Pub Date : 2026-02-05DOI: 10.1021/acs.jafc.5c09017
Martha Purnami Wulanjati, Johanna Trinkl, Xiran Wang, Thomas Hoffmann, Wilfried Schwab
Acylation is essential in plant metabolism, protecting metabolites from enzymatic degradation, aiding xenobiotic detoxification, and regulating cellular uptake. It also enhances the stability, solubility, and bioactivity of natural products, making it valuable for drug discovery. Since HDMF (4-hydroxy-2,5-dimethyl-3(2H)-furanone; Furaneol) 6'-O-malonyl glucoside was detected in strawberries, we hypothesized that strawberry malonyltransferases (FaMATs) acylate HDMF glucoside. Genome analysis of Fragaria × ananassa and biochemical assays identified FaMAT1C, FaMAT1S, and FaMAT4C1/S1 as enzymes catalyzing its malonylation, producing three isomers─likely due to keto-enol tautomerism. A screening revealed the broad substrate tolerance of FaMATs, with successful malonylation observed in 67 structurally different glycosides. Notably, FaMAT4C1/S1 malonylated maple furanone glucoside at the 6-OH position of the glucose moiety resulted in previously unknown metabolites. This modification stabilizes glycosides by preventing glycosidic bond cleavage by glycosidases. Understanding FaMAT function deepens insights into plant specialized metabolism and supports the development of natural product-based therapeutics.
酰化在植物代谢中是必不可少的，保护代谢物免受酶降解，帮助外源解毒，调节细胞摄取。它还提高了天然产物的稳定性，溶解度和生物活性，使其对药物发现有价值。自HDMF(4-羟基-2,5-二甲基-3(2H)-呋喃酮；在草莓中检测到呋喃醇6′- o -丙二醇基葡萄糖苷，我们假设草莓丙二醇基转移酶（famat）酰基化HDMF葡萄糖苷。Fragaria x ananassa的基因组分析和生化分析发现FaMAT1C、FaMAT1S和FaMAT4C1/S1是催化其丙二醛化的酶，产生三种异构体，可能是由于酮烯醇互变异构。筛选显示famat具有广泛的底物耐受性，在67种结构不同的糖苷中成功地观察到丙二醛化。值得注意的是，FaMAT4C1/S1在葡萄糖部分的6-OH位置丙二酰化枫呋喃酮葡萄糖苷导致了以前未知的代谢产物。这种修饰通过防止糖苷酶切割糖苷键来稳定糖苷。了解FaMAT功能可以加深对植物特化代谢的认识，并支持基于天然产物的治疗方法的发展。
{"title":"Promiscuous Transferases Malonylate Furaneol Glucoside in <i>Fragaria</i> × <i>ananassa</i>.","authors":"Martha Purnami Wulanjati, Johanna Trinkl, Xiran Wang, Thomas Hoffmann, Wilfried Schwab","doi":"10.1021/acs.jafc.5c09017","DOIUrl":"https://doi.org/10.1021/acs.jafc.5c09017","url":null,"abstract":"<p><p>Acylation is essential in plant metabolism, protecting metabolites from enzymatic degradation, aiding xenobiotic detoxification, and regulating cellular uptake. It also enhances the stability, solubility, and bioactivity of natural products, making it valuable for drug discovery. Since HDMF (4-hydroxy-2,5-dimethyl-3(2<i>H</i>)-furanone; Furaneol) 6'-<i>O</i>-malonyl glucoside was detected in strawberries, we hypothesized that strawberry malonyltransferases (FaMATs) acylate HDMF glucoside. Genome analysis of <i>Fragaria</i> × <i>ananassa</i> and biochemical assays identified FaMAT1C, FaMAT1S, and FaMAT4C<sub>1</sub>/S<sub>1</sub> as enzymes catalyzing its malonylation, producing three isomers─likely due to keto-enol tautomerism. A screening revealed the broad substrate tolerance of FaMATs, with successful malonylation observed in 67 structurally different glycosides. Notably, FaMAT4C<sub>1</sub>/S<sub>1</sub> malonylated maple furanone glucoside at the 6-OH position of the glucose moiety resulted in previously unknown metabolites. This modification stabilizes glycosides by preventing glycosidic bond cleavage by glycosidases. Understanding FaMAT function deepens insights into plant specialized metabolism and supports the development of natural product-based therapeutics.</p>","PeriodicalId":41,"journal":{"name":"Journal of Agricultural and Food Chemistry","volume":" ","pages":""},"PeriodicalIF":6.2,"publicationDate":"2026-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146117141","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-04DOI: 10.1021/acs.jafc.5c16340
Minmin Zhan, Chenxi Zhao, Yanhui Han, Bin Chen, Yilu Chen, Mingyue Song, Yong Cao, Hang Xiao
High-fat diet (HFD) is a recognized risk factor that exacerbates intestinal inflammation and complicates colitis pathology, posing challenges for treatment. This study evaluated citrus-derived exosome-like nanoparticles (CELNs) as a dietary intervention. Results demonstrated that CELNs effectively ameliorated HFD-aggravated colitis, improving the disease activity, colon length, and immune organ index. Mechanistically, CELNs restored gut barrier integrity (upregulating occludin and ZO-1), suppressed oxidative stress and pro-inflammatory signaling, and rebuilt microbial dysbiosis (enriching Faecalibaculum and Bacteroides). Furthermore, CELNs normalized critical metabolic pathways by increasing short-chain fatty acid production, reshaping bile acid profiles (increasing chenodeoxycholic acid and deoxycholic acid content), promoting anti-inflammatory indole derivatives (especially indole acrylic acid), and modulating branched-chain amino acid metabolism. This study highlights CELNs as a potent dietary intervention strategy that rectifies dysbiosis and subsequent metabolic disorders, strengthening the intestinal barrier, and suppressing inflammation. Therefore, CELNs represent a promising novel strategy for treating complex metabolic-inflammatory gut diseases.
{"title":"Citrus-Derived Exosome-like Nanoparticles Attenuate High-Fat Diet-Aggravated Colitis by Gut Microbiota-Metabolites Modulation.","authors":"Minmin Zhan, Chenxi Zhao, Yanhui Han, Bin Chen, Yilu Chen, Mingyue Song, Yong Cao, Hang Xiao","doi":"10.1021/acs.jafc.5c16340","DOIUrl":"https://doi.org/10.1021/acs.jafc.5c16340","url":null,"abstract":"<p><p>High-fat diet (HFD) is a recognized risk factor that exacerbates intestinal inflammation and complicates colitis pathology, posing challenges for treatment. This study evaluated citrus-derived exosome-like nanoparticles (CELNs) as a dietary intervention. Results demonstrated that CELNs effectively ameliorated HFD-aggravated colitis, improving the disease activity, colon length, and immune organ index. Mechanistically, CELNs restored gut barrier integrity (upregulating occludin and ZO-1), suppressed oxidative stress and pro-inflammatory signaling, and rebuilt microbial dysbiosis (enriching <i>Faecalibaculum</i> and <i>Bacteroides</i>). Furthermore, CELNs normalized critical metabolic pathways by increasing short-chain fatty acid production, reshaping bile acid profiles (increasing chenodeoxycholic acid and deoxycholic acid content), promoting anti-inflammatory indole derivatives (especially indole acrylic acid), and modulating branched-chain amino acid metabolism. This study highlights CELNs as a potent dietary intervention strategy that rectifies dysbiosis and subsequent metabolic disorders, strengthening the intestinal barrier, and suppressing inflammation. Therefore, CELNs represent a promising novel strategy for treating complex metabolic-inflammatory gut diseases.</p>","PeriodicalId":41,"journal":{"name":"Journal of Agricultural and Food Chemistry","volume":" ","pages":""},"PeriodicalIF":6.2,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146117105","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Biochanin A, a valuable O-methylated isoflavone, requires efficient P450 activity, regioselective methylation, and substantial cofactor availability. Here, we established a systematic strategy for its high-level production in Saccharomyces cerevisiae. We first constructed a genistein platform strain (16.10 mg/L) by optimizing the 2-hydroxyisoflavanone synthase gene (PlIFS) copy number. Next, a screen identified Pueraria lobata PlOMT9 as the optimal 4′-O-methyltransferase, yielding 14.29 mg/L biochanin A. As methylation was constrained by ATP supply, we augmented the cellular energy budget by expressing Vitreoscilla hemoglobin, increasing biochanin A titer to 19.48 mg/L. We then expanded the endoplasmic reticulum membrane capacity and coexpressed protein-folding chaperones, which profoundly enhanced the functional expression of the membrane-associated enzymes, skyrocketing the biochanin A titer to 39.89 mg/L. Finally, we increased the titer to 49.86 mg/L by improving the heme supply. The final strain in this study will facilitate the production of O-methylated isoflavones through the biochanin A biosynthetic pathway.
{"title":"De Novo Biosynthesis of Biochanin A in Saccharomyces cerevisiae via Integrated Metabolic and Organelle Engineering","authors":"Xinjia Tan,Fanglin Hu,Shasha Zuo,Yongtong Wang,Zhiqiang Xiao,Siqi Zhang,Jiaxu Chen,Liusha Fan,Juan Liu,Yang Shan","doi":"10.1021/acs.jafc.5c12010","DOIUrl":"https://doi.org/10.1021/acs.jafc.5c12010","url":null,"abstract":"Biochanin A, a valuable O-methylated isoflavone, requires efficient P450 activity, regioselective methylation, and substantial cofactor availability. Here, we established a systematic strategy for its high-level production in Saccharomyces cerevisiae. We first constructed a genistein platform strain (16.10 mg/L) by optimizing the 2-hydroxyisoflavanone synthase gene (PlIFS) copy number. Next, a screen identified Pueraria lobata PlOMT9 as the optimal 4′-O-methyltransferase, yielding 14.29 mg/L biochanin A. As methylation was constrained by ATP supply, we augmented the cellular energy budget by expressing Vitreoscilla hemoglobin, increasing biochanin A titer to 19.48 mg/L. We then expanded the endoplasmic reticulum membrane capacity and coexpressed protein-folding chaperones, which profoundly enhanced the functional expression of the membrane-associated enzymes, skyrocketing the biochanin A titer to 39.89 mg/L. Finally, we increased the titer to 49.86 mg/L by improving the heme supply. The final strain in this study will facilitate the production of O-methylated isoflavones through the biochanin A biosynthetic pathway.","PeriodicalId":41,"journal":{"name":"Journal of Agricultural and Food Chemistry","volume":"8 1","pages":""},"PeriodicalIF":6.1,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146111206","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Stevioside is a natural sweetener extracted from the perennial herb Stevia rebaudiana and has been approved by the FDA as an important dietary supplement. In addition, it possesses anti-inflammatory, antioxidant, and antiapoptotic properties. Nevertheless, its therapeutic efficacy against concanavalin A (Con A)-induced liver injury remains unclear. This study was designed to investigate the protective effect of stevioside on Con A-induced liver injury and to elucidate the underlying mechanisms. Using a Con A-induced mouse liver injury model, we evaluated liver damage via serum biochemistry and histopathology, identified key pathways through hepatic transcriptomics, and validated direct targets with molecular docking, CETSA, and DARTS assays. Compared with the model group, stevioside treatment dose-dependently reduced serum levels of hepatic injury markers and markedly ameliorated histopathological damage. Moreover, stevioside attenuated Con A-triggered hepatitis and hepatocyte apoptosis. Hepatic transcriptomic analyses revealed that differentially expressed genes were enriched in processes related to oxidoreductase activity, and stevioside effectively alleviated hepatic oxidative stress. Molecular docking, CETSA, and DARTS assays further identified AMPK may be the critical target for stevioside. In vitro experiments showed that stevioside suppressed Con A-induced inflammation and oxidative stress in RAW264.7 cells. In vivo, genetic knockout of Nrf2 or pharmacological inhibition of AMPK markedly diminished the hepatoprotective effects of stevioside. Collectively, stevioside activated the AMPK/NRF2 signaling pathway through its interaction with AMPK, thereby exerting hepatoprotective effects. Our study not only provides a theoretical basis for the application of stevioside in preventing liver diseases, but also opens new avenues for the treatment of liver injury.
{"title":"Stevioside Alleviates Con A-Induced Liver Injury by Activating the AMPK/NRF2 Signaling Pathway","authors":"Zhe Zhang,Yidan Wang,Jinping Hu,Yuxin Zhang,Lingling Qiu,Baoyin Wang,Xiwen Zhang,Yu Ding,Wenzhi Ren,Hongjuan Jin,Bao Yuan","doi":"10.1021/acs.jafc.5c11238","DOIUrl":"https://doi.org/10.1021/acs.jafc.5c11238","url":null,"abstract":"Stevioside is a natural sweetener extracted from the perennial herb Stevia rebaudiana and has been approved by the FDA as an important dietary supplement. In addition, it possesses anti-inflammatory, antioxidant, and antiapoptotic properties. Nevertheless, its therapeutic efficacy against concanavalin A (Con A)-induced liver injury remains unclear. This study was designed to investigate the protective effect of stevioside on Con A-induced liver injury and to elucidate the underlying mechanisms. Using a Con A-induced mouse liver injury model, we evaluated liver damage via serum biochemistry and histopathology, identified key pathways through hepatic transcriptomics, and validated direct targets with molecular docking, CETSA, and DARTS assays. Compared with the model group, stevioside treatment dose-dependently reduced serum levels of hepatic injury markers and markedly ameliorated histopathological damage. Moreover, stevioside attenuated Con A-triggered hepatitis and hepatocyte apoptosis. Hepatic transcriptomic analyses revealed that differentially expressed genes were enriched in processes related to oxidoreductase activity, and stevioside effectively alleviated hepatic oxidative stress. Molecular docking, CETSA, and DARTS assays further identified AMPK may be the critical target for stevioside. In vitro experiments showed that stevioside suppressed Con A-induced inflammation and oxidative stress in RAW264.7 cells. In vivo, genetic knockout of Nrf2 or pharmacological inhibition of AMPK markedly diminished the hepatoprotective effects of stevioside. Collectively, stevioside activated the AMPK/NRF2 signaling pathway through its interaction with AMPK, thereby exerting hepatoprotective effects. Our study not only provides a theoretical basis for the application of stevioside in preventing liver diseases, but also opens new avenues for the treatment of liver injury.","PeriodicalId":41,"journal":{"name":"Journal of Agricultural and Food Chemistry","volume":"232 1","pages":""},"PeriodicalIF":6.1,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146111187","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-04DOI: 10.1021/acs.jafc.5c13658
Wenjing Huang,Zhibin Ye,Shengmei Xie,Zihao Qi,Mengying Zhang,Shimao Fang,Jingming Ning
The sweetness of Keemun black tea (KBT) is a critical determinant of its overall sensory quality. This study used sensory analysis to quantitate the sweet odor and flavor of KBT. The results indicated that volatile compounds, rather than soluble sugars or free amino acids, are the main contributors to KBT’s sweet flavor. Ten odorants with an odor activity value > 1 were identified by the Sensomics approach and screened by applying the odor-induced taste enhancement (OITE) method, i.e. β-damascenone, (E)-β-ionone, linalool, methional, dimethyl sulfide, geraniol, β-myrcene, coumarin, citral, and 2-phenylacetaldehyde, which were identified as the key drivers of KBT’s sweet flavor. Omission and addition experiments confirmed that the intensity of sweet odor was correlated with sweet flavor (r = 0.71). These findings demonstrate that the sweet flavor of KBT mainly originates from its odorants, which synergistically enhance sweetness through OITE, resulting in the high overall flavor quality of KBT.
{"title":"Deciphering the Aroma-Driven Mechanism of Sweet Flavor in Keemun Black Tea","authors":"Wenjing Huang,Zhibin Ye,Shengmei Xie,Zihao Qi,Mengying Zhang,Shimao Fang,Jingming Ning","doi":"10.1021/acs.jafc.5c13658","DOIUrl":"https://doi.org/10.1021/acs.jafc.5c13658","url":null,"abstract":"The sweetness of Keemun black tea (KBT) is a critical determinant of its overall sensory quality. This study used sensory analysis to quantitate the sweet odor and flavor of KBT. The results indicated that volatile compounds, rather than soluble sugars or free amino acids, are the main contributors to KBT’s sweet flavor. Ten odorants with an odor activity value > 1 were identified by the Sensomics approach and screened by applying the odor-induced taste enhancement (OITE) method, i.e. β-damascenone, (E)-β-ionone, linalool, methional, dimethyl sulfide, geraniol, β-myrcene, coumarin, citral, and 2-phenylacetaldehyde, which were identified as the key drivers of KBT’s sweet flavor. Omission and addition experiments confirmed that the intensity of sweet odor was correlated with sweet flavor (r = 0.71). These findings demonstrate that the sweet flavor of KBT mainly originates from its odorants, which synergistically enhance sweetness through OITE, resulting in the high overall flavor quality of KBT.","PeriodicalId":41,"journal":{"name":"Journal of Agricultural and Food Chemistry","volume":"26 1","pages":""},"PeriodicalIF":6.1,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146111208","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The rapid post-mortem softening of abalone muscle is primarily attributed to collagen degradation mediated by matrix metalloproteinases (MMPs), although the synergistic mechanisms of different MMPs remain inadequately understood. In this study, we heterologously expressed MMP-3 and MMP-16 to investigate their combined effects on in vitro degradation of type I collagen and collagen fibers and then analyzed degradation products via mass spectrometry to elucidate the mechanism. Our findings showed that both enzymes degraded collagen individually, but their combined action accelerated collagen fiber degradation, causing more comprehensive breakdown. Mass spectrometry analysis revealed that MMP-3 initiated degradation by cleaving collagen telopeptides and disrupting the triple helix, facilitating MMP-16 infiltration into relaxed fibers to promote extensive proteolysis. This study elucidates a synergistic loosening-then-degradation mechanism of MMP-mediated collagen degradation, which underlies post-mortem muscle softening of abalone and thus provides a theoretical basis for seafood preservation strategies.
{"title":"Mechanistic Insights into Synergistic Collagen Degradation by MMP-3 and MMP-16 in Post-Mortem Abalone Muscle","authors":"Tian-Bo Zhang,Fu-Hao Zhang,Ling-Jing Zhang,Le-Chang Sun,Ru-Qing Yang,Yu-Lei Chen","doi":"10.1021/acs.jafc.5c16557","DOIUrl":"https://doi.org/10.1021/acs.jafc.5c16557","url":null,"abstract":"The rapid post-mortem softening of abalone muscle is primarily attributed to collagen degradation mediated by matrix metalloproteinases (MMPs), although the synergistic mechanisms of different MMPs remain inadequately understood. In this study, we heterologously expressed MMP-3 and MMP-16 to investigate their combined effects on in vitro degradation of type I collagen and collagen fibers and then analyzed degradation products via mass spectrometry to elucidate the mechanism. Our findings showed that both enzymes degraded collagen individually, but their combined action accelerated collagen fiber degradation, causing more comprehensive breakdown. Mass spectrometry analysis revealed that MMP-3 initiated degradation by cleaving collagen telopeptides and disrupting the triple helix, facilitating MMP-16 infiltration into relaxed fibers to promote extensive proteolysis. This study elucidates a synergistic loosening-then-degradation mechanism of MMP-mediated collagen degradation, which underlies post-mortem muscle softening of abalone and thus provides a theoretical basis for seafood preservation strategies.","PeriodicalId":41,"journal":{"name":"Journal of Agricultural and Food Chemistry","volume":"215 1","pages":""},"PeriodicalIF":6.1,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146111210","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lysine acetylation (Kac), 2-hydroxyisobutyrylation (Khib), and malonylation (Kma) represent three recently identified posttranslational modifications (PTMs) that regulate plant development and stress resilience. Herein, we constructed the first global proteomic atlas of Kac, Khib, and Kma modifications in developing cassava roots, identifying 11,253 Kac, 18,326 Khib, and 4068 Kma sites across 5165, 4832, and 1815 proteins, respectively. The PTM-modified proteins were involved in sucrose/starch metabolism, glycolysis/gluconeogenesis, pentose phosphate pathway, TCA cycle, and lignin biosynthesis, with the majority exhibiting multiple PTM co-occurrence. Hundreds of modified proteins associated with stress response, hormone metabolism, and transcription factors were also identified, of which a few proteins displayed significant type-specific modification preferences. Finally, the regulatory roles of Kac-, Khib-, and Kma-modified proteins in root development and stress responses were discussed, leading to a proposed mechanistic model for PTM-mediated regulation in cassava. These findings provide novel insights for elucidating the molecular mechanisms of PTM-driven regulation in plants.
{"title":"Deciphering the Atlas of Protein Acetylation, 2-Hydroxyisobutyrylation, and Malonylation in Developing Cassava Roots","authors":"Lili Fu,Yan Yan,Kaisen Huo,Weiwei Tie,Jinghao Yang,Deguan Tan,Wei Hu,Zehong Ding","doi":"10.1021/acs.jafc.5c14441","DOIUrl":"https://doi.org/10.1021/acs.jafc.5c14441","url":null,"abstract":"Lysine acetylation (Kac), 2-hydroxyisobutyrylation (Khib), and malonylation (Kma) represent three recently identified posttranslational modifications (PTMs) that regulate plant development and stress resilience. Herein, we constructed the first global proteomic atlas of Kac, Khib, and Kma modifications in developing cassava roots, identifying 11,253 Kac, 18,326 Khib, and 4068 Kma sites across 5165, 4832, and 1815 proteins, respectively. The PTM-modified proteins were involved in sucrose/starch metabolism, glycolysis/gluconeogenesis, pentose phosphate pathway, TCA cycle, and lignin biosynthesis, with the majority exhibiting multiple PTM co-occurrence. Hundreds of modified proteins associated with stress response, hormone metabolism, and transcription factors were also identified, of which a few proteins displayed significant type-specific modification preferences. Finally, the regulatory roles of Kac-, Khib-, and Kma-modified proteins in root development and stress responses were discussed, leading to a proposed mechanistic model for PTM-mediated regulation in cassava. These findings provide novel insights for elucidating the molecular mechanisms of PTM-driven regulation in plants.","PeriodicalId":41,"journal":{"name":"Journal of Agricultural and Food Chemistry","volume":"398 1","pages":""},"PeriodicalIF":6.1,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146111209","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Porcine epidemic diarrhea virus (PEDV) causes acute diarrhea and high mortality in piglets, and conventional control strategies are often limited by frequent viral mutations. Theaflavin (TF), a natural polyphenol from black tea, has demonstrated antiviral effects against several viruses; however, its efficacy against PEDV and its underlying mechanisms remain unclear. In this study, we established a PEDV infection model in Vero and IPI-HB1 cells and confirmed that TF significantly inhibited viral replication in a dose-dependent manner, particularly during internalization and replication. Network pharmacology and molecular docking identified 12 TF-related targets, four of which showed strong binding affinities. TF treatment downregulates the mRNA expression of these targets, contributing to its antiviral effects. Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) analyses suggested that the PI3K/Akt/mTOR pathway was central to the mechanism of TF. Western blotting confirmed that TF suppressed Akt and mTOR phosphorylation, while pathway activation reversed its antiviral effects. Furthermore, TF were found to directly bind to the PEDV nucleocapsid (N) and nonstructural protein 5 (Nsp5), suggesting additional virus-targeted activity. Therefore, TF exerts dual antiviral effects against PEDV by modulating host signaling and targeting viral proteins, thus offering a promising natural compound for antiviral drug development.
{"title":"Theaflavin Suppresses PEDV Replication via Inhibiting PI3K/Akt/mTOR Signaling and Directly Interacting with Viral Proteins","authors":"Qiong Wu,Yuxin Yang,Zijun Xiang,Keli Yang,Chang Li,Wei Liu,Ting Gao,Shuting Ni,Jiajia Zhu,Fangyan Yuan,Rui Guo,Ling Zhao,Yongxiang Tian,Danna Zhou","doi":"10.1021/acs.jafc.5c12020","DOIUrl":"https://doi.org/10.1021/acs.jafc.5c12020","url":null,"abstract":"Porcine epidemic diarrhea virus (PEDV) causes acute diarrhea and high mortality in piglets, and conventional control strategies are often limited by frequent viral mutations. Theaflavin (TF), a natural polyphenol from black tea, has demonstrated antiviral effects against several viruses; however, its efficacy against PEDV and its underlying mechanisms remain unclear. In this study, we established a PEDV infection model in Vero and IPI-HB1 cells and confirmed that TF significantly inhibited viral replication in a dose-dependent manner, particularly during internalization and replication. Network pharmacology and molecular docking identified 12 TF-related targets, four of which showed strong binding affinities. TF treatment downregulates the mRNA expression of these targets, contributing to its antiviral effects. Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) analyses suggested that the PI3K/Akt/mTOR pathway was central to the mechanism of TF. Western blotting confirmed that TF suppressed Akt and mTOR phosphorylation, while pathway activation reversed its antiviral effects. Furthermore, TF were found to directly bind to the PEDV nucleocapsid (N) and nonstructural protein 5 (Nsp5), suggesting additional virus-targeted activity. Therefore, TF exerts dual antiviral effects against PEDV by modulating host signaling and targeting viral proteins, thus offering a promising natural compound for antiviral drug development.","PeriodicalId":41,"journal":{"name":"Journal of Agricultural and Food Chemistry","volume":"88 1","pages":""},"PeriodicalIF":6.1,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146111205","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The exact mechanism through which dietary flavonoids alleviate metabolic syndrome (MetS) via the gut microbiota remains fully unclear. This study demonstrates that sinensetin markedly impeded the development of MetS and altered hepatic transcriptomic profiles by activating alternative bile acid biosynthesis signaling cascades both in vivo and in vitro. Importantly, sinensetin administration induced significant shifts in hepatic bile acid composition, notably increasing the relative abundance of non-12-hydroxy bile acids (non-12-OH BAs) in high-fat diet (HFD)-fed mice. Additionally, oral administration of sinensetin significantly relieved intestinal dysbiosis caused by HFD by altering the composition of gut microbiota in mice. The therapeutic efficacy of sinensetin against MetS was microbiota-dependent, as antibiotic-mediated depletion of gut microbiota abolished its beneficial effects, and fecal microbiota transplantation transmited this metabolic improvement. These findings suggest that sinensetin alleviated MetS by reshaping the gut microbiota to enhance non-12-OH BAs synthesis, offering novel mechanistic insights and promising avenues for therapeutic intervention.
{"title":"Sinensetin Ameliorates Metabolic Syndrome via Regulating Gut Microbiota and Bile Acid Metabolism","authors":"Min Luan,Sha Bao,Xueling Zhang,Yuhao Huang,Ruinan Yuan,Pengjun Zhong,Mengyuan Liu,Jue Li,Xuefei Liu,Lei Chen,Qingrong Huang,Rihui Wu","doi":"10.1021/acs.jafc.5c12920","DOIUrl":"https://doi.org/10.1021/acs.jafc.5c12920","url":null,"abstract":"The exact mechanism through which dietary flavonoids alleviate metabolic syndrome (MetS) via the gut microbiota remains fully unclear. This study demonstrates that sinensetin markedly impeded the development of MetS and altered hepatic transcriptomic profiles by activating alternative bile acid biosynthesis signaling cascades both in vivo and in vitro. Importantly, sinensetin administration induced significant shifts in hepatic bile acid composition, notably increasing the relative abundance of non-12-hydroxy bile acids (non-12-OH BAs) in high-fat diet (HFD)-fed mice. Additionally, oral administration of sinensetin significantly relieved intestinal dysbiosis caused by HFD by altering the composition of gut microbiota in mice. The therapeutic efficacy of sinensetin against MetS was microbiota-dependent, as antibiotic-mediated depletion of gut microbiota abolished its beneficial effects, and fecal microbiota transplantation transmited this metabolic improvement. These findings suggest that sinensetin alleviated MetS by reshaping the gut microbiota to enhance non-12-OH BAs synthesis, offering novel mechanistic insights and promising avenues for therapeutic intervention.","PeriodicalId":41,"journal":{"name":"Journal of Agricultural and Food Chemistry","volume":"100 1","pages":""},"PeriodicalIF":6.1,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146111207","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-03DOI: 10.1021/acs.jafc.5c15833
Hao-Yu Wang, Zheng-Heng Qian, Cui Zhang, Jia-Chang Li, Jian-Zhong Xu
Isoquercetin is a bioactive flavonoid whose biosynthesis from quercetin depends on glycosyltransferases (GTs); however, wild-type GTs exhibit a limited catalytic efficiency. Here, we combined virtual screening, molecular docking, and experimental validation to identify and engineer the GTs. From about 1000 homologous sequences screened via protein BLAST and deep learning-based kcat prediction, the glycosyltransferase MiCGT from Mangifera indica was selected for rational design. After molecular docking and phylogenetic analysis, the engineered variant PCAA (MiCGTS121P/M148C/K253A/S281A) exhibited a 103-fold higher activity than wild-type MiCGT. To enable cost-effective production, sucrose synthase GmSUS was coupled with PCAA to regenerate UDP-glucose during quercetin glycosylation, yielding 3.91 mM isoquercetin with a 78.1% conversion rate. This work overcomes a major bottleneck in isoquercetin biosynthesis and offers a practical strategy for its application in the food industry.
{"title":"Design Glycosyltransferases with High Glycosyl Transfer Efficiency to Efficiently Produce Isoquercetin from Quercetin","authors":"Hao-Yu Wang, Zheng-Heng Qian, Cui Zhang, Jia-Chang Li, Jian-Zhong Xu","doi":"10.1021/acs.jafc.5c15833","DOIUrl":"https://doi.org/10.1021/acs.jafc.5c15833","url":null,"abstract":"Isoquercetin is a bioactive flavonoid whose biosynthesis from quercetin depends on glycosyltransferases (GTs); however, wild-type GTs exhibit a limited catalytic efficiency. Here, we combined virtual screening, molecular docking, and experimental validation to identify and engineer the GTs. From about 1000 homologous sequences screened via protein BLAST and deep learning-based kcat prediction, the glycosyltransferase MiCGT from <i>Mangifera indica</i> was selected for rational design. After molecular docking and phylogenetic analysis, the engineered variant PCAA (MiCGT<sup>S121P/M148C/K253A/S281A</sup>) exhibited a 103-fold higher activity than wild-type MiCGT. To enable cost-effective production, sucrose synthase GmSUS was coupled with PCAA to regenerate UDP-glucose during quercetin glycosylation, yielding 3.91 mM isoquercetin with a 78.1% conversion rate. This work overcomes a major bottleneck in isoquercetin biosynthesis and offers a practical strategy for its application in the food industry.","PeriodicalId":41,"journal":{"name":"Journal of Agricultural and Food Chemistry","volume":"5 1","pages":""},"PeriodicalIF":6.1,"publicationDate":"2026-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146102018","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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