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BMC Plant Biology Jun 2024Early season carrot (Daucus carota) production is being practiced in Punjab, Pakistan to meet the market demand but high temperature hampers the seed germination and...
Early season carrot (Daucus carota) production is being practiced in Punjab, Pakistan to meet the market demand but high temperature hampers the seed germination and seedling establishment which cause marked yield reduction. Seed priming with potassium nitrate breaks the seed dormancy and improves the seed germination and seedling growth potential but effects vary among the species and ecological conditions. The mechanism of KNO priming in high temperature stress tolerance is poorly understood yet. Thus, present study aimed to evaluate high temperature stress tolerance potential of carrot seeds primed with potassium nitrate and impacts on growth, physiological, and antioxidant defense systems. Carrot seeds of a local cultivar (T-29) were primed with various concentration of KNO (T: unprimed (negative control), T: hydroprimed (positive control), T: 50 mM, T:100mM, T: 150 mM, T: 200 mM, T: 250 mM and T: 300 mM) for 12 h each in darkness at 20 ± 2℃. Seed priming with 50 mM of KNO significantly enhanced the seed germination (36%), seedling growth (28%) with maximum seedling vigor (55%) and also exhibited 16.75% more carrot root biomass under high temperature stress as compared to respective control. Moreover, enzymatic activities including peroxidase, catalase, superoxidase dismutase, total phenolic contents, total antioxidants contents and physiological responses of plants were also improved in response to seed priming under high temperature stress. By increasing the level of KNO, seed germination, growth and root biomass were reduced. These findings suggest that seed priming with 50 mM of KNO can be an effective strategy to improve germination, growth and yield of carrot cultivar (T-29) under high temperature stress in early cropping. This study also proposes that KNO may induces the stress memory by heritable modulations in chromosomal structure and methylation and acetylation of histones that may upregulate the hormonal and antioxidant activities to enhance the stress tolerance in plants.
Topics: Antioxidants; Seedlings; Nitrates; Seeds; Daucus carota; Potassium Compounds; Germination; Hot Temperature
PubMed: 38926658
DOI: 10.1186/s12870-024-05292-1 -
Microbial Biotechnology Jun 2024Pyruvate dehydrogenase (PDH) catalyses the irreversible decarboxylation of pyruvate to acetyl-CoA, which feeds the tricarboxylic acid cycle. We investigated how the loss...
Inactivation of Pseudomonas putida KT2440 pyruvate dehydrogenase relieves catabolite repression and improves the usefulness of this strain for degrading aromatic compounds.
Pyruvate dehydrogenase (PDH) catalyses the irreversible decarboxylation of pyruvate to acetyl-CoA, which feeds the tricarboxylic acid cycle. We investigated how the loss of PDH affects metabolism in Pseudomonas putida. PDH inactivation resulted in a strain unable to utilize compounds whose assimilation converges at pyruvate, including sugars and several amino acids, whereas compounds that generate acetyl-CoA supported growth. PDH inactivation also resulted in the loss of carbon catabolite repression (CCR), which inhibits the assimilation of non-preferred compounds in the presence of other preferred compounds. Pseudomonas putida can degrade many aromatic compounds, most of which produce acetyl-CoA, making it useful for biotransformation and bioremediation. However, the genes involved in these metabolic pathways are often inhibited by CCR when glucose or amino acids are also present. Our results demonstrate that the PDH-null strain can efficiently degrade aromatic compounds even in the presence of other preferred substrates, which the wild-type strain does inefficiently, or not at all. As the loss of PDH limits the assimilation of many sugars and amino acids and relieves the CCR, the PDH-null strain could be useful in biotransformation or bioremediation processes that require growth with mixtures of preferred substrates and aromatic compounds.
Topics: Pseudomonas putida; Catabolite Repression; Pyruvate Dehydrogenase Complex; Hydrocarbons, Aromatic; Biodegradation, Environmental; Acetyl Coenzyme A; Pyruvic Acid; Gene Deletion; Metabolic Networks and Pathways
PubMed: 38923400
DOI: 10.1111/1751-7915.14514 -
Toxics Jun 2024The associations between VOCs and sex hormones in adolescents remain unclear, and the role of serum albumin in these associations deserves to be explored. We conducted...
The associations between VOCs and sex hormones in adolescents remain unclear, and the role of serum albumin in these associations deserves to be explored. We conducted cross-sectional analyses using generalized linear models (GLMs), weighted quantile sum (WQS) regression, and mediation analysis, based on data from 584 adolescents from the National Health and Nutrition Examination Survey (NHANES). The GLM analyses revealed that seven kinds of mVOCs potentially affected sex hormone levels. According to the WQS regression results, 2-aminothiazoline-4-carboxylic acid (ATCA) was the major contributor to the significant associations of mixed mVOC exposure with testosterone, estradiol, and free androgen index in males; N-acetyl-S-(N-methylcarbamoyl)-L-cysteine (AMCC) was the major contributor to the significant associations of mixed mVOC exposure with sex hormone-binding globulin in males; and N-acetyl-S-(benzyl)-L-cysteine (BMA) was the major contributor to the significant associations of mixed mVOC exposure with the ratio of testosterone to estradiol in females. Moreover, serum albumin could mediate up to 9.2% of the associations between mixed exposure to mVOCs and sex hormones. Our findings could provide a reference for studies on the mechanisms underlying the effects of VOCs on sex hormones in adolescents and emphasize the necessity of reducing exposure to ATCA, AMCC, BMA, and their parent compounds.
PubMed: 38922118
DOI: 10.3390/toxics12060438 -
Marine Drugs Jun 2024To promote the bioconversion of marine chitin waste into value-added products, we expressed a novel pH-stable -derived chitinase, Chi1, in and subsequently purified,...
To promote the bioconversion of marine chitin waste into value-added products, we expressed a novel pH-stable -derived chitinase, Chi1, in and subsequently purified, characterized, and evaluated it for its chitin-converting capacity. Our results indicated that Chi1 is of the glycoside hydrolase (GH) family 18 with a molecular weight of approximately 57 kDa, consisting of a GH18 catalytic domain and a cellulose-binding domain. We recorded its optimal activity at pH 5.0 and 55 °C. It exhibited excellent stability in a wide pH range of 3.0-10.0. Mg (5 mM), and dithiothreitol (10 mM) significantly promoted Chi1 activity. Chi1 exhibited broad substrate specificity and hydrolyzed chitin, chitosan, cellulose, soluble starch, and -acetyl chitooligosaccharides with polymerization degrees ranging from three to six. Moreover, Chi1 exhibited an endo-type cleavage pattern, and it could efficiently convert colloidal chitin into -acetyl-D-glucosamine (GlcNAc) and (GlcNAc) with yields of 227.2 and 505.9 mg/g chitin, respectively. Its high chitin-degrading capacity and exceptional pH tolerance makes it a promising tool with potential applications in chitin waste treatment and bioactive oligosaccharide production.
Topics: Chitinases; Chitin; Hydrogen-Ion Concentration; Substrate Specificity; Micromonospora; Hydrolysis; Escherichia coli; Chitosan; Enzyme Stability
PubMed: 38921598
DOI: 10.3390/md22060287 -
Marine Drugs Jun 2024, a filamentous fungus widely distributed across terrestrial and marine environments, can produce a diverse array of natural products, including alkaloids, polyketones,...
, a filamentous fungus widely distributed across terrestrial and marine environments, can produce a diverse array of natural products, including alkaloids, polyketones, and polyketide-terpenoids. Among these, chrodrimanins represented a typical class of natural products. In this study, we isolated three previously undescribed pentaketide-sesquiterpenes, 8,9--chrodrimanins (-), along with eight known compounds (-). The structures of compounds - were elucidated using nuclear magnetic resonance (NMR) and mass spectrometry (MS), while their absolute configurations were determined through X-ray crystallography and electronic circular dichroism (ECD) computations. The biosynthetic pathways of compounds - initiate with 6-hydroxymellein and involve multiple stages of isoprenylation, cyclization, oxidation, and acetylation. We selected four strains of gastrointestinal cancer cells for activity evaluation. We found that compound selectively inhibited MKN-45, whereas compounds and exhibited no significant inhibitory activity against the four cell lines. These findings suggested that 8,9--chrodrimanins could serve as scaffold compounds for further structural modifications, potentially leading to the development of targeted therapies for gastric cancer.
Topics: Talaromyces; Humans; Cell Line, Tumor; Antineoplastic Agents; Crystallography, X-Ray; Biological Products; Aquatic Organisms; Magnetic Resonance Spectroscopy; Polyketides; Molecular Structure
PubMed: 38921585
DOI: 10.3390/md22060274 -
Metabolites Jun 2024Acetate is an important metabolite in metabolic fluxes. Its presence in biological entities originates from both exogenous inputs and endogenous metabolism. Because the...
Acetate is an important metabolite in metabolic fluxes. Its presence in biological entities originates from both exogenous inputs and endogenous metabolism. Because the change in blood acetate level has been associated with both beneficial and adverse health outcomes, blood acetate analysis has been used to monitor the systemic status of acetate turnover. The present study examined the use of urinary -acetyltaurine (NAT) as a marker to reflect the hyperacetatemic status of mice from exogenous inputs and endogenous metabolism, including triacetin dosing, ethanol dosing, and streptozotocin-induced diabetes. The results showed that triacetin dosing increased serum acetate and urinary NAT but not other -acetylated amino acids in urine. The co-occurrences of increased serum acetate and elevated urinary NAT were also observed in both ethanol dosing and streptozotocin-induced diabetes. Furthermore, the renal cortex was determined as an active site for NAT synthesis. Overall, urinary NAT behaved as an effective marker of hyperacetatemia in three experimental mouse models, warranting further investigation into its application in humans.
PubMed: 38921457
DOI: 10.3390/metabo14060322 -
Journal of Fungi (Basel, Switzerland) May 2024The acetylation of histone lysine residues regulates multiple life processes, including growth, conidiation, and pathogenicity in filamentous pathogenic fungi. However,...
The acetylation of histone lysine residues regulates multiple life processes, including growth, conidiation, and pathogenicity in filamentous pathogenic fungi. However, the specific function of each lysine residue at the N-terminus of histone H3 in phytopathogenic fungi remains unclear. In this study, we mutated the N-terminal lysine residues of histone H3 in , the main causal agent of Fusarium crown rot of wheat in China, which also produces deoxynivalenol (DON) toxins harmful to humans and animals. Our findings reveal that all the FpH3, FpH3, FpH3, and FpH3 mutants are vital for vegetative growth and conidiation. Additionally, FpH3K14 regulates the pathogen's sensitivity to various stresses and fungicides. Despite the slowed growth of the FpH3 and FpH3 mutants, their pathogenicity towards wheat stems and heads remains unchanged. However, the FpH3 mutant produces more DON. Furthermore, the FpH3 and FpH3 mutants exhibit significantly reduced virulence, with the FpH3 mutant producing minimal DON. In the FpH3, FpH3, FpH3, and FpH3 mutants, there are 1863, 1400, 1688, and 1806 downregulated genes, respectively, compared to the wild type. These downregulated genes include many that are crucial for growth, conidiation, pathogenicity, and DON production, as well as some essential genes. Gene ontology (GO) enrichment analysis indicates that genes downregulated in the FpH3 and FpH3 mutants are enriched for ribosome biogenesis, rRNA processing, and rRNA metabolic process. This suggests that the translation machinery is abnormal in the FpH3 and FpH3 mutants. Overall, our findings suggest that H3 N-terminal lysine residues are involved in regulating the expression of genes with important functions and are critical for fungal development and pathogenicity.
PubMed: 38921366
DOI: 10.3390/jof10060379 -
Open Biology Jun 2024is the predominant mould pathogen for humans. Adaption to host-imposed iron limitation has previously been demonstrated to be essential for its virulence. [2Fe-2S]...
is the predominant mould pathogen for humans. Adaption to host-imposed iron limitation has previously been demonstrated to be essential for its virulence. [2Fe-2S] clusters are crucial as cofactors of several metabolic pathways and mediate cytosolic/nuclear iron sensing in fungi including . [2Fe-2S] cluster trafficking has been shown to involve BolA family proteins in both mitochondria and the cytosol/nucleus. Interestingly, both homologues, termed Bol1 and Bol3, possess mitochondrial targeting sequences, suggesting the lack of cytosolic/nuclear versions. Here, we show by the combination of mutational, proteomic and fluorescence microscopic analyses that expression of the Bol3 encoding gene leads to dual localization of gene products to mitochondria and the cytosol/nucleus via alternative translation initiation downstream of the mitochondrial targeting sequence, which appears to be highly conserved in various species. Lack of either mitochondrial Bol1 or Bol3 was phenotypically inconspicuous while lack of cytosolic/nuclear Bol3 impaired growth during iron limitation but not iron sensing which indicates a particular importance of [2Fe-2S] cluster trafficking during iron limitation. Remarkably, cytosolic/nuclear Bol3 differs from the mitochondrial version only by N-terminal acetylation, a finding that was only possible by mutational hypothesis testing.
Topics: Aspergillus fumigatus; Fungal Proteins; Cytosol; Mitochondria; Iron; Adaptation, Physiological; Cell Nucleus; Protein Transport; Proteomics; Iron-Sulfur Proteins; Gene Expression Regulation, Fungal; Acetylation
PubMed: 38919062
DOI: 10.1098/rsob.240033 -
Journal of Translational Medicine Jun 2024Sorafenib resistance is becoming increasingly common and disadvantageous for hepatocellular carcinoma (HCC) treatment. Ferroptosis is an iron dependent programmed cell...
BACKGROUND
Sorafenib resistance is becoming increasingly common and disadvantageous for hepatocellular carcinoma (HCC) treatment. Ferroptosis is an iron dependent programmed cell death underlying the mechanism of sorafenib. Iron is crucial for synthesis of cofactors essential to mitochondrial enzymes and necessary for HCC proliferation, while mitochondrial iron overload and oxidative stress are associated with sorafenib induced ferroptosis. However, the crosstalk among iron homeostasis and sorafenib resistance is unclear.
METHODS
We conducted bioinformatics analysis of sorafenib treated HCC datasets to analyze GCN5L1 and iron related gene expression with sorafenib resistance. GCN5L1 deleted HCC cell lines were generated by CRISPR technology. Sorafenib resistant HCC cell line was established to validate dataset analysis and evaluate the effect of potential target.
RESULTS
We identified GCN5L1, a regulator of mitochondrial acetylation, as a modulator in sorafenib-induced ferroptosis via affecting mitochondrial iron homeostasis. GCN5L1 deficiency significantly increased sorafenib sensitivity in HCC cells by down-regulating mitochondrial iron transporters CISD1 expression to induce iron accumulation. Mitochondrial iron accumulation leads to an acceleration in cellular and lipid ROS. Sorafenib resistance is related to CISD1 overexpression to release mitochondrial iron and maintaining mitochondrial homeostasis. We combined CISD1 inhibitor NL-1 with sorafenib, which significantly enhanced sorafenib-induced ferroptosis by promoting mitochondrial iron accumulation and lipid peroxidation. The combination of NL-1 with sorafenib enhanced sorafenib efficacy in vitro and in vivo.
CONCLUSIONS
Our findings demonstrate that GCN5L1/CISD1 axis is crucial for sorafenib resistance and would be a potential therapeutic strategy for sorafenib resistant HCC.
Topics: Sorafenib; Carcinoma, Hepatocellular; Liver Neoplasms; Iron; Humans; Homeostasis; Mitochondria; Cell Line, Tumor; Animals; Ferroptosis; Drug Resistance, Neoplasm; Mice, Nude; Reactive Oxygen Species; Mice; Gene Expression Regulation, Neoplastic
PubMed: 38918793
DOI: 10.1186/s12967-024-05404-3 -
Biomedical Engineering Online Jun 2024Diabetic retinopathy (DR) is an eye disease that causes blindness and vision loss in diabetic. Risk factors for DR include high blood glucose levels and some... (Review)
Review
Diabetic retinopathy (DR) is an eye disease that causes blindness and vision loss in diabetic. Risk factors for DR include high blood glucose levels and some environmental factors. The pathogenesis is based on inflammation caused by interferon and other nuclear proteins. This review article provides an overview of DR and discusses the role of nuclear proteins in the pathogenesis of the disease. Some core proteins such as MAPK, transcription co-factors, transcription co-activators, and others are part of this review. In addition, some current advanced treatment resulting from the role of nuclear proteins will be analyzes, including epigenetic modifications, the use of methylation, acetylation, and histone modifications. Stem cell technology and the use of nanobiotechnology are proposed as promising approaches for a more effective treatment of DR.
Topics: Diabetic Retinopathy; Humans; Nuclear Proteins; Animals; Epigenesis, Genetic
PubMed: 38918766
DOI: 10.1186/s12938-024-01258-4