Regulation Of Metabolic Pathways Research Articles

Modulation of virulence and metabolic profiles in Klebsiella pneumoniae under indole-mediated stress response

Indole, a crucial bacterial signaling molecule, plays a fundamental role in regulating various physiological processes within bacteria, including growth, acid tolerance, biofilm development, motility, and other cellular functions. Its regulatory influence extends beyond indole-producing bacteria, significantly impacting the physiological activities in non-indole-producing species. In this study, we demonstrate that indole enhances the pathogenicity and viability of Klebsiella pneumoniae using the Galleria mellonella infection model and serum killing assay. Concurrently, indole has varying effects on biofilm formation in K. pneumoniae, with some strains showing enhanced biofilm formation ability. To elucidate the underlying molecular mechanisms, transcriptome analysis revealed that indole exposure in K. pneumoniae led to the upregulation of genes associated with pili formation and iron acquisition systems, while simultaneously inducing oxidative stress responses. Additionally, our analysis uncovered extensive metabolic remodeling. Specifically, we observed significant upregulation of genes involved in simple carbohydrate utilization pathways, including those responsible for galactose, mannose, and maltose metabolism, as well as enhanced expression of genes associated with pyrimidine biosynthesis. These findings collectively indicate that indole enhances the intestinal colonization and pathogenicity of K. pneumoniae primarily by modulation of fimbriae expression and metabolic pathway regulation.

The molecular code of kidney cancer: A path of discovery for gene mutation and precision therapy.

Renal cell carcinoma (RCC) is a malignant tumor with highly heterogeneous and complex molecular mechanisms. Through systematic analysis of TCGA, COSMIC and other databases, 24 mutated genes closely related to RCC were screened, including VHL, PBRM1, BAP1 and SETD2, which play key roles in signaling pathway transduction, chromatin remodeling and DNA repair. The PI3K/AKT/mTOR signaling pathway is particularly important in the pathogenesis of RCC. Mutations in genes such as PIK3CA, MTOR and PTEN are closely associated with metabolic abnormalities and tumor cell proliferation. Clinically, mTOR inhibitors and VEGF-targeted drugs have shown significant efficacy in personalized therapy. Abnormal regulation of metabolic reprogramming, especially glycolysis and glutamine metabolic pathways, provides tumor cells with continuous energy supply and survival advantages, and GLS1 inhibitors have shown promising results in preclinical studies. This paper also explores the potential of immune checkpoint inhibitors in combination with other targeted drugs, as well as the promising application of nanotechnology in drug delivery and targeted therapy. In addition, unique molecular mechanisms are revealed and individualized therapeutic strategies are explored for specific subtypes such as TFE3, TFEB rearrangement type and SDHB mutant type. The review summarizes the common gene mutations in RCC and their molecular mechanisms, emphasizes their important roles in tumor diagnosis, treatment and prognosis, and looks forward to the application prospects of multi-pathway targeted therapy, metabolic targeted therapy, immunotherapy and nanotechnology in RCC treatment, providing theoretical support and clinical guidance for individualized treatment and new drug development.

Oocyte transcriptomes and follicular fluid proteomics of ovine atretic follicles reveal the underlying mechanisms of oocyte degeneration

BackgroundIn mammals, female fertility is influenced by the result of follicular development (ovulation or atresia). Follicular atresia is a complex physiological process that results in the degeneration of oocytes from the ovary. However, the molecular mechanisms of oocyte degeneration and key protein markers of follicular atresia remain unclear. In this study, we investigated the complex transcriptional regulatory mechanisms and protein profiles in oocytes and follicular fluid in atretic follicle stages using single-cell RNA sequencing and tandem mass tag proteomics.ResultsFirst, through paired analysis of different follicle development stages, we identified 175 atresia-specific genes and eight candidate oocyte-secreted factors, including PKG1, YTHDF2, and MYC. Meanwhile, we also characterized unique features of the oocyte transcriptional landscape in the atretic follicle stage that displayed cell death-related transcriptional changes and mechanisms, such as autophagy (TBK1 and IRS4), necroptosis (PKR), and apoptosis (MARCKS). Moreover, we identified atresia-specific genes, namely FTH1, TF, and ACSL4, which may participate in regulation of oocyte ferroptosis in atretic follicles through a series of mechanisms including ferritinophagy, ferritin transport, and lipid metabolism. Additionally, we uncovered 333 differentially expressed proteins that may coordinate follicular atresia and revealed key pathways, such as negative regulation of angiogenesis, metabolic pathways, and transcription and mRNA splicing, that lead to oocyte degeneration. Finally, by combining transcriptome and proteomics analyses, we identified two oocyte-secreted biomarkers, PGK1 and ANGPT2, that may be associated with follicular atresia.ConclusionsIn conclusion, our work offers a thorough characterization of oocyte transcription mechanism and follicular fluid protein changes in ovine atretic follicles, which offers a crucial reference for analyzing the mechanism of follicular atresia and establishing an oocyte quality assessment system in sheep.

Lysine acetylation modulates drought stress responses in birch (Betula platyphylla) through metabolic and transcriptional pathway regulation.

Acetylation modifies protein subcellular localization, stability, enzymatic activity, and protein-protein and protein-DNA interactions, playing a crucial role in mediating protein function. However, research on non-histone acetylation remains limited. This study investigates changes in lysine acetylation (Kac) in proteins of birch (Betula platyphylla) in response to drought using 4D label-free quantitative lys-acetylproteome analysis. We identified a total of 15 064 acetylated peptides across 4393 proteins, with 2486 Kac sites exhibiting significant changes: 246 prteins showed increased Kac levels, while 1406 displayed reductions. Notably, proteins associated with metabolic pathways, such as nucleotide sugar biosynthesis, proteasome, glutamate decarboxylase and the tricarboxylic acid (TCA) cycle, were significantly impacted. The alterations in Kac levels correlated with various KEGG pathways, suggesting that acetylation plays a regulatory role in drought response mechanisms. Furthermore, we identified specific acetylation sites in transcription factors (TFs), highlighting their involvement in this process. Functional validation demonstrated that mutations in Kac sites of five randomly selected TFs resulted in significant changes in drought tolerance, emphasizing the critical role of lysine acetylation in modulating stress responses. Overall, our findings indicate that Kac modification serves as a key regulatory mechanism in birch adaptation to drought stress, influencing both metabolic processes and transcriptional regulation.

Effect of glyphosate on renal function: A study integrating epidemiological and experimental evidence.

Glyphosate, a widely used herbicide globally, has prompted concerns regarding its potential health impacts. This study aimed to explore the link between glyphosate exposure and renal function by combining NHANES, a zebrafish model, and metabolomics. A cross-sectional analysis of 2013-2014 NHANES data investigated the relationship between glyphosate exposure and renal function [albumin-to-creatinine ratio (ACR) and estimated glomerular filtration rate (eGFR)]. A subsequent zebrafish experiment was conducted to verify this association. Embryos (0.75 hpf-96 hpf) were exposed to different glyphosate concentrations dissolved in water (0, 30, 60, 90, 120 μg/mL). The underlying mechanism of the association between glyphosate and renal function was explored by the real-time quantitative polymerase chain reaction (RT-qPCR) and non-targeted metabolomics analysis [embryos (0.75 hpf-96 hpf) were exposed to 90 μg/mL glyphosate]. 1170 participants were enrolled in the NHANES study. The NHANES-based study found a positive association between glyphosate and ACR [0.07 (0.01, 0.13)]. Higher urinary glyphosate levels, particularly in the third quartile group, were negatively linked to eGFR [-3.72 (-5.98, -1.46)]. Further zebrafish experiments indicated that zebrafish exposed to 90 μg/mL glyphosate exhibited increased mortality rates, higher fluorescence intensity, up-regulated the havcr1 expression level, and cystic dilatation of the kidney. Non-targeted metabolomics analysis identified differential metabolites (e.g., 5-Hydroxyindole acetic acid) and pathways (e.g., ABC transporters) influenced by glyphosate. Glyphosate exposure is negatively associated with renal function in community adults. The damage to the kidneys caused by glyphosate may be mediated through the regulation of metabolic pathways, and the specific mechanisms require further experimental investigation.

24-epibrassinolide regulates oxytetracycline-induced phytotoxicity and its detoxification mechanism.

Oxytetracycline (OTC), a crop-absorbable antibiotic, poses a health risk to humans through the food chain. Conversely, 24-epibrassinolide (EBL), a plant growth hormone, mitigates the toxic effects of various pollutants on plants. However, the mechanism by which exogenous EBL affects the growth of rape seedlings exposed to OTC remains largely unknown. In this study, we found that environmental OTC concentrations significantly inhibited plant growth and metabolism, whereas exogenous EBL could restore plant growth characteristics. Exogenous EBL significantly decreased reactive oxygen species (ROS) accumulation, alleviating OTC-induced cell membrane lipid peroxidation. This was achieved by increasing the antioxidant capacity and secondary metabolism levels. Notably, our findings suggested that EBL stimulated glutathione S-transferase (GST) and glutathione reductase (GR) activities, enhancing reduced glutathione synthesis and participating in plant OTC detoxification. OTC residues in EBL + OTC-treated seedlings at 21 d were significantly reduced by 29 % compared with OTC alone. Further transcriptomic and metabolomic analyses revealed that the differentially expressed genes and metabolites in the EBL and OTC alone or combined treatment groups were primarily involved in the regulation of phenylpropanoid biosynthesis, glutathione metabolism, and lant hormone signal transduction pathways in response to phytotoxic effects and detoxification mechanisms, as compared to the control group.

Different expression of circulating microRNA profile in tibetan OSAHS with metabolic syndrome patients

Recent empirical investigations reinforce the understanding of a profound interconnection between metabolic functions and Obstructive Sleep Apnea-hypopnea Syndrome (OSAHS). This study identifies distinctive miRNA signatures in OSAHS with Metabolic Syndrome (Mets) patients from healthy subjects, that could serve as diagnostic biomarkers or describe differential molecular mechanisms with potential therapeutic implications. In this study, OSAHS with MetS patients showed significantly higher Apnea Hyponea Index(AHI), but lower oxygen desaturation index(ODI 4/h) and minimum pulse oxygen saturation(SpO2). A total of 33 differentially expressed miRNAs by Limma method, and 31 differentially expressed miRNAs by DEseq2 method were screened. In addition, GO enrichment analysis of target genes associated with differentially expressed miRNAs revealed significant enrichment in metabolic processes, suggesting that the differential expression of OSAHS-induced miRNAs may contribute to the progression of metabolic disorders through the regulation of metabolic pathways. Furthermore, KEGG pathway enrichment analysis revealed significant enrichment in the p53 signaling pathway and several other pathways. Notably, the Wnt signaling pathway, PI3K-Akt signaling pathway, cAMP signaling pathway, and AMPK signaling pathway are implicated in the metabolic processes of glucose dysregulation and lipid homeostasis, as well as the pathogenesis of hypertension associated with OSAHS. We identified IKBKB, PIK3R1, and MAP2K1 as the target genes most associated with Mets pathogenesis in OSAHS, regulated by miR-503-5p, miR-497-5p, and miR-497-5p, respectively. Additionally, the target genes of differentially expressed miRNAs between Tibetan OSAHS patients with MetS and healthy individuals are regulated by transcription factors such as NR2C1, STAT3, STAT5a, HIF1a, ETV4, NANOG, RELA, SP1, E2F1, NFKB1, AR, and MYC. In conlusion, we found differentially expressed miRNAs in Tibetan OSAHS patients with Metabolic Syndrome for the first time. Enrichment analysis results suggest that differentially expressed miRNAs may involved in the development of OSAHS-related metabolic disorders by regulating metabolic pathways. We also revealed that IKBKB, PIK3R1, and MAP2K1 are mostly associated with metabolic disorder in OSAHS, and miR-503-5p and miR-497-5p may regulate the development of MetS associated with OSAHS by modulating IKBKB, PIK3R1, and MAP2K1.

The (un)known crosstalk between metabolism and mechanotransduction: Implications for metabolic syndrome (MetS)-associated neurological complications.

Metabolic syndrome (MetS) has been associated with disruptions in tissue mechanical homeostasis and inflammatory and metabolic derangements. However, the direct correlation between metabolic alterations and changes in tissue stiffness, and whether they could play a role as upstream initiators of disease pathology remains to be investigated. This emerging concept has yet to be put into clinical practice as many questions concerning the interplay between extracellular matrix mechanical properties and regulation of metabolic pathways remain unsolved. This review will highlight key foundational studies examining mutual regulation of cell metabolism and mechanotransduction, and opening questions lying ahead for better understanding MetS pathophysiology.

Smu_1558c-mediated regulation of growth and biofilm formation in Streptococcus mutans.

Streptococcus mutans is a key etiological agent in dental caries, owing to its strong ability to form biofilms through carbohydrate fermentation. Protein acetylation, facilitated by GNAT family acetyltransferases, plays a critical regulatory role in bacterial physiology, but its impact on S. mutans remains largely unexplored. In this study, we investigated the role of the GNAT family acetyltransferase encoded by smu_1558c in regulating the growth and biofilm formation of S. mutans. The deletion of smu_1558c resulted in impaired growth, reduced biofilm formation, and diminished synthesis of water-insoluble extracellular polysaccharides (EPS). Proteomic analysis revealed 166 differentially expressed proteins in the deletion mutant, with significant enrichment in pathways related to carbohydrate transport and metabolism, and translation. Notably, glucosyltransferases GtfB and GtfC, key enzymes in biofilm formation, were significantly downregulated in the deletion mutant, while ClpL, a Clp-like ATP-dependent protease involved in protein homeostasis under stress conditions, was highly upregulated. These findings highlight that acetyltransferase smu_1558c plays a crucial role in the growth, biofilm formation, and EPS synthesis of S. mutans through its regulation of carbohydrate transport and metabolism pathways, as well as stress response mechanisms. This study provides novel insights into the molecular mechanisms governing S. mutans pathogenicity and suggests potential therapeutic targets for caries prevention.

Vaccinia growth factor-dependent modulation of the mTORC1-CAD axis upon nutrient restriction.

The molecular mechanisms by which vaccinia virus (VACV), the prototypical member of the poxviridae family, reprograms host cell metabolism remain largely unexplored. Additionally, cells sense and respond to fluctuating nutrient availability, thereby modulating metabolic pathways to ensure cellular homeostasis. Understanding how VACV modulates metabolic pathways in response to nutrient signals is crucial for understanding viral replication mechanisms, with the potential for developing antiviral therapies. In this study, we establish the importance of de novo pyrimidine synthesis during VACV infection. We report the significance of vaccinia growth factor (VGF), a viral early protein and a homolog of cellular epidermal growth factor (EGF), in enabling VACV to phosphorylate the key enzyme CAD of the de novo pyrimidine pathway at serine 1859, a site known to positively regulate CAD activity. Although nutrient-poor conditions typically inhibit mTORC1 activation, VACV activates CAD via the mTORC1-S6K1 signaling axis in a VGF-dependent manner, especially upon glutamine and asparagine limitation. However, unlike its cellular homolog EGF, the VGF peptide alone, in the absence of VACV infection, has minimal ability to activate CAD. This suggests the involvement of other viral factors yet to be identified. Our research provides a foundation for understanding the regulation of a significant metabolic pathway, de novo pyrimidine synthesis during VACV infection, shedding new light on viral regulation under distinct nutritional environments. This study not only has the potential to contribute to the advancement of antiviral treatments but also improve the development of VACV as an oncolytic agent and vaccine vector.IMPORTANCEViruses often reprogram host cell metabolism to facilitate replication. How poxviruses, such as the prototype member, vaccinia virus (VACV), modulate host cell metabolism is not well understood. Understanding how VACV affects these metabolic pathways is key to learning about viral replication and developing antiviral treatments. This study highlights the importance of de novo pyrimidine synthesis during VACV infection. We found that the vaccinia growth factor (VGF), a viral protein similar to the cellular epidermal growth factor (EGF), helps VACV activate the enzyme CAD of the de novo pyrimidine pathway. Upon nutrient limitation, VGF is needed for the activation of CAD through mTORC1-S6K signaling. VGF peptide alone is unable to activate this pathway independent of infection, suggesting the involvement of other viral factor(s). Our research not only sheds light on how VACV regulates metabolism but also holds promise for improving VACV as a cancer treatment and vaccine.

The Entry of Pollinating Fig Wasps Plays a Pivotal Role in the Developmental Phase and Metabolic Expression Changes in Ficus hookeriana Figs

The fig (the syconium of the Ficus tree) and its pollinating fig wasp represent exceptional examples for researching plant–insect interactions due to their remarkable specificity in species interaction and mutually beneficial symbiotic relationship. However, the mechanisms underlying the developmental process of monoecious figs in response to the entry of pollinating fig wasps (pollinators) and the metabolic changes occurring during this process remain elusive. Our study employed a combination of controlled experiments in the field and LC-MS methods to investigate the impact of pollinating fig wasp entry on the developmental phase of figs, as well as the metabolic alterations occurring during this process. A total of 381 metabolites and 155 differential metabolites were identified, with the predominant classes of metabolites being organic acids, lipids, and benzene aromatic compounds. The results suggest that in the absence of wasp entry, the receptive phase of fig would exhibit an extended duration. However, upon the entry of fig wasps, the receptive phase of figs would terminate within a span of 1 to 2 days, concomitant with substantial fluctuations in the composition and proportions of metabolites within the fig. Our research focuses on the analysis of linoleic acid metabolism, phenylpropanoid biosynthesis, and flavonoid biosynthesis pathways. Our findings suggest that the entry of wasps triggers alterations in the metabolic regulatory mechanisms of figs. Prior to wasp entry, metabolites primarily regulate fig growth and development. However, after wasp entry, metabolites predominantly govern lipid accumulation and the establishment of defense mechanisms, indicating a transition in fig development. This metabolic perspective explains why figs promptly enter an interflower phase that is not attractive to pollinating fig wasps after their entry, and how figs achieve reproductive balance through the regulation of different metabolic pathways. This study provides scientific evidence for elucidating the stability mechanism of the fig wasp mutualistic system.

The effects of Fraxini cortex and Andrographis herba on Escherichia coli-induced diarrhea in chicken.

Escherichia coli (E. coli) is a type of pathogenic bacteria that often causes diarrhea in poultry. While antibiotics can control E. coli-induced diarrhea in chickens, it can lead the ongoing proliferation of antibiotic resistance. Traditional Chinese medicines (TCMs) that effectively protect against and treat chicken diarrhea caused by E. coli are an encouraging alternative. That enhance poultry immunity, curtail antibiotic resistance, and provide a secure, eco-friendly, and efficacious option for the livestock and poultry industry. In this study, the model of chicken diarrhea induced by E. coli was established, and different TCM formulas were used for treatment, and finally the formula with the best effect was screened out. The research also investigated the impact of these formulas on gut microbiota and serum metabolites in chickens, using 16S rRNA sequencing technology and metabolomics. Mass spectrometry technology and network pharmacology were used to analyze the optimal TCM formula corroborated by molecular docking and qPCR for further explore mechanism exploration. The findings indicated that Fraxini cortex and Andrographis herba dramatically lowered mortality rates and alleviated pathologic changes in cases of avian E. coli diarrhea (P < 0.05). Fraxini cortex and Andrographis herba significantly boosted the abundance of Bacteroidetes (P < 0.05) and mainly enhanced cysteine and methionine metabolic pathways. Moreover, 97 active ingredients in Fraxini cortex and Andrographis herba were identified, along with 1425 diarrhea-related targets, primarily enriched in the MAPK signaling pathway. Molecular docking and qPCR revealed that the crucial active ingredients in Fraxini cortex and Andrographis herba bonded effectively with disease targets and treated diarrhea by regulating the MAPK signaling pathway. This suggests that Fraxini cortex and Andrographis herba exerts an optimal effect on diarrhea by multi-target and multi-pathway regulation of metabolic pathways and gut microbiota.

Linking microRNA to metabolic reprogramming and gut microbiota in the pathogenesis of colorectal cancer (Review).

Colorectal cancer (CRC), an emerging public health concern, is one of the leading causes of cancer morbidity and mortality worldwide. An increasing body of evidence shows that dysfunction in metabolic reprogramming is a crucial characteristic of CRC progression. Specifically, metabolic reprogramming abnormalities in glucose, glutamine and lipid metabolism provide the tumour with energy and nutrients to support its rapid cell proliferation and survival. More recently, microRNAs (miRNAs) appear to be involved in the pathogenesis of CRC, including regulatory roles in energy metabolism. In addition, it has been revealed that dysbiosis in CRC might play a key role in impairing the host metabolic reprogramming processes, and while the exact interactions remain unclear, the link may lie with miRNAs. Hence, the aims of the current review include first, to delineate the metabolic reprogramming abnormalities in CRC; second, to explain how miRNAs mediate the aberrant regulations of CRC metabolic pathways; third, linking miRNAs with metabolic abnormalities and dysbiosis in CRC and finally, to discuss the roles of miRNAs as potential biomarkers.

PbMYB5 transcription factor plays a role in regulating anthocyanin biosynthesis in pear (Pyrus bretschneideri Rehd) skin.

The phenylacetone pathway, which encompasses flavonoids, lignin, and other compounds, is of paramount importance in determining the quality of pear fruit. Nevertheless, the precise regulatory functions of R2R3-MYB transcription factors in the metabolic pathways that regulate pear color changes remain unclear. In this study, we isolated an R2R3-PbMYB5(PbMYB5) transcription factor from 'Red Zaosu' pears and demonstrated that it influenced the expression of several genes, including PbCAD1, PbF5H, PbLAR, PbANR, and PbUFGT. The overexpression of PbMYB5 resulted in a notable elevation in anthocyanin concentration within the pear epidermis. Further research has shown that PbMYB5 is able to bind to PbANS and also has interactions with PbbHLH3 and PbbHLH33.We proposed that PbMYB5 forms a complex with PbbHLH3, PbbHLH33, and PbWD40 to activate PbANS and promote anthocyanin accumulation. This study offers new insights into the regulation of various metabolic pathways that impact fruit coloration.

Molecular Mechanisms and Therapeutic Potential of Mulberry Fruit Extract in High-Fat Diet-Induced Male Reproductive Dysfunction: A Comprehensive Review.

High-fat diet (HFD)-induced obesity represents a significant challenge to male reproductive health, affecting approximately 13% of the global adult population. This comprehensive review synthesizes current evidence regarding mulberry (Morus alba L.) fruit extract's therapeutic potential for HFD-induced male reproductive dysfunction. Through comprehensive analysis of the peer-reviewed literature from multiple databases (PubMed, Web of Science, Scopus, and Google Scholar; 2005-2024), we evaluated mulberry extract's effects on testicular morphology, spermatogenesis, sperm parameters, and the underlying molecular mechanisms. Mechanistic studies reveal that standardized mulberry extract mediates protective effects through multiple pathways: enhanced antioxidant enzyme activities (SOD: +45%, Catalase: +38%, GPx: +35%), reduced inflammatory markers (TNF-α: -64%, IL-6: -58%), and modulated NF-κB signaling (-42.3%). These effects are facilitated by mulberry's rich phytochemical profile, particularly anthocyanins (2.92-5.35 mg/g dry weight) and polyphenols (4.23-6.38 mg/g). The extract demonstrates particular efficacy in preserving seminiferous tubule integrity and maintaining blood-testis barrier function, with treated groups maintaining up to 85% of normal tubular architecture compared to HFD controls. Key molecular mechanisms include AMPK/SIRT1 pathway activation (2.3-fold increase), enhanced mitochondrial function (67% increase in mtDNA copy number), and epigenetic regulation of metabolic pathways. Temporal analysis indicates optimal therapeutic effects after 28 days of treatment, with initial improvements observable within 14 days. While current evidence is promising, limitations include predominant reliance on rodent models and lack of standardized extraction protocols. Future research priorities include well-designed human clinical trials, standardization of preparation methods, and investigation of potential synergistic effects with other therapeutic agents. This comprehensive review indicates that mulberry extract is a promising therapeutic candidate for obesity-related male infertility, warranting further clinical investigation.

Genome-Wide Identification of the Uridine Diphosphate Glucotransferase Gene Family and Expression Profiling Analysis in the Stem Development of Prunus mume

Prunus mume, a traditional ornamental species native to China, is highly valued for both its captivating weeping variety and economic value. The glycosylation of metabolites, which is mediated by UDP-glycosyltransferases (UGTs), is essential for the regulation of secondary metabolic pathways in plants. Here, we systematically identified and analyzed the UGTs in P. mume. A total of 182 PmUGTs were identified using genomic data and categorized into 16 distinct subfamilies (A–P). All PmUGTs were distributed unevenly across the eight chromosomes, with clear evidence of tandem duplication. Additionally, synteny analysis revealed a close evolutionary relationship between P. mume and Prunus persica. A promoter cis-acting element analysis indicated that PmUGTs may respond to light, hormones, and external stresses. A heatmap analysis revealed that PmUGTs had specific expression patterns across different tissues, under various hormone treatments, and in different developmental stages of stem lignification. Notably, qRT-PCR verification showed significant differences in PmUGT163 expression between straight and weeping stems, underscoring its role in regulating plant architecture formation. Taken together, our study elucidates the evolutionary trajectory of PmUGTs and lays the groundwork for the further validation of the candidate genes involved in plant architectural formation.

The OsGATA gene family as a promising candidate for applying the CRISPR/Cas genome editing technology to improve the nutritional and yield qualities of rice (Oryza sativa L.)

Molecular breeding of rice (Oryza sativa L.) for yield is of great importance for ensuring food security of the population. Living organisms manifest genetically determined responses to environmental factors, including stressors. Photosynthetic activity affects all metabolic processes in plant cells. The genes involved in photosynthesis, in their turn, are regulated by differentially expressed genes associated with circadian rhythms. Plants, as sedentary organisms, require more efficient regulation of gene expression. GATA factors are transcription factors (TFs) that affect the production of phytohormones and mediate the stress response. GATA factors are divided into four main classes (A to D), based on the difference in the structure of the zinc finger domain, and into seven subfamilies, depending on the availability of additional domains. GATA TFs incorporate domain structures that may be involved in the regulation of circadian rhythms. Effects on the circadian rhythms influence other regulatory metabolic pathways in plants, which makes the study of genes associated with circadian rhythms relevant and significant. The most well-known and popular method of gene editing at the moment is the CRISPR/Cas technology. More than 30 rice genes were successfully genomically edited using the CRISPR/Cas technology in the period from 2018 through 2023. This helped to improve their valuable agronomic traits.This review summarizes all information about the classification and known functions of OsGATA genes and OsGATA TFs and provides evidence for the possibility of influencing the regulation of rice photoperiodicity by editing these genes.

Metabolic Reprogramming at the Edge of Redox: Connections Between Metabolic Reprogramming and Cancer Redox State.

The importance of redox systems as fundamental elements in biology is now widely recognized across diverse fields, from ecology to cellular biology. Their connection to metabolism is particularly significant, as it plays a critical role in energy regulation and distribution within organisms. Over recent decades, metabolism has emerged as a relevant focus in studies of biological regulation, especially following its recognition as a hallmark of cancer. This shift has broadened cancer research beyond strictly genetic perspectives. The interaction between metabolism and redox systems in carcinogenesis involves the regulation of essential metabolic pathways, such as glycolysis and the Krebs cycle, as well as the involvement of redox-active components like specific amino acids and cofactors. The feedback mechanisms linking redox systems and metabolism in cancer highlight the development of redox patterns that enhance the flexibility and adaptability of tumor processes, influencing larger-scale biological phenomena such as circadian rhythms and epigenetics.

PH-dependent medium-chain fatty acid synthesis in waste activated sludge fermentation: Metabolic pathway regulation.

Transforming waste activated sludge (WAS) into medium-chain fatty acids (MCFAs) via chain elongation (CE) technology is sustainable, yet pH effects on this process are poorly understood. In this study, semi-continuous flow experiments demonstrated that WAS degradation was highest under alkaline pH (10) but unsuitable for CE. Continuous output of MCFAs indicated that CE could be successfully performed under acidic pH (5) and neutral pH (7). Moreover, neutral pH optimized MCFAs production, achieving higher MCFAs yield (8.9±1.2g COD/L), MCFAs selectivity (51.2±7.3%), and WAS degradation (25.4±0.4%) than acidic pH. Further metagenomic and metatranscriptomic analysis revealed that the reverse β-oxidation cycle was the primary CE pathway. The absence of CE-related microorganisms and enzymes under alkaline pH hindered MCFAs synthesis, while under acidic pH, carboxylate accumulation may reduce cellular protection capabilities and affect energy metabolism, thereby inhibiting anaerobic fermentation. Conversely, neutral pH enhanced amino acid and butyrate metabolic pathways, facilitating WAS degradation and SCFAs production, providing precursor substrates for MCFAs production. Additionally, neutral pH promoted the enrichment and activity of CE-related microorganisms and enzymes, contributing to the accumulation of high-concentration MCFAs. Notably, Clostridium_kluyveri and Sporanaerobacter_acetigenes were key CE-functional bacteria at neutral pH.

Fecal fatty acid profile reveals the therapeutic effect of red ginseng acidic polysaccharide on type 2 diabetes mellitus in rats.

This study aimed to investigate the potential hypoglycemic mechanism of red ginseng acidic polysaccharides (RGAP) from the perspective of fatty acid (FA) regulation. A high-glucose/high-fat diet in conjunction with streptozotocin administration was employed to establish type 2 diabetes mellitus (T2DM) rat models, and their fecal FAs were detected using the liquid chromatography-mass spectrometry (LC-MS) method. RGAP treatment alleviated the polyphagia, polydipsia, weight loss, and hyperglycemia observed in T2DM rats. FA profile was disturbed by T2DM modeling, and 11 marker FAs were selected from statistical analysis, whose intensities were reversely changed by RGAP administration. Among these marker FAs, short-chain FAs were negatively correlated with the fasting blood glucose (FBG) level, while positive correlations were observed between long-chain FA and the FBG level. Combined with the metabolite-enzyme-gene network analysis, we inferred that the mechanistic mechanism RGAP on T2DM may be associated with the regulation of FA metabolism and inflammation-related signaling pathways. This study confirmed the regulatory effect of RGAP on fecal FA, which can provide a scientific basis and new ideas for developing red ginseng as a functional food for supplementary treatment of T2DM.