-viral immune processes. CONCLUSION: The PCC transcriptome is characterized by a modest overexpression of interferon-stimulated genes, pointing to a subtle ongoing inflammatory response.

Sexually concordant selection on floral traits despite greater opportunity for selection through male fitness.

Pollinators are important drivers of floral trait evolution, yet plant populations are not always perfectly adapted to their pollinators. Such apparent maladaptation may result from conflicting selection through male and female sexual functions in hermaphrodites. We studied sex-specific mating patterns and phenotypic selection on floral traits in Aconitum gymnandrum. After genotyping 1786 offspring, we partitioned individual fitness into sex-specific selfed and outcrossed components and estimated phenotypic selection acting through each. Relative fitness increased with increasing mate number, and more so for male function. This led to greater opportunity for selection through outcrossed male fitness, though patterns of phenotypic selection on floral traits tended to be similar, and with better support for selection through female rather than male fitness components. We detected directional selection through one or more fitness component for larger flower number, larger flowers, and more negative nectar gradients within inflorescences. Our results are consistent with Bateman's principles for sex-specific mating patterns and illustrate that, despite the expected difference in opportunity for selection, patterns of variation in selection across traits can be rather similar for the male and female sexual functions. These results shed new light on the effect of sexual selection on the evolution of floral traits.

A rice amino acid transporter OsMP1 acts as a quantitative trait locus against blast fungus and leaf-blight bacterium.

Amino acid homeostasis is interconnected with the immune network of plants. During plant-pathogen interaction, amino acid transporters (AATs) have been shown to be involved in plant immune responses. However, the molecular mechanism by which how AATs function in this process remains elusive. In this study, we identify OsMP1 that acts as a quantitative trait locus against blast fungus from a joint analysis of GWAS and QTL mapping in rice. Heterogeneous expression of OsMP1 in yeast supports its function in transporting a wide range of amino acids, including Thr, Ser, Phe, His and Glu. OsMP1 could also mediate 15N-Glu efflux and influx in Xenopus oocyte cells. The expression of OsMP1 is dramatically induced by Magnaporthe oryzae in the resistant landrace Heikezijing, while remaining unresponsive in the susceptible landrace Suyunuo. Overexpressing OsMP1 in Suyunuo enhances disease resistance to blast fungus and leaf-blight bacterium without yield penalty. Furthermore, the overexpression of OsMP1 leads to increased accumulation of Thr, Ser, Phe and His in the leaves. And the heightened levels of these amino acids contribute to reduced disease susceptibility, which is associated with upregulated jasmonic acid pathway. Thus, our results elucidate the pivotal role of OsMP1 in disease resistance and provide a potential target for breeding more resistant rice cultivars without compromising yield.

Drug-Drug Cocrystal Alloy and Nanoformulation of Cytarabine: Optimized Biopharmaceutical Property and Synergistic Antitumor Efficacy.

An integrated strategy by combining cocrystallization with nanotechnology is developed to optimize in vitro/vivo performances of marine antitumor drug cytarabine (ARA) and further obtain innovative insights into the exploitation of cocrystal alloy nanoformulation. Therein, the optimization of properties and synergistic effects of ARA mainly depends on assembling with uracil (U) and antitumor drug 5-fluorouracil (FU) into the same crystal by cocrystallization technology, while the long-term efficacy is primarily maintained by playing the superiority of nanotechnology. Along this line, the first cocrystal alloy of ARA, viz., ARA-FU-U (0.6:0.4), is successfully obtained and then transformed into a nanocrystal. Single-crystal X-ray diffraction analysis demonstrates that this cocrystal alloy consists of two isomorphic cocrystals of ARA, namely, ARA-FU and ARA-U, in 0.6:0.4 ratio. An R22(8) hydrogen-bonding cyclic system formed by a cytosine fragment of ARA with U or FU can protect and stabilize the amine group on ARA, laying the foundation for regulating its properties. The in vitro/in vivo properties of the cocrystal alloy and its nanocrystals are investigated by theoretical and experimental means. It reveals that both the alloy and nanocrystal can improve physicochemical properties and promote drug absorption, thus bringing to optimized pharmacokinetic behaviors. The nanocrystal produces superior effects than the alloy that helps to extend therapeutic time and action. Particularly, relative to the corresponding binary cocrystal, the synergistic antitumor activity of ARA and FU in the cocrystal alloy is heightened obviously. It may be that U contributes to reducing the degradation of FU, specifically increasing its concentration in tumors to enhance the synergistic effects of FU and ARA. These findings provide new thoughts for the application of cocrystal alloys in the marine drug field and break fresh ground for cocrystal alloy formulations to optimize drug properties.