PubMed

J Nutr. 2023 Dec 11:S0022-3166(23)72798-3. doi: 10.1016/j.tjnut.2023.12.011. Online ahead of print.ABSTRACTBACKGROUND: Provision of zinc supplementation to young children has been associated with reduced infectious morbidity and better growth outcomes. However, the metabolic pathways underlying these outcomes are unclear, and metabolomic data from humans undergoing zinc supplementation, particularly infants, are generally lacking.OBJECTIVE: To examine the effect of zinc supplementation on metabolic profiles in Tanzanian infants ages 6 weeks and 6 months METHODS: Blood samples were collected at age 6 weeks and 6 months from 50 Tanzanian infants who were enrolled in a randomized placebo-controlled trial of zinc supplementation (5 mg oral daily). Metabolomic analysis using an ultrahigh-performance liquid chromatography/tandem mass spectroscopy (UPLC-MS/MS) platform were performed to identify potential metabolomic profiles and biomarkers associated with zinc supplementation. Principal component analysis (PCA) was used to summarize metabolomic data from all samples. Two-way repeated measures ANOVAs with compound symmetry covariance structures were used to compare metabolome levels over time between infants in the two treatment arms.RESULTS: In PCA, our samples tended to be more separated by child age (6 weeks versus 6 months) than by zinc supplementation status. We found that zinc supplementation affected a variety of metabolites associated with amino acid, lipid, nucleotide, and xenobiotic metabolism, including indoleacetate in the tryptophan metabolism pathway,3-methoxytrosine and 4-hydrxoyphenylphruvate in the tyrosine pathway, eicosanedioate, 2-aminooctanoate, and N-acetyl-2-aminooctanoate in the fatty acid pathway, and N6-succinyladenosine in the purine metabolism pathway. Compared to the relatively small number of metabolites associated with zinc supplements, many infant metabolites changed significantly from age 6 weeks to 6 months.CONCLUSIONS: Zinc supplementation, despite having overall clinical benefits, appears to induce limited metabolomic changes in blood metabolites in young infants. Future larger studies may be warranted to further examine metabolic pathways associated with zinc supplementation.PMID:38092153 | DOI:10.1016/j.tjnut.2023.12.011

J Nutr. 2023 Dec 11:S0022-3166(23)72797-1. doi: 10.1016/j.tjnut.2023.12.010. Online ahead of print.ABSTRACTBACKGROUND: Folic acid (FA) is the oxidized form of folate found in supplements and FA-fortified foods. Most FA is reduced by dihydrofolate reductase to 5-methyltetrahydrofolate (5mTHF); the latter is the form of folate naturally found in foods. Ingestion of FA increases plasma levels of both 5mTHF and unmetabolized FA (UMFA). Limited information is available on downstream metabolic effects of supplemental FA intake, including potential effects associated with UMFA.OBJECTIVE: We aimed to assess the metabolic effects of FA-supplementation, and the associations of plasma 5mTHF and UMFA with the metabolome in FA-naïve Bangladeshi adults.METHODS: Sixty participants were selected from the Folic Acid and Creatine Trial (FACT); half received 800 μg FA/day for 12 weeks and half placebo. Plasma metabolome profiles were measured by high-resolution mass spectrometry, including 170 identified metabolites and 26,541 metabolic features. Penalized regression methods were used to assess the associations of targeted metabolites with FA-supplementation, 5mTHF, and UMFA. Pathway analyses were conducted using Mummichog.RESULTS: In penalized models of identified metabolites, FA-supplementation was associated with higher choline. Changes in 5mTHF concentrations were positively associated with metabolites involved in amino acid metabolism (5-hydroxyindoleacetic acid, acetylmethionine, creatinine, guanidinoacetate, hydroxyproline/n-acetylalanine) and two fatty acids (docosahexaenoic acid and linoleic acid). Changes in 5mTHF concentrations were negatively associated with acetylglutamate, acetyllysine, carnitine, propionyl carnitine, cinnamic acid, homogentisate, arachidonic acid and nicotine. UMFA concentrations were associated with lower levels of arachidonic acid. Together, metabolites selected across all models were related to lipids, aromatic amino acid metabolism, and the urea cycle. Analyses of nontargeted metabolic features identified additional pathways associated with FA supplementation.CONCLUSION: In addition to the recapitulation of several expected metabolic changes associated with 5mTHF, we observed additional metabolites/pathways associated with FA-supplementation. Further studies are needed to confirm these associations and assess their potential implications for human health.CLINICAL TRIAL REGISTRY: This trial was registered at https://clinicaltrials.gov as NCT01050556.PMID:38092151 | DOI:10.1016/j.tjnut.2023.12.010

Int J Biol Macromol. 2023 Dec 11:128727. doi: 10.1016/j.ijbiomac.2023.128727. Online ahead of print.ABSTRACTDicranostigma leptopodum (Maxim) Fedde (DLF) is a renowned medicinal plant in China, known to be rich in alkaloids. However, the unavailability of a reference genome has impeded investigation into its plant metabolism and genetic breeding potential. Here we present a high-quality chromosomal-level genome assembly for DLF, derived using a combination of Nanopore long-read sequencing, Illumina short-read sequencing and Hi-C technologies. Our assembly genome spans a size of 621.81 Mb with an impressive contig N50 of 93.04 Mb. We show that the species-specific whole-genome duplication (WGD) of DLF and Papaver somniferum corresponded to two rounds of WGDs of Papaver setigerum. Furthermore, we integrated comprehensive homology searching, gene family analyses and construction of a gene-to-metabolite network. These efforts led to the discovery of co-expressed transcription factors, including NAC and bZIP, alongside sanguinarine (SAN) pathway genes CYP719 (CFS and SPS). Notably, we identified P6H as a promising gene for enhancing SAN production. By providing the first reference genome for Dicranostigma, our study confirms the genomic underpinning of SAN biosynthesis and establishes a foundation for advancing functional genomic research on Papaveraceae species. Our findings underscore the pivotal role of high-quality genome assemblies in elucidating genetic variations underlying the evolutionary origin of secondary metabolites.PMID:38092109 | DOI:10.1016/j.ijbiomac.2023.128727

J Hazard Mater. 2023 Dec 8;465:133202. doi: 10.1016/j.jhazmat.2023.133202. Online ahead of print.ABSTRACTWheat is susceptible to atmospheric ozone (O3) pollution, thus the increasing O3 is a serious threat to wheat production. γ-aminobutyric acid (GABA) is found to play key roles in the tolerance of plants to stress. However, few studies elaborated the function of GABA in response of wheat to O3. Here, we incorporated metabolome and transcriptome data to provide a more comprehensive insight on the role of GABA in enhancing the O3-tolerance of wheat. In our study, there were 31, 23, and 32 differentially accumulated flavonoids in the carbon-filtered air with GABA, elevated O3 with or without GABA treatments compared to the carbon-filtered air treatment, respectively. Elevated O3 triggered the accumulation of dihydroflavone, flavonols, and flavanols. Exogenous GABA enhanced dihydroflavone and dihydroflavonol, and also altered the expression of genes encoding some key enzymes in the flavonoid synthesis pathway. Additionally, GABA stimulated proline accumulation and antioxidant enzyme activities under elevated O3, resulting in the less accumulation of H2O2 and malondialdehyde. Consequently, GABA alleviated the grain yield loss from 19.6% to 9.6% induced by elevated O3. Our study provided comprehensive insight into the role of GABA in the alleviating the detrimental effects of elevated O3 on wheat, and a new avenue to mitigate O3 damage to the productivity of crops.PMID:38091801 | DOI:10.1016/j.jhazmat.2023.133202

Nat Rev Genet. 2023 Dec 13. doi: 10.1038/s41576-023-00674-x. Online ahead of print.ABSTRACTModern health care faces several serious challenges, including an ageing population and its inherent burden of chronic diseases, rising costs and marginal quality metrics. By assessing and optimizing the health trajectory of each individual using a data-driven personalized approach that reflects their genetics, behaviour and environment, we can start to address these challenges. This assessment includes longitudinal phenome measures, such as the blood proteome and metabolome, gut microbiome composition and function, and lifestyle and behaviour through wearables and questionnaires. Here, we review ongoing large-scale genomics and longitudinal phenomics efforts and the powerful insights they provide into wellness. We describe our vision for the transformation of the current health care from disease-oriented to data-driven, wellness-oriented and personalized population health.PMID:38093095 | DOI:10.1038/s41576-023-00674-x

Cell Mol Life Sci. 2023 Dec 13;81(1):8. doi: 10.1007/s00018-023-05041-x.ABSTRACTCystatin F, a cysteine peptidase inhibitor, is a potent modulator of NK cytotoxicity. By inhibiting granule-mediated cytotoxicity pathway, cystatin F induces formation of non-functional NK cell stage, called split-anergy. We show that N-glycosylation determines the localization and cellular function of cystatin F. Cystatin F mostly exhibited high-mannose glycosylation in U-937 cells, both high-mannose and complex glycosylation in NK-92 and primary NKs, and predominantly complex glycosylation in super-charged NKs. Manipulating N-glycosylation with kifunensine increased high-mannose glycosylation of cystatin F and lysosome localisation, which decreased cathepsin C activity and reduced NK cytotoxicity. Mannose-6-phosphate could significantly reduce the internalization of extracellular cystatin F. By comparing NK cells with different cytotoxic potentials, we found that high-mannose cystatin F was strongly associated with lysosomes and cathepsin C in NK-92 cell line. In contrast, in highly cytotoxic super-charged NKs, cystatin F with complex glycosylation was associated with the secretory pathway and less prone to inhibit cathepsin C. Modulating glycosylation to alter cystatin F localisation could increase the cytotoxicity of NK cells, thereby enhancing their therapeutic potential for treating cancer patients.PMID:38092995 | DOI:10.1007/s00018-023-05041-x

NPJ Microgravity. 2023 Dec 13;9(1):90. doi: 10.1038/s41526-023-00337-5.ABSTRACTThe adverse effects of microgravity exposure on mammalian physiology during spaceflight necessitate a deep understanding of the underlying mechanisms to develop effective countermeasures. One such concern is muscle atrophy, which is partly attributed to the dysregulation of calcium levels due to abnormalities in SERCA pump functioning. To identify potential biomarkers for this condition, multi-omics data and physiological data available on the NASA Open Science Data Repository (osdr.nasa.gov) were used, and machine learning methods were employed. Specifically, we used multi-omics (transcriptomic, proteomic, and DNA methylation) data and calcium reuptake data collected from C57BL/6 J mouse soleus and tibialis anterior tissues during several 30+ day-long missions on the international space station. The QLattice symbolic regression algorithm was introduced to generate highly explainable models that predict either experimental conditions or calcium reuptake levels based on multi-omics features. The list of candidate models established by QLattice was used to identify key features contributing to the predictive capability of these models, with Acyp1 and Rps7 proteins found to be the most predictive biomarkers related to the resilience of the tibialis anterior muscle in space. These findings could serve as targets for future interventions aiming to reduce the extent of muscle atrophy during space travel.PMID:38092777 | DOI:10.1038/s41526-023-00337-5

NPJ Biofilms Microbiomes. 2023 Dec 14;9(1):99. doi: 10.1038/s41522-023-00466-5.ABSTRACTSpinal cord injury (SCI) can reshape gut microbial composition, significantly affecting clinical outcomes in SCI patients. However, mechanisms regarding gut-brain interactions and their clinical implications have not been elucidated. We hypothesized that short-chain fatty acids (SCFAs), intestinal microbial bioactive metabolites, may significantly affect the gut-brain axis and enhance functional recovery in a mouse model of SCI. We enrolled 59 SCI patients and 27 healthy control subjects and collected samples. Thereafter, gut microbiota and SCFAs were analyzed using 16 S rDNA sequencing and gas chromatography-mass spectrometry, respectively. We observed an increase in Actinobacteriota abundance and a decrease in Firmicutes abundance. Particularly, the SCFA-producing genera, such as Faecalibacterium, Megamonas, and Agathobacter were significantly downregulated among SCI patients compared to healthy controls. Moreover, SCI induced downregulation of acetic acid (AA), propionic acid (PA), and butyric acid (BA) in the SCI group. Fecal SCFA contents were altered in SCI patients with different injury course and injury segments. Main SCFAs (AA, BA, and PA) were administered in combination to treat SCI mice. SCFA supplementation significantly improved locomotor recovery in SCI mice, enhanced neuronal survival, promoted axonal formation, reduced astrogliosis, and suppressed microglial activation. Furthermore, SCFA supplementation downregulated NF-κB signaling while upregulating neurotrophin-3 expression following SCI. Microbial sequencing and metabolomics analysis showed that SCI patients exhibited a lower level of certain SCFAs and related bacterial strains than healthy controls. SCFA supplementation can reduce inflammation and enhance nourishing elements, facilitating the restoration of neurological tissues and the improvement of functional recuperation. Trial registration: This study was registered in the China Clinical Trial Registry ( www.chictr.org.cn ) on February 13, 2017 (ChiCTR-RPC-17010621).PMID:38092763 | DOI:10.1038/s41522-023-00466-5

Environ Sci Technol. 2023 Dec 13. doi: 10.1021/acs.est.3c07515. Online ahead of print.ABSTRACTPer- and polyfluoroalkyl substances (PFAS) are ubiquitous and persistent chemicals associated with multiple adverse health outcomes; however, the biological pathways affected by these chemicals are unknown. To address this knowledge gap, we used data from 264 mother-infant dyads in the Health Outcomes and Measures of the Environment (HOME) Study and employed quantile-based g-computation to estimate covariate-adjusted associations between a prenatal (∼16 weeks' gestation) serum PFAS mixture [perfluorooctanesulfonic acid (PFOS), perfluorooctanoic acid (PFOA), perfluorohexanesulfonic acid (PFHxS), and perfluorononanoic acid (PFNA)] and 14,402 features measured in cord serum. The PFAS mixture was associated with four features: PFOS, PFHxS, a putatively identified metabolite (3-monoiodo-l-thyronine 4-O-sulfate), and an unidentified feature (590.0020 m/z and 441.4 s retention time; false discovery rate <0.20). Using pathway enrichment analysis coupled with quantile-based g-computation, the PFAS mixture was associated with 49 metabolic pathways, most notably amino acid, carbohydrate, lipid and cofactor and vitamin metabolism, as well as glycan biosynthesis and metabolism (P(Gamma) <0.05). Future studies should assess if these pathways mediate associations of prenatal PFAS exposure with infant or child health outcomes, such as birthweight or vaccine response.PMID:38091497 | DOI:10.1021/acs.est.3c07515

Environ Sci Pollut Res Int. 2023 Dec 13. doi: 10.1007/s11356-023-31285-y. Online ahead of print.ABSTRACTImidacloprid (IM) is a systemic insecticide persistent in the environment and possesses a negative impact on the non-targeted ecosystem. The objective of the present study was to evaluate the dissipation and degradation mechanism of IM residues in grape rhizosphere soil and to investigate its residual effect on soil enzyme activity at different IM spiking levels. The half-life of IM residue in soil was 27, 36, and 43.5 days at a spiking level of 1, 10, and 50 mg kg-1, respectively following a bi-phasic first + first-order dissipation kinetics. UHPLC-Orbitrap™-MS analysis by targeted metabolomics approach revealed that IM metabolites such as IM-amine analogue, guanidine (reduction), 5-hydroxy IM (hydroxylation), IM-Urea (oxidation), reduced NO analogue of IM (oxidation), and olefin of guanidine IM (dehydrogenation) were identified and proposed the degradation mechanism in grape rhizosphere soil. Toxicity of IM residues on five extracellular enzymes, viz., dehydrogenase, acid phosphatase, alkaline phosphatase, β-glucosidase, and urease revealed that activity of dehydrogenase, acid phosphatase, and alkaline phosphatase remained unaffected at 60th day of sampling. The β-glucosidase and urease were negatively affected throughout the incubation period indicating the influence of IM residues on carbon and nitrogen mineralization in soil. Thus, long-term exposure of IM to grape rhizosphere through soil drenching could affect soil enzyme activity which has a negative effect on the soil nutrient cycle and soil microbiome.PMID:38091217 | DOI:10.1007/s11356-023-31285-y

Naunyn Schmiedebergs Arch Pharmacol. 2023 Dec 13. doi: 10.1007/s00210-023-02864-0. Online ahead of print.ABSTRACTNon-alcoholic fatty liver disease (NAFLD) is a hepatic manifestation of metabolic syndrome. Vitamin E (VE) has antioxidant properties and can mediate lipid metabolism. Non-targeted metabolomics technology was employed to uncover comprehensively the metabolome of VE in NAFLD rats. NAFLD model was created with a high-fat and high-cholesterol diet (HFD) in rats. NAFLD rats in the VE group were given 75 mg/(kg day) VE. The metabolites in the serum of rats were identified via UPLC and Q-TOF/MS analysis. KEGG was applied for the pathway enrichment. VE improved the liver function, lipid metabolism, and oxidative stress in NAFLD rats induced by HFD. Based on the metabolite profile data, 132 differential metabolites were identified between VE group and the HFD group, mainly including pyridoxamine, betaine, and bretylium. According to the KEGG results, biosynthesis of cofactors was a key metabolic pathway of VE in NAFLD rats. VE can alleviate NAFLD induced by HFD, and the underlying mechanism is associated with the biosynthesis of cofactors, mainly including pyridoxine and betaine.PMID:38091076 | DOI:10.1007/s00210-023-02864-0

Saudi Pharm J. 2024 Jan;32(1):101897. doi: 10.1016/j.jsps.2023.101897. Epub 2023 Dec 6.ABSTRACTThe steady increase in the use of electronic cigarettes (ECs) has reached an epidemic level, increasing mortality and morbidity, mainly due to pulmonary toxicity. Several mechanisms are involved in EC-induced toxicity, including oxidative stress and increased inflammation. Concurrently, the integrity of cellular metabolism is essential for cellular homeostasis and mitigation of toxic insults. However, the effects of EC on cellular metabolism remain largely unknown. In this study, we investigated the metabolic changes induced by EC in human lung epithelial cells (A549) using an untargeted metabolomics approach. A549 cells were exposed to increasing EC vapor extract concentrations, and cell viability, oxidative stress, and metabolomic changes were assessed. Our findings show that ECs induce cell death and increase oxidative stress in a concentration-dependent manner. Metabolomic studies demonstrated that ECs induce unique metabolic changes in key cellular metabolic pathways. Our results revealed that exposure to ECs induced clear segregation in metabolic responses which is driven significantly by number of essential metabolites such as aminoacids, fatty acids, glutathione, and pyruvate. Interstingly, our metabolomics results showed that each concentration of ECs induced unqiues pattern of metabolic changes, suggesting the complexity of ECs induced cytotoxcity. Disrupted metabolites were linked to essential cellular pathways, such as fatty acid biosynthesis, as well as glutathione, pyruvate, nicotinate and nicotinamide, and amino acid metabolisms. These results highlight the potential adverse effects of ECs on cellular metabolism and emphasize the need for further research to fully understand the long-term consequences of EC use. Overall, this study demonstrates that ECs not only induce cell death and oxidative stress but also disrupt cellular metabolism in A549 lung epithelial cells.PMID:38090735 | PMC:PMC10714235 | DOI:10.1016/j.jsps.2023.101897

Front Immunol. 2023 Nov 28;14:1331366. doi: 10.3389/fimmu.2023.1331366. eCollection 2023.ABSTRACT[This corrects the article DOI: 10.3389/fimmu.2023.1149107.].PMID:38090584 | PMC:PMC10715422 | DOI:10.3389/fimmu.2023.1331366

Int J Nanomedicine. 2023 Dec 8;18:7483-7503. doi: 10.2147/IJN.S436866. eCollection 2023.ABSTRACTPURPOSE: Fatty oil of Descurainia Sophia (OIL) has poor stability and low solubility, which limits its pharmacological effects. We hypothesized that fatty oil nanoparticles (OIL-NPs) could overcome this limitation. The protective effect of OIL-NPs against monocrotaline-induced lung injury in rats was studied.METHODS: We prepared OIL-NPs by wrapping fatty oil with polylactic-polyglycolide nanoparticles (PLGA-NPs) and conducted in vivo and in vitro experiments to explore its anti-pulmonary hypertension (PH) effect. In vitro, we induced malignant proliferation of pulmonary artery smooth muscle cells (RPASMC) using anoxic chambers, and studied the effects of OIL-NPs on the malignant proliferation of RPASMC cells and phospholipase C (PLC)/inositol triphosphate receptor (IP3R)/Ca2+ signal pathways. In vivo, we used small animal echocardiography, flow cytometry, immunohistochemistry, western blotting (WB), polymerase chain reaction (PCR) and metabolomics to explore the effects of OIL-NPs on the heart and lung pathological damage and PLC/IP3R/Ca2+ signal pathway of pulmonary hypertension rats.RESULTS: We prepared fatty into OIL-NPs. In vitro, OIL-NPs could improve the mitochondrial function and inhibit the malignant proliferation of RPASMC cells by inhibiting the PLC/IP3R/Ca2+signal pathway. In vivo, OIL-NPs could reduce the pulmonary artery pressure of rats and alleviate the pathological injury and inflammatory reaction of heart and lung by inhibiting the PLC/IP3R/Ca2+ signal pathway.CONCLUSION: OIL-NPs have anti-pulmonary hypertension effect, and the mechanism may be related to the inhibition of PLC/IP3R/Ca2+signal pathway.PMID:38090366 | PMC:PMC10714987 | DOI:10.2147/IJN.S436866

Mass Spectrom (Tokyo). 2023;12(1):A0138. doi: 10.5702/massspectrometry.A0138. Epub 2023 Dec 8.ABSTRACTNon-targeted metabolome analysis studies comprehensively acquire product ion spectra from the observed ions by the data-dependent acquisition (DDA) mode of tandem mass spectrometry (MS). A DDA dataset redundantly contains closely similar product ion spectra of metabolites commonly existing among the biological samples analyzed in a metabolome study. Moreover, a single DDA data file often includes two or more closely similar raw spectra obtained from an identical precursor ion. The redundancy of product ion spectra has been used to generate an averaged product ion spectrum from a set of similar product ion spectra recorded in a DDA dataset. The spectral averaging improved the accuracy of m/z values and signal-to-noise levels of product ion spectra. However, the origins of redundancy, variations among datasets, and these effects on the spectral averaging procedure needed to be better characterized. This study investigated the nature of the redundancy by comparing the averaging results of eight DDA datasets of non-targeted metabolomics studies. The comparison revealed a significant variation in redundancy among datasets. The DDA datasets obtained by the quadrupole (Q)-Orbitrap-MS datasets had more significant intrafile redundancy than that of the Q-time-of-flight-MS. For evaluating the similarity score between two production spectra, the optimal threshold level of the cosine-product method was approximately 0.8-0.9. Moreover, contamination of biological samples such as plasticizers was another origin of spectral redundancy. The results will be the basis for further development of methods for processing of product ion spectra data. Copyright © 2023 Fumio Matsuda. This is an open-access article distributed under the terms of Creative Commons Attribution Non-Commercial 4.0 International License, which permits use, distribution, and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes. Please cite this article as: Mass Spectrom (Tokyo) 2023; 12(1): A0138.PMID:38090113 | PMC:PMC10713281 | DOI:10.5702/massspectrometry.A0138

Cureus. 2023 Dec 11;15(12):e50318. doi: 10.7759/cureus.50318. eCollection 2023 Dec.ABSTRACTAntibiotic therapy is a cornerstone of modern medicine, yet the development of antibiotic resistance threatens to render these therapies ineffective. The gut microbiota, a complex ecosystem of microorganisms residing in the gastrointestinal tract, plays a critical role in modulating antibiotic efficacy and resistance. This review delves into the intricate relationship between gut microbiota, antibiotic therapy, and resistance and discusses the potential applications of gut microbiota research in guiding personalized antibiotic therapy and resistance mitigation strategies. Recent advancements in metagenomics, metatranscriptomics, and metabolomics have demonstrated the potential for tailored antibiotic regimens that minimize collateral damage to commensal bacteria and reduce the risk of resistance. Adjuvant therapies, such as probiotics, prebiotics, and synbiotics, have shown promise in restoring gut microbial balance and mitigating the adverse effects of antibiotic therapy. We address the challenges associated with this emerging field, including the need for standardized methodologies, ethical considerations, and interdisciplinary collaboration. With continued interdisciplinary collaboration and the implementation of standardized methodologies, gut microbiota research can contribute to the global fight against antibiotic resistance and improve patient outcomes.PMID:38089944 | PMC:PMC10714069 | DOI:10.7759/cureus.50318

Front Plant Sci. 2023 Nov 16;14:1287997. doi: 10.3389/fpls.2023.1287997. eCollection 2023.ABSTRACTINTRODUCTION: Paprika (Capsicum annuum L.) is prone to chilling injury (CI) during low-temperature storage. Although recent findings suggest that CO2 treatment may protect against CI, the effects of short-term CO2 treatment on CI and the underlying molecular mechanisms in paprika remain unknown. Therefore, this study aimed to examine the effect of short-term CO2 treatment on CI and postharvest quality in paprika during storage at cold storage and retail condition at physio-biochemical-molecular level.METHODS: Paprika was treated with 20 and 30% CO2 for 3 h and stored at 4°C for 14 days, followed by additional storage for 2 days at 20°C (retail condition). Fruit quality parameters, including weight loss, firmness, color, and pitting were assessed, and the molecular mechanism of the treatment was elucidated using transcriptomic and metabolomic analyses.RESULTS: Short-term treatment with 20 and 30% CO2 effectively maintained paprika quality during cold storage and retailer conditions, with reduced surface pitting, a common symptom of CI. Additionally, transcriptomic and metabolomic analyses revealed that 20% CO2 treatment induced genes associated with biosynthesis of phosphatidic acid (PA), diacylglycerol, triacylglycerol, and stress response, metabolites associated with phasphatidyl inositol signaling, inositol phosphate metabolism, and starch and sucrose metabolism.CONCLUSION: CO2 treatment activates PA biosynthesis through PLD and PLC-DGK pathways, and induces inositol phosphate, starch, and sucrose metabolism, thereby regulating chilling stress response via the ICE-CBF pathway. These findings suggest that short-term CO2 treatment enhances resistance to cold-induced injury and preserves postharvest quality in non-climacteric fruits, such as paprika, through activation of PA signaling, which improves membrane stability during cold storage and distribution.PMID:38089806 | PMC:PMC10711834 | DOI:10.3389/fpls.2023.1287997

Front Plant Sci. 2023 Nov 28;14:1277762. doi: 10.3389/fpls.2023.1277762. eCollection 2023.ABSTRACTINTRODUCTION: Salt stress is a major constraint affecting crop productivity worldwide. Investigation of halophytes could provide valuable information for improving economically important crops to tolerate salt stress and for more effectively using halophytes to remediate saline environments. Sesuvium portulacastrum L. is a halophyte species widely distributed in tropical and subtropical coastal regions and can absorb a large amount of sodium (Na). This study was to analyze S. portulacastrum responses to salt stress at morphological, physiological, proteomic, and metabolomic levels and pursue a better understanding of mechanisms behind its salt tolerance.METHODS: The initial experiment evaluated morphological responses of S. portulacastrum to different concentrations of NaCl in a hydroponic system, and subsequent experiments compared physiological, proteomic, and metabolomic changes in S. portulacastrum after being exposed to 0.4 M NaCl for 24 h as immediate salt stress (IS) to 14 days as adaptive salt stress (AS). Through these analyses, a working model to illustrate the integrative responses of S. portulacastrum to salt stress was proposed.RESULTS: Plants grown in 0.4 M NaCl were morphologically comparable to those grown in the control treatment. Physiological changes varied in control, IS, and AS plants based on the measured parameters. Proteomic analysis identified a total of 47 and 248 differentially expressed proteins (DEPs) in leaves and roots, respectively. KEGG analysis showed that DEPs, especially those occurring in roots, were largely related to metabolic pathways. Root metabolomic analysis showed that 292 differentially expressed metabolites (DEMs) occurred in IS plants and 371 in AS plants. Among them, 20.63% of upregulated DEMs were related to phenolic acid metabolism.DISCUSSION: Based on the integrative analysis of proteomics and metabolomics, signal transduction and phenolic acid metabolism appeared to be crucial for S. portulacastrum to tolerate salt stress. Specifically, Ca2+, ABA, and JA signalings coordinately regulated salt tolerance in S. portulacastrum. The stress initially activated phenylpropanoid biosynthesis pathway through Ca2+ signal transduction and increased the content of metabolites, such as coniferin. Meanwhile, the stress inhibited MAPK signaling pathway through ABA and JA signal transduction, which promoted Na sequestration into the vacuole to maintain ROS homeostasis and enhanced S. portulacastrum tolerance to salt stress.PMID:38089796 | PMC:PMC10714944 | DOI:10.3389/fpls.2023.1277762

Front Plant Sci. 2023 Nov 27;14:1260429. doi: 10.3389/fpls.2023.1260429. eCollection 2023.ABSTRACTSpaceflight presents a unique environment with complex stressors, including microgravity and radiation, that can influence plant physiology at molecular levels. Combining transcriptomics and proteomics approaches, this research gives insights into the coordination of transcriptome and proteome in Arabidopsis' molecular and physiological responses to Spaceflight environmental stress. Arabidopsis seedlings were germinated and grown in microgravity (µg) aboard the International Space Station (ISS) in NASA Biological Research in Canisters - Light Emitting Diode (BRIC LED) hardware, with the ground control established on Earth. At 10 days old, seedlings were frozen in RNA-later and returned to Earth. RNA-seq transcriptomics and TMT-labeled LC-MS/MS proteomic analysis of cellular fractionates from the plant tissues suggest the alteration of the photosynthetic machinery (PSII and PSI) in spaceflight, with the plant shifting photosystem core-regulatory proteins in an organ-specific manner to adapt to the microgravity environment. An overview of the ribosome, spliceosome, and proteasome activities in spaceflight revealed a significant abundance of transcripts and proteins involved in protease binding, nuclease activities, and mRNA binding in spaceflight, while those involved in tRNA binding, exoribonuclease activity, and RNA helicase activity were less abundant in spaceflight. CELLULOSE SYNTHASES (CESA1, CESA3, CESA5, CESA7) and CELLULOSE-LIKE PROTEINS (CSLE1, CSLG3), involved in cellulose deposition and TUBULIN COFACTOR B (TFCB) had reduced abundance in spaceflight. This contrasts with the increased expression of UDP-ARABINOPYRANOSE MUTASEs, involved in the biosynthesis of cell wall non-cellulosic polysaccharides, in spaceflight. Both transcripts and proteome suggested an altered polar auxin redistribution, lipid, and ionic intracellular transportation in spaceflight. Analyses also suggest an increased metabolic energy requirement for plants in Space than on Earth, hence, the activation of several shunt metabolic pathways. This study provides novel insights, based on integrated RNA and protein data, on how plants adapt to the spaceflight environment and it is a step further at achieving sustainable crop production in Space.PMID:38089794 | PMC:PMC10712242 | DOI:10.3389/fpls.2023.1260429

iScience. 2023 Nov 23;26(12):108546. doi: 10.1016/j.isci.2023.108546. eCollection 2023 Dec 15.ABSTRACTEnvironmental variation selects for the adaptive plasticity of maternal provisioning. Even though developing honeybees find themselves in a protected colony environment, their reproductively specialized queens actively adjust their maternal investment, even among worker-destined eggs. However, the potentially adaptive consequences of this flexible provisioning strategy and their mechanistic basis are unknown. Under natural conditions, we find that the body size of larvae hatching from small eggs in large colonies converges with that of initially larger larvae hatching from large eggs typically produced in small colonies. However, large eggs confer a persistent body size advantage when small and large eggs are cross-fostered in small and large colonies, respectively. We substantiate the increased maternal investment by identifying growth-promoting metabolomes and proteomes in large eggs compared to small eggs, which are primarily enriched in amino acid metabolism and cell maturation. Thus, our study provides a comprehensive adaptive explanation for the worker egg size plasticity of honeybees.PMID:38089582 | PMC:PMC10711493 | DOI:10.1016/j.isci.2023.108546