Gain-of-function of the 1-aminocyclopropane-1-carboxylate synthase gene ACS1G induces female flower development in cucumber gynoecy.

Unisexual flowers provide a useful system for studying plant sex determination. In cucumber (Cucumis sativus L.), three major Mendelian loci control unisexual flower development, Female (F), androecious [a; 1-aminocyclopropane-1-carboxylate {ACC} synthase 11, acs11], and Monoecious (M; ACS2), referred to here as the Female, Androecious, Monoecious (FAM) model, in combination with two genes, gynoecious (g, the WIP family C2H2 zinc finger transcription factor gene WIP1) and the ethylene biosynthetic gene ACC oxidase 2 (ACO2). The F locus, conferring gynoecy and the potential for increasing fruit yield, is defined by a 30.2-kb tandem duplication containing three genes. However, the gene that determines the Female phenotype, and its mechanism, remains unknown. Here, we created a set of mutants and revealed that ACS1G is responsible for gynoecy conferred by the F locus. The duplication resulted in ACS1G acquiring a new promoter and expression pattern; in plants carrying the F locus duplication, ACS1G is expressed early in floral bud development, where it functions with ACO2 to generate an ethylene burst. The resulting ethylene represses WIP1 and activates ACS2 to initiate gynoecy. This early ACS1G expression bypasses the need for ACS11 to produce ethylene, thereby establishing a dominant pathway for female floral development. Based on these findings, we propose a model for how these ethylene biosynthesis genes cooperate to control unisexual flower development in cucumber.

DC-SIGN(+) Macrophages Control the Induction of Transplantation Tolerance.

Tissue effector cells of the monocyte lineage can differentiate into different cell types with specific cell function depending on their environment. The phenotype, developmental requirements, and functional mechanisms of immune protective macrophages that mediate the induction of transplantation tolerance remain elusive. Here, we demonstrate that costimulatory blockade favored accumulation of DC-SIGN-expressing macrophages that inhibited CD8(+) T cell immunity and promoted CD4(+)Foxp3(+) Treg cell expansion in numbers. Mechanistically, that simultaneous DC-SIGN engagement by fucosylated ligands and TLR4 signaling was required for production of immunoregulatory IL-10 associated with prolonged allograft survival. Deletion of DC-SIGN-expressing macrophages in vivo, interfering with their CSF1-dependent development, or preventing the DC-SIGN signaling pathway abrogated tolerance. Together, the results provide new insights into the tolerogenic effects of costimulatory blockade and identify DC-SIGN(+) suppressive macrophages as crucial mediators of immunological tolerance with the concomitant therapeutic implications in the clinic.

Pharmacological and mechanistic study of PS1, a Pdia4 inhibitor, in ß-cell pathogenesis and diabetes in db/db mice.

Pdia4 has been characterized as a key protein that positively regulates ß-cell failure and diabetes via ROS regulation. Here, we investigated the function and mechanism of PS1, a Pdia4 inhibitor, in ß-cells and diabetes. We found that PS1 had an IC50 of 4 µM for Pdia4. Furthermore, PS1 alone and in combination with metformin significantly reversed diabetes in db/db mice, 6 to 7 mice per group, as evidenced by blood glucose, glycosylated hemoglobin A1c (HbA1c), glucose tolerance test, diabetic incidence, survival and longevity (P < 0.05 or less). Accordingly, PS1 reduced cell death and dysfunction in the pancreatic ß-islets of db/db mice as exemplified by serum insulin, serum c-peptide, reactive oxygen species (ROS), islet atrophy, and homeostatic model assessment (HOMA) indices (P < 0.05 or less). Moreover, PS1 decreased cell death in the ß-islets of db/db mice. Mechanistic studies showed that PS1 significantly increased cell survival and insulin secretion in Min6 cells in response to high glucose (P < 0.05 or less). This increase could be attributed to a reduction in ROS production and the activity of electron transport chain complex 1 (ETC C1) and Nox in Min6 cells by PS1. Further, we found that PS1 inhibited the enzymatic activity of Pdia4 and mitigated the interaction between Pdia4 and Ndufs3 or p22 in Min6 cells (P < 0.01 or less). Taken together, this work demonstrates that PS1 negatively regulated ß-cell pathogenesis and diabetes via reduction of ROS production involving the Pdia4/Ndufs3 and Pdia4/p22 cascades.

Statin Use and Delirium Risk: An Updated Systematic Review and Meta-Analysis.

BACKGROUND: Findings on the association of statin use with delirium risk are inconsistent. THE STUDY QUESTION: Is statin use associated with delirium risk? STUDY DESIGN: We searched PubMed, the Cochrane Library, and the EMBASE database, limiting the search to human patients and articles in English published until December 31, 2021. The effect size and 95% confidence interval (CI) were defined as the odds ratio (OR) and 95% CI, respectively, to indicate the difference in the incidence of delirium between statin use and nonuse groups. A random-effects model was selected in the case of high heterogeneity of study populations. We used funnel plots, Egger test, Duval and Tweedie trim-and-fill approach, and the classic fail-safe N to assess publication bias. RESULTS: Of a total of 264 identified studies, 13 were selected for the qualitative review-4 RCTs and 9 observational cohort studies. Statin use was not associated with low delirium risk (pooled OR, 0·82; 95% CI, 0·64-1·04; P = 0·09). Substantial statistical heterogeneity was observed ( I2 , 90%). Visual inspection of the funnel plot of ORs from the studies revealed symmetry. Using the Grading of Recommendations Assessment, Development, and Evaluation approach, we assigned the evidence a rating of C and a weak recommendation for this review. CONCLUSIONS: Statin use is not associated with delirium risk. More comprehensive RCTs are required to confirm the results.

Anticoagulant drugs with or without proton pump inhibitor and colorectal cancer risk: a population-based, case-control study.

BACKGROUND: Low-dose aspirin and clopidogrel have demonstrated potential chemoprevention for colorectal cancer (CRC). Proton-pump inhibitors (PPI) are commonly prescribed with anticoagulation drugs, but the relationship between PPI and CRC is unclear. Moreover, evidence of CRC risk under direct oral anticoagulant (DOAC) is limited. This study aimed to investigate the effects of anticoagulation drugs combined with or without PPI on the risks of CRC in Taiwan. METHODS: A retrospective case-control study of 1,024,227 cases based on the Chang Gung Research Database from 2010 to 2017 was performed. Clinical characteristics, indications, duration of anticoagulation and PPI use, and CRC occurrence data were collected. Logistic regression was employed to adjust for known confounders of CRC risk. RESULTS: Monotherapy of clopidogrel decreased the risk of CRC (AOR 0.70; 95% CI 0.60-0.83), while no protective effect was observed in aspirin alone or aspirin plus clopidogrel. DOAC did not affect CRC significantly. The risk of CRC increased in patients with PPI (AOR 1.38; 95% CI 1.28-1.49) and PPI plus DOAC (OR 3.91; 95% CI 1.49-10.27), while PPI plus aspirin decreased the risk of CRC (OR 0.48; 95% CI 0.32-0.73). PPI plus clopidogrel showed no significant effect on the CRC. CONCLUSION: This study suggests clopidogrel alone and PPI plus aspirin offer a preventative benefit against CRC in the Taiwanese population studied. The same effect was not observed in DOAC. Moreover, a significant increase in CRC was observed in patients on PPI monotherapy and PPI plus DOAC, suggesting a possible risk.

CALML6 Controls TAK1 Ubiquitination and Confers Protection against Acute Inflammation.

Proper regulation of innate immune response is important for individual health. The NF-κB signaling pathway plays crucial roles in innate immunity and inflammation, and its aberrant activation is implicated in diverse diseases and disorders. In this study, we report that calmodulin-like 6 (CALML6), a member of the EF-hand protein family, is a negative regulator of the NF-κB signaling pathway. CALML6 attenuated TNF-stimulated phosphorylation of proteins downstream of TGF-ß-activated kinase 1 (TAK1) and inhibited TAK1-induced NF-κB activation. Further studies showed that CALML6 interacted with TAK1 and recruited the deubiquitylating enzyme cylindromatosis to repress the K63-linked polyubiquitination of TAK1. CALML6 transgenic mice had higher tolerances to lethal LPS treatment in vivo. These findings suggest that CALML6 is a negative regulator of the NF-κB signaling pathway, which is important for maintaining the balance of the innate immune response.

Associations between dietary patterns and stages of chronic kidney disease.

BACKGROUND: Studies have revealed that patients with chronic kidney disease (CKD) have dietary patterns different from those of the general population. However, no studies have compared the dietary patterns of between patients with early-stages (stages 1-3a) and late-stages (stages 3b-5) of CKD. Our objective was to investigate the associations between dietary patterns in early and late-stage CKD. METHODS: We analyzed 4480 participants with CKD at various stages based on the data recorded between 2007 and 2016 from the database of the American National Health and Nutrition Examination Survey. RESULTS: In total, 3683 and 797 participants had early and late-stage CKD, respectively. Through principal components analysis, the dietary intake dimension was reduced from 63 variables to 3 dietary patterns. We adopted logistic regression for analysis. The three dietary patterns are as follows: (1) saturated fatty acids and mono-unsaturated fatty acids (MUFA); (2) vitamins and minerals; and (3) cholesterols and polyunsaturated fatty acids (PUFA). These 3 patterns explained > 50% of dietary nutrient intake. Results indicated that among participants with dietary patterns 2 (vitamins and minerals) and 3 (cholesterols and PUFA), those with low intakes were more likely to have late-stage CKD. The odds ratios for patterns 2 and 3 were 1.74 (95% CI: 1.21-2.50) and 1.66 (95% CI: 1.13-2.43), respectively. CONCLUSIONS: This study revealed that intakes of vitamins and minerals and cholesterols and PUFA were associated with the stages of CKD.

The Formation of Hollow Trait in Cucumber (Cucumis sativus L.) Fruit Is Controlled by CsALMT2.

The hollow trait is crucial for commercial quality of cucumber (Cucumis sativus L.) fruit, and its molecular regulatory mechanism is poorly understood due to its environmental sensitivity. In the previous research, we obtained the hollow and the non-hollow materials of ecotype cucumbers of South China, which were not easily affected by the external environment through a systematic breeding method. In this study, first, we proposed to use the percentage of the hollow area as the criterion to compare the hollow characteristics between two materials, and to analyze the formation mechanism of early hollow trait from the perspective of cytology. The results showed that the hollow trait occurred in the early stage of fruit development, and formed with the opening of carpel ventral zipped bi-cell layer, which formed rapidly from 2 to 4 days, and then slowed to a constant rate from 14 to 16 days. Meanwhile, the different genetic populations were constructed using these materials, and fine mapping was performed by bulked segregant analysis (BSA) and kompetitive allele specific PCR (KASP) method. The Csa1G630860 (CsALMT2), encoding protein ALMT2, was determined as a candidate gene for regulating the hollow trait in fruit. Furthermore, the expression profile of CsALMT2 was analyzed by qRT-PCR and fluorescence in situ hybridization. The expression of CsALMT2 had obvious tissue specificity, and it was abundantly expressed in the ovule development zone inside the fruit. In the hollow material of cucumber fruit, the expression of CsALMT2 was significantly downregulated. The subcellular localization in tobacco leaves indicated that CsALMT2 was distributed on the plasma membrane. In conclusion, in this study, for the first time, we found the regulatory gene of hollow trait in cucumber fruit, which laid the foundation for subsequent research on the molecular mechanism of hollow trait formation in cucumber fruit, and made it possible to apply this gene in cucumber breeding.

Nutrient supplements from selected botanicals mediated immune modulation of the tumor microenvironment and antitumor mechanism.

Specific extracts of selected vegetables (SV) have been shown to benefit the survival of stage IIIb/IV non-small cell lung cancer patients in phase I/II studies and is currently in a phase III trial. However, the underlying mechanism of SV-mediated antitumor immune responses has not been elucidated. Our results indicate that SV modulated the NK and adoptive T cell immune responses in antitumor efficacy. Furthermore, antitumor effects of SV were also mediated by innate myeloid cell function, which requires both TLR and ß-glucan signaling in a MyD88/TRIF and Dectin-1-dependent manner, respectively. Additionally, SV treatment reduced granulocytic myeloid-derived suppressor cell (MDSC) infiltration into the tumor and limited monocytic MDSC toward the M2-like functional phenotype. Importantly, SV treatment enhanced antigen-specific immune responses by augmenting the activation of antigen-specific TH1/TH17 cells in secondary lymphoid organs and proliferative response, as well as by reducing the Treg population in the tumor microenvironment, which was driven by SV-primed activated M-MDSC. Our results support the idea that SV can subvert immune-tolerance state in the tumor microenvironment and inhibit tumor growth. The present study suggests that features, such as easy accessibility, favorable clinical efficacy, no detectable side effects and satisfactory safety make SV a feasible, appealing and convincing adjuvant therapy for the treatment of cancer patients and prevent tumor recurrence and/or metastases.

Current Advancements of Plant-Derived Agents for Triple-Negative Breast Cancer Therapy through Deregulating Cancer Cell Functions and Reprogramming Tumor Microenvironment.

Triple-negative breast cancer (TNBC) is defined based on the absence of estrogen, progesterone, and human epidermal growth factor receptor 2 receptors. Currently, chemotherapy is the major therapeutic approach for TNBC patients; however, poor prognosis after a standard chemotherapy regimen is still commonplace due to drug resistance. Abnormal tumor metabolism and infiltrated immune or stromal cells in the tumor microenvironment (TME) may orchestrate mammary tumor growth and metastasis or give rise to new subsets of cancer cells resistant to drug treatment. The immunosuppressive mechanisms established in the TME make cancer cell clones invulnerable to immune recognition and killing, and turn immune cells into tumor-supporting cells, hence allowing cancer growth and dissemination. Phytochemicals with the potential to change the tumor metabolism or reprogram the TME may provide opportunities to suppress cancer metastasis and/or overcome chemoresistance. Furthermore, phytochemical intervention that reprograms the TME away from favoring immunoevasion and instead towards immunosurveillance may prevent TNBC metastasis and help improve the efficacy of combination therapies as phyto-adjuvants to combat drug-resistant TNBC. In this review, we summarize current findings on selected bioactive plant-derived natural products in preclinical mouse models and/or clinical trials with focus on their immunomodulatory mechanisms in the TME and their roles in regulating tumor metabolism for TNBC prevention or therapy.

Integrated Metabolome and Transcriptome Analysis Unveils Novel Pathway Involved in the Formation of Yellow Peel in Cucumber.

Yellow peel will adversely affect the appearance quality of cucumber fruit, but the metabolites and the molecular mechanism of pigment accumulation in cucumber peel remain unclear. Flavonoid metabolome and transcriptome analyses were carried out on the young peel and old peel of the color mutant L19 and the near-isogenic line L14. The results showed that there were 165 differential flavonoid metabolites in the old peel between L14 and L19. The total content of representative flavonoid metabolites in the old peel of L14 was 95 times that of L19, and 35 times that of young peel of L14, respectively. This might explain the difference of pigment accumulation in yellow peel. Furthermore, transcriptome analysis showed that there were 3396 and 1115 differentially expressed genes in the yellow color difference group (Young L14 vs. Old L14 and Old L14 vs. Old L19), respectively. These differentially expressed genes were significantly enriched in the MAPK signaling pathway-plant, plant-pathogen interaction, flavonoid biosynthesis and cutin, suberine and wax biosynthesis pathways. By analyzing the correlation between differential metabolites and differentially expressed genes, six candidate genes related to the synthesis of glycitein, kaempferol and homoeriodictyol are potentially important. In addition, four key transcription factors that belong to R2R3-MYB, bHLH51 and WRKY23 might be the major drivers of transcriptional changes in the peel between L14 and L19. Then, the expression patterns of these important genes were confirmed by qRT-PCR. These results suggested that the biosynthesis pathway of homoeriodictyol was a novel way to affect the yellowing of cucumber peel. Together, the results of this study provide a research basis for the biosynthesis and regulation of flavonoids in cucumber peel and form a significant step towards identifying the molecular mechanism of cucumber peel yellowing.

Untargeted LC-MS-based metabonomics revealed that aristolochic acid I induces testicular toxicity by inhibiting amino acids metabolism, glucose metabolism, ß-oxidation of fatty acids and the TCA cycle in male mice.

As the main toxic component of aristolochic acid, aristolochic acid I (AAI) is primarily found in Aristolochiaceae plants such as Aristolochia, Aristolochia fangchi and Caulis aristolochiae manshuriensis. AAI has been proven to be carcinogenic, mutagenic and nephrotoxic. Although the role of AAI in testicular toxicity has been reported, its mechanism of action is unknown. Using metabonomics and molecular biology techniques, we tried to identify the differential endogenous metabolites of AAI that may affect the changes in testicular function in mice, map the network of metabolic pathways, and systematically reveal the molecular mechanism of AAI-induced testicular toxicity. We found that AAI inhibited amino acid metabolism in mouse testicular cells, impeded the uptake and oxidative decomposition of fatty acids, prevented normal glucose uptake by testicular cells, which inhibited glycolysis and gluconeogenesis, affected the mitochondrial tricarboxylic acid (TCA) cycle, which impaired the ATP energy supply, decreased the number of spermatogenic cells and sperm in the testes, induced changes in the mitochondrial state of spermatogonial cells, and ultimately led to physiological and pathological changes in the testes. AAI also regulated the testicular physiological activity by regulating the androgen receptor and hormone levels. This study used metabonomics and other methods to elucidate the mechanism of AAI-induced testicular toxicity from a new angle.

Highly Secure Physically Unclonable Cryptographic Primitives Based on Interfacial Magnetic Anisotropy.

Information security is of great importance for the approaching Internet of things (IoT) era. Physically unclonable functions (PUFs) have been intensively studied for information security. However, silicon PUFs are vulnerable to hazards such as modeling and side-channel attacks. Here we demonstrate a magnetic analogue PUF based on perpendicularly magnetized Ta/CoFeB/MgO heterostructures. The perpendicular magnetic anisotropy originates from the CoFeB/MgO interface, which is sensitive to the subnanometer variation of MgO thickness within a certain range (0.6-1.3 nm). When the MgO layer is thinned, a thickness variation resulting from ion milling nonuniformity induces unclonable random distributions of eas y-axis magnetization orientations in heterostructures. The analogue PUF can provide a much larger key size than a conventional binary-bit counterpart. Moreover, after the thinning process, the unique eas y-axis magnetization orientation in each single device was formed, which can avoid setting random states to realize low power consumption and high-density integration. This magnetic PUF is a promising innovative primitive for secret key generation and storage with high security in the IoT era.

Influence of fillers on the removal of rainwater runoff pollutants by a permeable brick system with a frame structure base.

To fully investigate the effectiveness of fillers in the removal of pollutants from rainwater, gravel, zeolite, slag, volcanic rock and iron filings with a 3-5 cm particle size were applied to construct a brick paving system with a frame structure for the removal of pollutants. Total suspended solids (TSS), chemical oxygen demand (COD), ammonia nitrogen (NH3-N), total nitrogen (TN), total phosphorus (TP) and heavy metals (Cu, Zn, and Pb) in the influent and effluent were measured, and the effectiveness and mechanism of pollutant removal were further investigated. The results showed that the permeable brick system effectively reduced TSS, TP, Zn, Cu and Pb and was relatively ineffective in reducing NH3-N, TN and COD. The removal results obtained using different materials show that (1) physical interception is the main reason for TSS and TP removal, (2) the adsorption and ion exchange properties of zeolite enable it to highly absorb ammonia nitrogen, (3) iron filings can effectively reduce NO3-N, and (4) adding fillers rich in iron oxide, such as volcanic rock or slag, can contribute to COD adsorption. The study provides a feasible technical path for improving the practicability of permeable pavement.

Genome-Wide Mapping of Structural Variations Reveals a Copy Number Variant That Determines Reproductive Morphology in Cucumber.

Structural variations (SVs) represent a major source of genetic diversity. However, the functional impact and formation mechanisms of SVs in plant genomes remain largely unexplored. Here, we report a nucleotide-resolution SV map of cucumber (Cucumis sativas) that comprises 26,788 SVs based on deep resequencing of 115 diverse accessions. The largest proportion of cucumber SVs was formed through nonhomologous end-joining rearrangements, and the occurrence of SVs is closely associated with regions of high nucleotide diversity. These SVs affect the coding regions of 1676 genes, some of which are associated with cucumber domestication. Based on the map, we discovered a copy number variation (CNV) involving four genes that defines the Female (F) locus and gives rise to gynoecious cucumber plants, which bear only female flowers and set fruit at almost every node. The CNV arose from a recent 30.2-kb duplication at a meiotically unstable region, likely via microhomology-mediated break-induced replication. The SV set provides a snapshot of structural variations in plants and will serve as an important resource for exploring genes underlying key traits and for facilitating practical breeding in cucumber.

Quadrupole Orbitrap Mass Spectrometer-Based Metabonomic Elucidation of Influences of Short-Term Di(2-ethylhexyl) phthalate Exposure on Cardiac Metabolism in Male Mice.

Di(2-ethylhexyl) phthalate (DEHP) can cause severe environmental pollution. Effects of DEHP on cardiac metabolism have been reported, but its mechanism(s) of action is not fully clear. Here, we used high-resolution mass spectrometry for metabonomics and molecular biological methods to identify the different endogenous metabolites affected by DEHP that might cause changes in cardiac metabolism in mice, map the network of metabolic pathways, and reveal (at the molecular level) how DEHP affects cardiac metabolism. The results showed that DEHP could inhibit the ß-oxidation of fatty acids and gluconeogenesis, promote glycolysis, and inhibit the tricarboxylic acid cycle in cardiomyocytes. DEHP caused mitochondrial dysfunction by inhibiting the synthesis and transport of fatty acids and, thus, inhibiting the synthesis and breakdown of adenosine triphosphate in mitochondria. Pathology revealed that DEHP could change the normal structures and functions of the heart and bodies of mice. DEHP can interfere with the physiological and metabolic function of the heart in mice by disrupting the endogenous metabolite and gene levels.

LILRB receptor-mediated regulation of myeloid cell maturation and function.

The leukocyte immunoglobulin-like receptor (LILR) family comprises a set of paired immunomodulatory receptors expressed among human myeloid and lymphocyte cell populations. While six members of LILR subfamily A (LILRA) associate with membrane adaptors to signal via immunoreceptor tyrosine-based activating motifs (ITAM), LILR subfamily B (LILRB) members signal via multiple cytoplasmic immunoreceptor tyrosine-based inhibitory motifs (ITIM). Ligand specificity of some LILR family members has been studied in detail, but new perspective into the immunoregulatory aspects of this receptor family in human myeloid cells has been limited. LILRB receptors and the murine ortholog, paired immunoglobulin-like receptor B (PIRB), have been shown to negatively regulate maturation pathways in myeloid cells including mast cells, neutrophils, dendritic cells, as well as B cells. Our laboratory further demonstrated in mouse models that PIRB regulated functional development of myeloid-derived suppressor cell and the formation of a tumor-permissive microenvironment. Based on observations from the literature and our own studies, our laboratory is focusing on how LILRs modulate immune homeostasis of human myeloid cells and how these pathways may be targeted in disease states. Integrity of this pathway in tumor microenvironments, for example, permits a myeloid phenotype that suppresses antitumor adaptive immunity. This review presents the evidence supporting a role of LILRs as myeloid cell regulators and ongoing efforts to understand the functional immunology surrounding this family.

Interaction of NS2 with AIMP2 facilitates the switch from ubiquitination to SUMOylation of M1 in influenza A virus-infected cells.

UNLABELLED: Influenza A viruses (IAVs) rely on host factors to support their life cycle, as viral proteins hijack or interact with cellular proteins to execute their functions. Identification and understanding of these factors would increase our knowledge of the molecular mechanisms manipulated by the viruses. In this study, we searched for novel binding partners of the influenza A virus NS2 protein, the nuclear export protein responsible for overcoming host range restriction, by a yeast two-hybrid screening assay and glutathione S-transferase-pulldown and coimmunoprecipitation assays and identified AIMP2, a potent tumor suppressor that usually functions to regulate protein stability, as one of the major NS2-binding candidates. We found that the presence of NS2 protected AIMP2 from ubiquitin-mediated degradation in NS2-transfected cells and AIMP2 functioned as a positive regulator of IAV replication. Interestingly, AIMP2 had no significant effect on NS2 but enhanced the stability of the matrix protein M1. Further, we provide evidence that AIMP2 recruitment switches the modification of M1 from ubiquitination to SUMOylation, which occurs on the same attachment site (K242) on M1 and thereby promotes M1-mediated viral ribonucleoprotein complex nuclear export to increase viral replication. Collectively, our results reveal a new mechanism of AIMP2 mediation of influenza virus replication. IMPORTANCE: Although the ubiquitination of M1 during IAV infection has been observed, the precise modification site and the molecular consequences of this modification remain obscure. Here, we demonstrate for the first time that ubiquitin and SUMO compete for the same lysine (K242) on M1 and the interaction of NS2 with AIMP2 facilitates the switch of the M1 modification from ubiquitination to SUMOylation, thus increasing viral replication.

A major quantitative trait locus conferring subgynoecy in cucumber.

KEY MESSAGE: A major QTL conditioning high degree of femaleness in cucumber was identified by marker analysis and next generation sequencing. Cucumber (Cucumis sativus L.) is a model species for sex determination studies, and its yield is associated with the degree of femaleness. Subgynoecy represents a sex form with a high degree of femaleness for which the genetic basis remains elusive. In this study, genetic analysis in the F2 and BC1 populations developed from a cross between subgynoecious S-2-98 and monoecious M95 suggested a quantitative nature of subgynoecy. Application of simple sequence repeat markers between subgynoecious and monoecious bulks constructed from BC1 plants identified three QTLs: sg3.1, sg6.1, and sg6.2. The major QTL sg3.1 contributed to 54.6% of the phenotypic variation, and its presence was confirmed by genome-wide comparison of SNP profiles between parental lines and a subgynoecious bulk constructed from BC6 plants. Using PCR-based markers developed from the SNP profile, sg3.1 was further delimited to a genomic region of 799 kb. The genetic basis of subgynoecy revealed here shall shed light on the development of elite cultivars with high yield potential.

Identification and mapping of Tril, a homeodomain-leucine zipper gene involved in multicellular trichome initiation in Cucumis sativus.

KEY MESSAGE: Using map-based cloning of Tril gene, we identified a homeodomain-leucine zipper gene involved in the initiation of multicellular trichomes (including the spines of fruit) in cucumber. ABSTRACT: Fruit spines are a special type of trichome that impacts the quality and appearance of cucumber (Cucumis sativus L.) fruit. Scanning electron microscopy revealed that the trichome-less (tril) mutant originating from European greenhouse cucumber has a completely glabrous phenotype on cotyledons, hypocotyls, young leaves, fruits, and fruit stalks. Genetic analysis revealed that tril was inherited as a recessive allele at a single locus. Using 1058 F2 individuals derived from a cross between cucumber tril mutant CGN19839 and the micro-trichome (mict) mutant 06-2, tril was mapped to chromosome 6, and narrowed down to a 37.4 kb genomic region which carries seven predicted genes. Genetic and molecular analyses revealed that gene Cucsa.045360 is a possible candidate gene for the differentiation of epidermal cells to trichomes. It is a member of the class IV homeodomain-leucine zipper (HD-Zip IV) family and encodes homeodomain and START domain, sharing 66.7% predicted amino acid sequence identity to PROTODERMAL FACTOR2 (PDF2) and 35.0% to GLABRA2 (GL2) of Arabidopsis. The homeobox domain had changed amino acid sequence because of an insertion in tril mutant. The results of genetic analysis and transcriptome profiling indicated that the Tril gene had an epistatic effect on the Mict gene in trichome development. Phenotypes of the tril mutant such as glabrous fruits and female flowers at every node could be used in developing new cultivars.