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Gluten subfractions of wheat storage proteins are affected by high night temperature during grain formation
Abstract
Gluten (gliadin + glutenin) protein in wheat flour is affected by high temperature (day and/or night) resulting in undesirable consequences on dough quality. A study was conducted with early and late-maturing wheat genotypes, to assess the spatial (superior- central and inferior- apical and basal spikelets) variation in the composition of gluten subfractions in the developing ear under high night temperature (HNT). We hypothesised that protein content in the superior and inferior grains may show a differential quantitative and qualitative response to HNT. HNT resulted in a significant increase in protein content which exhibited a strong (r = −0.44*) negative correlation with sedimentation volume (SV) that determines baking quality. The late-maturity genotypes were more responsive to HNT with changes in ω-5 and γ gliadin subfractions of both superior and inferior spikelets, though a consistent trend was not established. The proportion of high molecular weight (HMW) glutenins increased, whereas low molecular weight (LMW) glutenins reduced in most of the genotypes under HNT. Both HMW and LMW glutenins revealed significant positive (r = 0.43* and r = 0.81***, respectively) correlation with SV. The expression analysis of genes for gluten subfractions showed a significant decrease in transcript abundance of α, ω-5, γ, HMW, and LMW fractions under HNT.
Protein concentrations and activities of fatty acid desaturase and elongase enzymes in liver, brain, testicle, and kidney from mice: Substrate dependency
The liver had the highest capacity for PUFA biosynthesis, with limited activity in the brain, testicles, and kidney, while we failed to detect activity in the heart and lung. The protein content and activity of the enzymes were significantly correlated. The capacity for PUFA synthesis in mice mainly resides in the liver, with enzymes having preference for n-3 PUFAs.
Abstract
The synthesis rates of n-3 and n-6 polyunsaturated fatty acids (PUFAs) in rodents and humans are not agreed upon and depend on substrate availability independently of the capacity for synthesis. Therefore, we aimed to assess the activities of the enzymes for n-3 and n-6 PUFA synthesis pathways in liver, brain, testicle, kidney, heart, and lung, in relation to their protein concentration levels. Eight-week-old Balb/c mice (n = 8) were fed a standard chow diet (6.2% fat, 18.6% protein, and 44.2% carbohydrates) until 14 weeks of age, anesthetized with isoflurane and tissue samples were collected (previously perfused) and stored at −80°C. The protein concentration of the enzymes (Δ-6D, Δ-5D, Elovl2, and Elovl5) were assessed by ELISA kits; their activities were assayed using specific PUFA precursors and measuring the respective PUFA products as fatty acid methyl esters by gas chromatographic analysis. The liver had the highest capacity for PUFA biosynthesis, with limited activity in the brain, testicles, and kidney, while we failed to detect activity in the heart and lung. The protein concentration and activity of the enzymes were significantly correlated. Furthermore, Δ-6D, Δ-5D, and Elovl2 have a higher affinity for n-3 PUFA precursors compared to n-6 PUFA. The capacity for PUFA synthesis in mice mainly resides in the liver, with enzymes having preference for n-3 PUFAs.
Greater rate of nitrogen fertilizer application increases root rot caused by Phytophthora cinnamomi and P. plurivora in container‐grown rhododendron
Application of nitrogen accelerated Phytophthora root rot disease symptoms in rhododendron plants inoculated with Phytophthora cinnamomi and P. plurivora.
Abstract
Phytophthora root rot, caused by many Phytophthora species, decreases the health of rhododendrons produced in nurseries. Optimizing nitrogen (N) fertilizer is often used to improve nursery stock quality, but there is little information on how N fertilizers influence root rot caused by these pathogens. To understand the impact of N fertilizer and pathogen species on root rot development, rhododendrons were grown with no (0 g N/pot), low (1.04 g N/pot) or high (3.12 g N/pot) rates of N and inoculated with either P. cinnamomi or P. plurivora. Noninoculated plants at low and high N rates had greater biomass, leaf greenness and enhanced N, potassium, magnesium, phosphorus, sulphur and manganese uptake compared to plants grown with no N. When either Phytophthora species was present, N application increased aboveground disease symptoms (wilting, chlorosis, reduced stomatal conductance and biomass), but had no effect on root rot severity belowground. In addition, P. cinnamomi restricted uptake of several nutrients while P. plurivora had less influence on nutrient uptake. Nurseries frequently apply high amounts of N to promote fast growth. However, our results show that this can exacerbate root rot when P. cinnamomi or P. plurivora is present. Although decreasing N can reduce the number of overtly symptomatic plants, this may conversely increase the risk for selling apparently asymptomatic plants with low levels of infection. Additional studies are needed to determine how N fertilization influences Phytophthora root rot for a broader range of rhododendron cultivars and nursery crop species.
Effect of drought stress and subsequent re-watering on the physiology and nutrition of Pistacia vera and Pistacia atlantica
Genetic variants associated with leaf spot disease resistance in oil palm (Elaeis guineensis): A genome‐wide association study
Genome-wide association study using a diverse genetic background of the oil palm population reveals associated genes contributing to leaf spot disease resistance.
Abstract
Leaf spot is considered as a common disease of oil palm, caused primarily by Curvularia spp. fungi. This disease mainly affects the early stages of oil palm and if not adequately controlled can cause plant death. Among the methods available to control the disease, breeding resistant varieties is the most economically effective and promising strategy. A genome-wide association study for leaf spot resistance was conducted on 210 individual tenera palms from seven different (origin) crosses. These palms were subsequently infected with Curvularia spp. pathogenic inoculum in a nursery trial located in an endemic area. The area under the disease progress curve was used as a phenotypic measure. In addition, a genotyping-by-sequencing (GBS) approach was used to obtain the genotyping data of each individual. We found two loci, at chromosome 2 and chromosome 13, that were significantly associated with leaf spot disease resistance. Six genetic variants at the two loci (five variants at chromosome 2 and one variant at chromosome 13) surpassed the threshold for genome-wide significance (p < 106). These loci are linked with three widely known disease-related genes, namely, resistance gene analogue 3 (RGA3), resistance gene analogue 4 (RGA4) and receptor-like protein 9a (RLP9a). The loci identified here can be used for marker-assisted selection when developing leaf spot disease-resistant oil palm varieties.
Sodium Danshensu ameliorates cerebral ischemia/reperfusion injury by inhibiting CLIC4/NLRP3 inflammasome‐mediated endothelial cell pyroptosis
Mechanism of SDSS in inhibiting endothelial cell pyroptosis. In the priming step, NLRP3, pro-Caspase-1, GSDMD-full, pro-IL-1β, and pro-IL-18 were up-regulated. Furthermore, the translocation of CLIC4 from cytoplasm to the membrane induced chloride outflow, resulting in the assembly of NLRP3, ASC and Pro-Caspase-1 into a platform (activation step). By binding CLIC4 and blocking its membrane localization, SDSS inhibited chloride outflow, thus inhibiting the activation of NLRP3 inflammasome and then the cleavage of pro-Caspase-1 into Caspase-1. This inhibited pyroptosis along with the release of IL-1β and IL-18, resulting from Caspase-1-dependent GSDMD-N cleavage.
Abstract
Endothelial pyroptosis promotes cerebral ischemia/reperfusion injury (CIRI). Sodium Danshensu (SDSS) has been shown to attenuate CIRI and have anti-inflammatory properties in endothelial cells. However, the mechanism and effect of SDSS on alleviating endothelial pyroptosis after CIRI remains poorly understood. Thus, we aimed to investigate the efficacy and mechanism of SDSS in reducing endothelial pyroptosis. It has been shown that SDSS administration inhibited NLRP3 inflammasome-mediated pyroptosis. As demonstrated by protein microarrays, molecular docking, CETSA and ITDRFCETSA, SDSS bound strongly to CLIC4. Furthermore, SDSS can decrease its expression and inhibit its translocation. Its effectiveness was lowered by CLIC4 overexpression but not by knockdown. Overall The beneficial effect of SDSS against CIRI in this study can be ascribed to blocking endothelial pyroptosis by binding to CLIC4 and then inhibiting chloride efflux-dependent NLRP3 inflammasome activation.
What plant breeding may (and may not) look like in 2050?
Abstract
At the turn of 2000 many authors envisioned future plant breeding. Twenty years after, which of those authors’ visions became reality or not, and which ones may become so in the years to come. After two decades of debates, climate change is a “certainty,” food systems shifted from maximizing farm production to reducing environmental impact, and hopes placed into GMOs are mitigated by their low appreciation by consumers. We revise herein how plant breeding may raise or reduce genetic gains based on the breeder's equation. “Accuracy of Selection” has significantly improved by many experimental-scale field and laboratory implements, but also by vulgarizing statistical models, and integrating DNA markers into selection. Pre-breeding has really promoted the increase of useful “Genetic Variance.” Shortening “Recycling Time” has seen great progression, to the point that achieving a denominator equal to “1” is becoming a possibility. Maintaining high “Selection Intensity” remains the biggest challenge, since adding any technology results in a higher cost per progeny, despite the steady reduction in cost per datapoint. Furthermore, the concepts of variety and seed enterprise might change with the advent of cheaper genomic tools to monitor their use and the promotion of participatory or citizen science. The technological and societal changes influence the new generation of plant breeders, moving them further away from field work, emphasizing instead the use of genomic-based selection methods relying on big data. We envisage what skills plant breeders of tomorrow might need to address challenges, and whether their time in the field may dwindle.
P38α contributes to TNF‐α‐induced IL‐8 production in human gingival cells
When phosphorylated at threonine 180 and tyrosine 182, p38α contributes to the induction of IL-8 by TNF-α in Ca9-22 cells. TNF-α-induced phosphorylation translocates NF-κB into the nucleus and then increases both IL-8 mRNA expression and secretion. Thus, p38α plays an important role in TNF-α-induced IL-8 production, providing a potential therapeutic target to prevent and treat periodontal disease.
Abstract
Tumor necrosis factor-alpha (TNF-α) is a major inflammatory cytokine that induces interleukin (IL)-8 production. Although some studies have reported the involvement of the p38 MAPK signaling pathway in TNF-α-induced IL-8 production, its specific regulatory mechanisms in gingival epithelial cells (GECs) are still poorly understood. In the present study, Ca9-22 cells were used as representative GECs to investigate the effect of p38 signaling on TNF-α-induced IL-8 production. We found that TNF-α enhanced IL-8 production in Ca9-22 cells by activating the p38 signaling pathway, and one of its isoforms, p38α, played a key role. P38α deletion markedly inhibited TNF-α-induced IL-8 expression in Ca9-22 cells, while p38α gene rescue could reverse this effect. Further studies revealed that TNF-α-induced IL-8 production was markedly reduced when the threonine 180 and tyrosine 182 p38α phosphorylation sites were targeted for mutagenesis to alanine and phenylalanine, respectively, suggesting their critical role in the process. In conclusion, p38α plays an important role in TNF-α-induced IL-8 production, providing a potential therapeutic target to prevent and treat periodontal disease.
Genetic characterization and prevalence of Pseudomonas syringae strains from sweet cherry orchards in New Zealand
The study identified prevalent Pseudomonas syringae strains in New Zealand cherry orchards, with P. syringae pv. syringae as the predominant pathovar in Central Otago, providing valuable insights for future epidemiology research.
Abstract
Bacterial canker of cherry, caused by Pseudomonas syringae pathovars, is a major constraint to cherry growing in New Zealand. The prevalence of strains from cherry orchards in Central Otago, the main growing area for cherries in New Zealand, was studied, to better understand the epidemiology of the disease. Pseudomonas spp. isolates were collected from symptomatic and asymptomatic cherry tissue from 23 commercial cherry orchards in 2015. Isolates were classified into strains belonging to three different taxonomic groups by determining their phylogeny using the gltA gene sequence for all the strains and multilocus sequence analysis (MLSA) of four housekeeping genes for 35 strains. Pathogenicity of all Central Otago strains was tested on immature cherry fruit to support the phylogenetic classification. The two main taxonomic groups were P. syringae pv. syringae (Pss) and P. syringae pv. morsprunorum race 1 (Psm1), in Phylogroup 2 (PG2) and Phylogroup 3 (PG3), respectively. The third group comprised nonpathogenic strains classified as Pseudomonas spp. Strains of Psm1 formed a monophyletic group, representing an almost clonal population. There was more variation detected within strains of Pss, although they were restricted to group PG2d. Nonpathogenic Pseudomonas spp. and pathogenic Pss and Psm1 strains coexisted in the same orchard. It was concluded that Pss is the predominant pathovar in Central Otago. This is the first detailed study of the P. syringae species complex in cherry orchards in New Zealand and provides the basis for future epidemiology studies.