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Detection of CpG methylations in human mismatch repair gene hMLH1 promoter by denaturing high-performance liquid chromatography (DHPLC) 认领 引用 被引量：4
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作者 邓大君 邓国仁 +1 位作者 周静 辛慧君 《Chinese Journal of Cancer Research》 CAS 2000年第3期18-171,38,共154页
Objectives: To develop a novel method to detect CpG methylation by DHPLC. Methods: After DNA was treated with sodium bisulfite, mismatch repair gene hMLH1 promoter was amplified by polymerase chain reaction (PCR). DHP... Objectives: To develop a novel method to detect CpG methylation by DHPLC. Methods: After DNA was treated with sodium bisulfite, mismatch repair gene hMLH1 promoter was amplified by polymerase chain reaction (PCR). DHPLC was used to separate the PCR products at their partially denaturing temperatures. BstUI digestion assay was also used for comparison study. Results: A 294bp band was obtained by PCR from each DNA samples of colon cancer cell line RKO and gastric cancer cell line PACM82. These two bands could be separated completely by DHPLC at 53°C (retention time 6.7 min for RKO vs. 6.2 min for PACM82). We concluded that the hMLH1 promoter in RKO cells is methylated, while PACM82 is not methylated, since methylation can protect the conversion of C to T and keep higher C/G content after bisulfite treatment, leading to the delayed time. These results consistent with those from BstUI digestion assay. Conclusion: Methylation in CpG islands of hMLH1 could be detected conveniently by DHPLC after bisulfite modification. 展开更多
关键词 hMLH1,CpG islands Methylation DHPLC
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Coordinated regulation of active and repressive histone methylations by a dual-specificity histone demethylase ceKDM7A from Caenorhabditis elegans 认领 引用 被引量：3
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作者 Hanqing Lin Yiqin Wang +11 位作者 Yanru Wang Feng Tian Pu Pu Yi Yu Hailei Mao Ying Yang Ping Wang Lulu Hu Yan Lin Yi Liu Yanhui Xu Charlie Degui Chen 《Cell Research》 SCIE CAS 2010年第8期899-907,共9页
H3K9me2 and H3K27me2 are important epigenetic marks associated with transcription repression, while H3K4me3 is associated with transcription activation. It has been shown that active and repressive histone methylation... H3K9me2 and H3K27me2 are important epigenetic marks associated with transcription repression, while H3K4me3 is associated with transcription activation. It has been shown that active and repressive histone methylations distribute in a mutually exclusive manner, but the underlying mechanism was poorly understood. Here we identified ceKDM7A, a PHD （plant homeodomain）- and JmjC domain-containing protein, as a histone demethylase specific for H3K9me2 and H3K27me2. We further demonstrated that the PHD domain of ceKDM7A bound H3K4me3 and H3K4me3 co-localized with ceKDM7A at the genome-wide level. Disruption of the PHD domain binding to H3K4me3 reduced the demethylase activity in vivo, and loss of ceKDM7A reduced the expression of its associated target genes. These results indicate that ceKDM7A is recruited to the promoter to demethylate H3K9me2 and H3K27me2 and activate gene expression through the binding of the PHD domain to H3K4me3. Thus, our study identifies a dual-specificity histone demethylase and provides novel insights into the regulation of histone methylation. 展开更多
关键词 KDM7A demethylase H3K9me2 H3K27me2 PHD JmjC histone methylation
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FcMET1 mediates low DNA methylation and promotes peel coloring in Ficus carica 认领 引用 被引量：2
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作者 Kairong Sun Xiaoxiao Wang +5 位作者 Hantang Huang Yuan Wang Zhiyi Fan Yutian Xia Huiqin Ma Miaoyu Song 《Horticultural Plant Journal》 SCIE CAS CSCD 2026年第2期345-355,共11页
Fig(Ficus carica L.)with purple-red peel cultivars are popular among consumers and exhibit better storability.While DNA methylation influences fruit ripening and color development,its specific role in fig fruit remain... Fig(Ficus carica L.)with purple-red peel cultivars are popular among consumers and exhibit better storability.While DNA methylation influences fruit ripening and color development,its specific role in fig fruit remains unclear.This study explores the impact of DNA methylation on the fig peel coloration.Enzymatic colorimetric detection revealed that the level of‘Purple Peel’fig DNA methylation decreases with fig fruit ripening and coloring.Treatment of young fruit with the DNA-methylation inhibitor azacytidine induced peel coloration,suggesting that a decrease in DNA-methylation level promotes fig peel coloration.Seven members of DNA methyltransferases and three members of DNA demethylases were identified from a high-level fig genome,highlighting FcMET1 and FcDRM2 as stable proteins,ensuring functional expression.Reference to the Arabidopsis protein interaction network map predicted that FcMET1 is in a central position,suggesting a crucial regulatory role in multiple biological processes.Correlation analysis revealed a positive correlation between FcMET1 expression during peel development and the level of total DNA methylation.Weighted gene co-expression network analysis identified co-expression of FcMET1 with the color-related transcription factors MYB,bHLH and WD40,as well as with eight structural genes in the flavonoid-biosynthesis pathway.The expression of FcUFGT3 was negatively correlated with that of FcMET1.McrBC-PCR and Bisulfite Sequencing detection showed that a low methylation level of the FcUFGT3 promoter corresponds with its high expression in colored fig.This investigation of the mechanism of DNA methylation provides a theoretical basis for understanding the role of DNA-methylation modifications in fig ripening and coloring. 展开更多
关键词 Ficus carica L. DNA methylation FcMET1 Coloring Peel
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DaMYB75 and DaMYB56 antagonistically regulate anthocyanin biosynthesis by binding to the DaANS promoter in Dioscorea alata 认领 引用 被引量：1
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作者 Xin Chen Jingyu Sun +11 位作者 Nan Shan Asjad Ali Sha Luo Shenglin Wang Qianglong Zhu Yao Xiao Zihao Li Yufan Fang Jiali Lin Xiaorong Chen Qinghong Zhou Yingjin Huang 《The Crop Journal》 SCIE CSCD 2026年第1期255-270,共16页
The yam Dioscorea alata L.is widely cultivated globally.Purple-fleshed varieties of this important crop have enhanced market value due to their high anthocyanin contents,but how anthocyanin biosynthesis in D.alata tub... The yam Dioscorea alata L.is widely cultivated globally.Purple-fleshed varieties of this important crop have enhanced market value due to their high anthocyanin contents,but how anthocyanin biosynthesis in D.alata tubers is regulated remains poorly understood.In this study,we identified and functionally validated key transcription factors that regulate anthocyanin biosynthesis based on a comparative transcriptome and metabolome analysis of three D.alata cultivars with different colored tubers(dark purple,light purple,and white).The anthocyanin glycoside cyanidin-3-O-(2′′-O-glucosyl)glucoside was abundant during early tuber development,and we determined that its accumulation is regulated in opposite manners by two R2R3-MYB transcription factors:DaMYB75 and DaMYB56.Yeast two-hybrid and bimolecular fluorescence complementation assays in Nicotiana benthamiana and co-expression assays in D.alata demonstrated that DaMYB75 promotes anthocyanin biosynthesis by specifically activating the promoter of the late anthocyanin biosynthesis gene DaANS and enhancing its expression through an interaction with DabHLH72.By contrast,DaMYB56 is a negative regulator of anthocyanin biosynthesis that binds to the DaANS promoter together with DabHLH72.Furthermore,the methylation levels of the DaMYB75 promoter were significantly lower in purple tubers than in white tubers.These findings shed light on the regulation of anthocyanin biosynthesis by MYBs and provide the basis for genetically improving anthocyanin content in D.alata. 展开更多
关键词 Dioscorea alata L Anthocyanin biosynthesis DaMYB75 DaMYB56 DNA methylation
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Neuromodulatory role and therapeutic potential of N6-methyladenosine RNA methylation in neurodegenerative diseases 认领 引用 被引量：2
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作者 Jinyu Zhang Wenjing Ma +3 位作者 Ranxu Liu Xiaoheng Li Zengqiang Yuan Jinbo Cheng 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第6期2191-2204,共14页
N6-methyladenosine RNA methylation,an essential post-transcriptional modification,dynamically regulates RNA metabolism and plays a crucial role in neuronal function.Growing evidence suggests that dysregulated N6... N6-methyladenosine RNA methylation,an essential post-transcriptional modification,dynamically regulates RNA metabolism and plays a crucial role in neuronal function.Growing evidence suggests that dysregulated N6-methyladenosine modification contributes to the pathogenesis of neurodegenerative diseases,including Alzheimer’s disease,Parkinson’s disease,multiple sclerosis,and amyotrophic lateral sclerosis.However,the precise mechanisms by which N6-methyladenosine modification influences these conditions remain unclear.This review summarizes the role of m6A modification and its associated regulators in neurodegeneration,focusing on their involvement in key pathological processes.In Alzheimer’s disease,m6A modification contributes to synaptic dysfunction,mitochondrial damage,and neuronal apoptosis.Evidence from APP/PS1,5xFAD,tau transgenic,and Drosophila models demonstrates that regulators such as methyltransferase-like 3 and fat mass and obesity-associated protein influence Alzheimer’s disease progression through neuroinflammation,circular RNAs dysregulation,and autophagy-related mechanisms.In Parkinson’s disease,altered N6-methyladenosine regulator expression affects dopaminergic neuron survival and stress responses by modulating mRNA stability and autophagy-related lncRNAs.In multiple sclerosis and amyotrophic lateral sclerosis,N6-methyladenosine affects immune activation,myelin repair,and the regulation of disease-associated genes such as TDP-43.Beyond N6-methyladenosine,other RNA methylation modifications-such as m1A,m5C,m7G,uracil,and pseudouridine-are implicated in neurodegenerative diseases through their regulation of mitochondrial function,RNA metabolism,and neuronal stress responses.Additionally,N6-methyladenosine exhibits cell type-specific functions:in microglia,it regulates inflammatory activation and phagocytic function;in astrocytes,it modulates metabolic homeostasis and glutamate-associated neurotoxicity;in neurons,it affects synaptic function and neurodegeneration-related gene expression;and in adult neural stem cells,it controls differentiation,neurogenesis,and cognitive plasticity.Recently,several small-molecule inhibitors targeting methyltransferase-like 3 or fat mass and obesity-associated protein have been developed to modulate N6-methyladenosine modification,providing new opportunities for disease intervention,with the targeting of N⁶-methyladenosine-related pathways emerging as a promising therapeutic strategy.However,challenges persist in optimizing the specificity and delivery of these therapeutic approaches. 展开更多
关键词 Alzheimer’s disease amyotrophic lateral sclerosis cell type m6A RNA methylation methyltransferase-like 3 multiple sclerosis neurodegeneration neuroinflammation Parkinson’s disease RNA modification therapeutic strategy
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GiMYB76,a MeJA-inducible R2R3-type transcription factor,regulates licochalcone A biosynthesis in licorice(Glycyrrhiza inflata) 认领 引用 被引量：1
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作者 Yuping Li Zhigeng Wu +6 位作者 Jixiang Zhu Jiangyi Zeng Yongliang Liu Jihua Wang Ling Yuan Ying Wang Yongqing Li 《The Crop Journal》 SCIE CSCD 2026年第1期235-246,共12页
Licochalcone A(LCA)is a characteristic compound in licorice Glycyrrhiza inflata and is widely utilized in pharmaceutical and cosmetic industries.However,the biosynthetic pathway and regulatory mechanisms of LCA remain... Licochalcone A(LCA)is a characteristic compound in licorice Glycyrrhiza inflata and is widely utilized in pharmaceutical and cosmetic industries.However,the biosynthetic pathway and regulatory mechanisms of LCA remain poorly understood.In this study,we first found the accumulation of LCA is induced by methyl jasmonate(MeJA).Given that MYB transcriptional factors are well-documented as key regulators of flavonoid biosynthesis,we identified a total of 147 GiR2R3-MYB genes in G.inflata,which were classified into 28 subgroups.The chromosome distributions,sequence characteristics,gene structures,duplication events and cis-acting elements were also investigated.Through integrated analysis of GiR2R3-MYBs expression patterns across different tissues and under MeJA treatment,along with phylogenetic relationship,we identified GiMYB76—a MeJA-inducible MYB transcription factor—as a potential regulator of LCA accumulation.Functional validation showed that transgenic hairy roots overexpressing GiMYB76 exhibited a significant increase in LCA content.DAP-seq analysis of GiMYB76 revealed potential target genes involved in flavonoid biosynthesis regulation.Subsequent promoter activity assay verified that GiMYB76 can bind to the promoter and activate the expression of GiCHS4.Consistently,overexpression of GiCHS4 in G.inflata hairy roots also significantly enhanced LCA production.This study not only clarifies that GiMYB76 transcriptionally activated GiCHS4 to promote LCA biosynthesis but also provides valuable insights for basic research on licorice and the development of related industries. 展开更多
关键词 R2R3-MYB Licochalcone A DAP-Seq Methyl JA Glycyrrhiza inflata
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Beta 2-adrenergic pathway combats Alzheimer's disease:Restoring cognition and synaptic integrity 认领 引用 被引量：2
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作者 Shaomin Li Shan-Xue Jin 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第10期4832-4842,共11页
Alzheimer's disease is typified by amyloid-beta oligomer-mediated synaptic disruption,neuroinflammation,and mitochondrial loss of function,culminating in cognitive decline.Recent evidence points toward the β2-... Alzheimer's disease is typified by amyloid-beta oligomer-mediated synaptic disruption,neuroinflammation,and mitochondrial loss of function,culminating in cognitive decline.Recent evidence points toward the β2-adrenergic receptor as a target through its regulation of synaptic plasticity,neuroinflammation,and epigenetic control.Activation of β2-adrenergic receptor potentiates long-term potentiation,reverses amyloid-beta-mediated synaptic loss,and stimulates neuroprotective gene expression through cyclic adenosine monophosphateprotein kinase A-cyclic AMP response element-binding protein.Moreover,β2-adrenergic receptor suppression of histone deacetylase 2/3 promotes transcriptional reprogramming,supporting synaptic function.Beyond synaptic maintenance,activation of β2-adrenergic receptor prevents neuroinflammation by polarizing microglia toward an anti-inflammatory phenotype and augmenting amyloid-beta degradation.Additionally,mitochondrial metabolism is regulated by β2-adrenergic receptor,diminishing oxidative stress and allowing for bioenergetic resilience.Enriched environments mediate their neuroprotective effects through,in part,activation of β2-adrenergic receptor,supporting its role in promoting synaptic resilience.Pharmacological activation of β2-adrenergic receptor with specific agonists such as formoterol and clenbuterol has shown promise in preclinical models of Alzheimer's disease by restoring cognitive function and synaptic integrity.In this review,the molecular mechanisms of β2-adrenergic receptor-mediated neuroprotection are examined,with specific emphasis on its regulation of synaptic plasticity,neuroinflammation,mitochondrial function,and epigenetic control.Due to its multi-faceted action for maintenance of neuronal health,activation of β2-adrenergic receptor is an appealing therapy for Alzheimer's disease.Future research needs to target optimizing brain-penetrant β2-adrenergic receptor agonists and determining their longterm effects on Alzheimer's disease pathology. 展开更多
关键词 Alzheimer’s disease amyloid-beta β2-adrenergic receptor DNA methylation enriched environments histone modification long-term potentiation microglia microRNAs mitochondria neuroinflammation synaptic plasticity
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Methyl donor micronutrients orchestrate lipid metabolism:The role of DNA methylation modification 认领 引用
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作者 Li Han Qiyu Tian +3 位作者 Qi Han Yulong Yin Jie Yin Xingguo Huang 《Journal of Integrative Agriculture》 SCIE CAS CSCD 2026年第4期1343-1358,共16页
DNA methylation,a key epigenetic modification,plays a crucial role in regulating lipid metabolism.Consistent correlations have been observed between aberrant DNA methylation patterns and lipid metabolic disorders.Emer... DNA methylation,a key epigenetic modification,plays a crucial role in regulating lipid metabolism.Consistent correlations have been observed between aberrant DNA methylation patterns and lipid metabolic disorders.Emerging evidence indicates that methyl donor micronutrients could influence DNA methylation patterns,consequently exerting an influence on lipid metabolism.Specifically,the deficiency or excesses of methyl donor micronutrients(folate,choline,betaine,B vitamins and methionine)have been associated with altered DNA methylation patterns linked to lipid metabolism.These alteration in DNA methylation levels,occurring globally and within promoter regions,could affect gene expression related to lipid metabolism.However,the mechanisms through which methyl donor micronutrients regulate lipid metabolism via the DNA methylation modification and the role of methyl donor micronutrients supplementation on DNA methylation profiles remain unclear.In this review,we summarized the regulatory role of DNA methylation in lipid metabolism,and highlighted recent findings investigating the impact of methyl donor micronutrients on lipid metabolism,as well as DNA methylationmediated adipogenesis and adipose deposition.Taken together,this review deepened our understanding of how the complex interplay between methyl donor micronutrients,DNA methylation,and lipid metabolism,and provides valuable information for accurately regulating lipid metabolism of livestock and poultry,thereby improving meat quality,and promoting the development of animal husbandry. 展开更多
关键词 DNA methylation epigenetic lipid metabolism methyl donor micronutrients
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Synthesis of methyl diphenylmethane dicarbamate by methyl phenylcarbamate condensation catalyzed by NKC-9:Non-phosgene preparation of key precursors for diphenylmethane diisocyanate 认领 引用
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作者 Junya Cao Yi Hui +6 位作者 Yan Cao Jiaqiang Chen Zheng Zheng Liyan Zhao Peng He Huiquan Li Liguo Wang 《Chinese Journal of Chemical Engineering》 SCIE EI CAS CSCD 2026年第4期333-342,共10页
Methyl diphenylmethane dicarbamate(MDC)was synthesized by condensation of methyl phenylcarbamate(MPC)using trioxane as methylenation reagents over sulfonic acid resin catalyst.The effect of Brønsted's acid am... Methyl diphenylmethane dicarbamate(MDC)was synthesized by condensation of methyl phenylcarbamate(MPC)using trioxane as methylenation reagents over sulfonic acid resin catalyst.The effect of Brønsted's acid amount on the condensation reaction was investigated,and the optimal sulfonic acid resin(NKC-9)with an acid amount of 4.57 was determined.2-MDC,featuring a methylene-bridged biphenyl structure,achieved 91.6%selectivity and 83.2%yield after response surface methodology optimization.In situ FTIR spectroscopy was employed to monitor the condensation process.The spectroscopic results unequivocally demonstrate that trioxane undergoes catalytic depolymerization to formaldehyde over NKC-9 resin,which subsequently reacts with MPC to form MDC.After sulfuric acid regeneration,NKC-9 maintains its catalytic performance after 4 cycles. 展开更多
关键词 Methyl diphenylmethane dicarbamate Multiphase reaction Catalysis Chemical reaction Response surface optimization Reaction mechanism
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Revealing the formation of nanoparticulate mercury sulfide in Hg(Ⅱ)-DOM-Sulfide(-Ⅱ)systems with nanomolar Hg(Ⅱ)by using liquid chromatography-ICP-MS analysis 认领 引用
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作者 Ying Chen Peijie Yang +8 位作者 Yingying Guo Yanwei Liu Tao Jiang Maoyong Song Jianbo Shi Ligang Hu Yongguang Yin Yong Cai Guibin Jiang 《Journal of Environmental Sciences》 SCIE EI CAS CSCD 2026年第3期445-453,共9页
Sulfidation of mercury(Hg)in Hg(Ⅱ)-dissolved organic matter(DOM)-sulfide(S(-Ⅱ))systems has crucial impacts on its transport,transformation,and bioavailability risks in food chains(e.g.,from fish to humans)under anox... Sulfidation of mercury(Hg)in Hg(Ⅱ)-dissolved organic matter(DOM)-sulfide(S(-Ⅱ))systems has crucial impacts on its transport,transformation,and bioavailability risks in food chains(e.g.,from fish to humans)under anoxic environments.Probing this process remains a significant challenge due to low Hg concentrations and poor sensitivity of conventional characterization methods.Here,we systematically identified nanoparticulate mercury sulfide(nano-HgS)formation in Hg(Ⅱ)-DOM-S(-Ⅱ)systems at nanomolar Hg(Ⅱ)levels and deciphered its environmental factors by integrating liquid chromatography(LC)-ICP-MS combined with ultrafiltration-transmission electron microscopy(TEM).Ultrafiltration-TEM with energy dispersive spectroscopy confirmed the spherical nano-Hg S(~5 nm)formation.Formation kinetics demonstrated a rapid formation of nano-HgS,followed by a slow size increase.Environmental factors,including pH,DOM,S(-Ⅱ),and Ca2+,modulated nano-HgS size distributions by altering surface charge interactions(e.g.,electrostatic repulsion),whereas natural ligands(Cl-,citrate,mercaptopropionic acid)showed negligible effects.Crucially,nano-HgS was the predominant Hg species in the Hg(Ⅱ)-DOM-S(-Ⅱ)systems,rather than dissolved HgS species(e.g.,HgSaq0 and HgS22-).Although nano-Hg S,especially aged nano-HgS exhibits lower methylmercury production than Hg(Ⅱ)-DOM complex at 24 h incubation by Geobacter sulfurreducens PCA,higher methylation for newborn nano-HgS at the initial 8 h further highlights the previously proposed“Trojan horse”mechanism of uptake followed by intracellular dissolution of nano-HgS.This work provides a significant analytical tool for accurately identifying and quantifying nano-HgS in the Hg(Ⅱ)-DOM-S(-Ⅱ)systems and highlights the importance of assessing the methylation of newborn nano-HgS because it may amplify Hg toxicity in food chains through providing higher methylation production. 展开更多
关键词 Nanoparticulate mercury sulfide Dissolved organic matter Sulfide Ultrafiltration LC-ICP-MS Methylation
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DNA methylation landscapes of in vitro matured oocytes retrieved during endoscopic gynaecological procedures 认领 引用
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作者 Cui-Ling Lu Xue-Ling Song +6 位作者 Xiao-Ying Zheng Tian-Shu Song Xiao-Na Wang Jie Yan Rui Yang Rong Li Jie Qiao 《Journal of Genetics and Genomics》 SCIE CAS CSCD 2026年第1期121-130,共10页
In vitro maturation(IvM)of human oocytes offers cost efficiency and minimal invasiveness,serving as a valuable supplementary tool in assisted reproduction for fertility preservation,ovarian hyperstimulation syndrome p... In vitro maturation(IvM)of human oocytes offers cost efficiency and minimal invasiveness,serving as a valuable supplementary tool in assisted reproduction for fertility preservation,ovarian hyperstimulation syndrome prevention,and other reproductive strategies.Despite its availability for three decades,the clinical use of IVM remains limited due to efficacy and safety concerns.This study examines the DNA methylation profile of IVM oocytes collected during laparoscopic/hysteroscopic surgeries compared to in vivo matured oocytes via reduced representation bisulfite sequencing.Results indicate IVM oocytes exhibit a higher global methylation level.Differentially methylated regions(DMRs)analysis reveals that the in vitro group displays more hypermethylated and fewer hypomethylated DMRs compared to the in vivo group.Additionally,the in vitro group exhibits a higher level of non-CpG methylation than the in vivo group.However,no significant correlation between methylation levels and transcriptional activity in these oocytes is found,especially for those specific imprinted genes or genes related to embryonic development.These findings shed light on the epigenetic landscape of IvM oocytes,contributing to the ongoing assessment of their clinical feasibility and safety in assisted reproduction. 展开更多
关键词 In vitro maturation(IVM) DNA methylation Reduced representation bisulfite sequencing (RRBS) Differentially methylated regions(DMRs) Oocyte
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Tissue-specific epigenetic regulation of fat metabolism in pigs through integrated analysis of DNA methylation and gene expression networks 认领 引用
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作者 Do-Young Kim Byeonghwi Lim +3 位作者 Rajesh Kumar Pathak Woncheoul Park Jong-Eun Park Jun-Mo Kim 《Journal of Animal Science and Biotechnology》 SCIE CAS CSCD 2026年第3期1328-1344,共17页
Background Fat metabolism in pigs is controlled by tissue-specific molecular mechanisms that ultimately affect growth performance and meat quality.Understanding how epigenetic modifications interact with gene expressi... Background Fat metabolism in pigs is controlled by tissue-specific molecular mechanisms that ultimately affect growth performance and meat quality.Understanding how epigenetic modifications interact with gene expression across key metabolic and fat-depositing tissues is essential for identifying regulatory processes and potential biomarkers to improve pork quality traits.Therefore,this study aimed to elucidate tissue specific epigenetic regulation of fat metabolism by integrating DNA methylation and gene expression profiles from liver,backfat,and loin(longissimus dorsi)tissues at two physiologically developmental stages(10 and 26 weeks),representing the early post-weaning growth phase and near-market weight,respectively.By explicitly comparing these ages and tissues,the study was designed to capture the transition from muscle-dominated growth to increased lipid deposition and to identify tissue-and stage-specific regulatory signatures that may serve as biomarkers for pork quality.Results Genome-wide DNA methylation exhibited weak clustering by tissue,whereas gene expression showed clear tissue separation.The liver harbored fewer genes with differential methylation across stage and tissue but a greater number of genes with differential expression than backfat and loin,suggesting distinct regulatory modes.Integrative analysis of the overlap genes between methylation and expression signals highlighted epigenetically mediated regulation of extracellular matrix organization,lipid metabolism,and muscle development pathways.Furthermore,weighted gene co-expression network analysis revealed distinct tissue-specific correlations between co-methylated and co-expressed modules,with enrichment in cholesterol biosynthesis,muscle contractility,and extracellular matrix remodeling.Together,these findings suggest that methylation changes are more subtle than transcriptional shifts,yet they are aligned with key functional pathways,consistent with a role for methylation as a fine-tuning mechanism that shapes tissue-specific transcriptional networks during growth.Conclusions Across liver,backfat,and loin,DNA methylation modulates transcriptional programs in a tissue-dependent manner,prioritizing pathways central to lipid handling,extracellular matrix remodeling,and muscle function.This integrated multi-omics framework highlights candidate epigenetic markers and regulatory modules with potential utility for improving pork quality traits through selection or management strategies. 展开更多
关键词 DNA methylation Epigenetic Gene expression Multi-omics integration analysis Porcine
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Revealing low-temperature reaction mechanism of cobalt-doped CeO2 catalyst for catalytic removal of methyl mercaptan 认领 引用
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作者 Zijun Huang Xiaohua Cao +5 位作者 Huaiyu Xu Miao Lin Dedong He Dingkai Chen Jichang Lu Yongming Luo 《Journal of Rare Earths》 SCIE EI CAS CSCD 2026年第3期811-821,I0003,共11页
Methyl mercaptan(CH3SH)is notorious for global air pollution owing to its odorous characteristics and adverse health effects.Although CeO2 is currently regarded as a promising catalyst for CH3SH decomposition... Methyl mercaptan(CH3SH)is notorious for global air pollution owing to its odorous characteristics and adverse health effects.Although CeO2 is currently regarded as a promising catalyst for CH3SH decomposition,the high conversion temperature followed by high energy consumption is still a bottleneck.Herein,the cobalt-doped CeO2 catalyst was synthesized by a facile one-pot preparation strategy and successfully reduces the decomposition temperature from 450 to 250℃.Further studies demonstrate that the excellent low-temperature catalytic activity of Co0.6Ce0.4O2-σis attributed to its abundant oxygen vacancies and reactive oxygen species.Oxygen vacancies promote the adsorption and dissociation of CH3SH,while reactive oxygen species facilitate the decomposition of CH3SH.Moreover,Co acts as a sacrificial agent for the adsorption of sulfur species in CH3SH,while Ce is responsible for the adsorption and activation of CH3SH as the active metal phase.Furthermore,the migration and transformation mechanism of CH3SH on the surface of Co0.6Ce0.4O2-δwas determined via in situ diffuse reflectance infrared Fourier transform spectra(in situ-DRIFTS).This work provides a new strategy to synthesize highperformance catalysts for decomposing sulfur-containing volatile organic compounds(VOCs)at low temperatures,which is beneficial to decreasing the energy consumption. 展开更多
关键词 CoxCeyO2-δ Methyl mercaptan Catalytic decomposition Oxygen vacancies Reaction mechanism Rare earths
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Genetic and pathway complexity in Alzheimer's disease:Insights from multi-omic data about the immune response and mitochondrial function 认领 引用
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作者 Xuan Xu Jiang Li +4 位作者 Fei Wang Ke Xue Junwen He Xiangyu Meng Yin Shen 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第9期4406-4423,共18页
Despite recent developments,the genetics and biology of Alzheimer's disease remain insufficiently characterized.As an important first step toward developing effective treatment strategies to slow or prevent Alzhei... Despite recent developments,the genetics and biology of Alzheimer's disease remain insufficiently characterized.As an important first step toward developing effective treatment strategies to slow or prevent Alzheimer's disease onset,the identification of relevant genetic markers is crucial.In the present study,we analyzed transcriptomic and multi-omic datasets across multiple cohorts(the Alzheimer's Disease Neuroimaging Initiative,Religious Orders Study and Rush Memory and Aging Project,Mount Sinai Brain Bank,and Mayo Clinic Alzheimer's Disease Genetics Studies) using gene set enrichment analysis,machine learning algorithms,and polygenic risk scoring to identify gene sets relevant to Alzheimer's disease risk and pathological features.For prioritized gene sets,we performed epigenome-wide association studies to assess DNA methylation patterns,and used multi-omic mediation analysis to characterize the causal gene regulatory networks.Overall,we identified several key gene sets relevant to Alzheimer's disease pathology—particularly,those related to immune system function and mitochondrial dysfunction.Upregulated pathways,including neutrophil degranulation and tumor necrosis factor-α signaling pathways,correlated strongly with aspects of neuroinflammation in Alzheimer's disease.By contrast,downregulated oxidative phosphorylation pathways further suggested mitochondrial dysfunction.Gene sets that contained mitochondrially located genes(e.g.,SGK1 and LRRK1) were identified as significantly contributing to neurodegeneration.Moreover,genes such as CXCL1,TGFB2,and DUSP1 were consistently implicated in all datasets,thus emphasizing their involvement in immune modulation and mitochondrial function.The multimodal investigation outlined in the current study represents useful steps toward comprehending the genetic architecture of Alzheimer's disease,including an expanded understanding of the spatial interactions of genes associated with disease susceptibility.Mitochondrial dysfunction and immune modulation were pathological pathways that converged on Alzheimer's disease and future treatment novel options.Using the frameworks provided in the current comprehensive study,we present opportunities to explore targeted treatment strategies that may alter immune systems and mitochondrial function to optimize treatment outcomes for individuals at increased risk of or living with Alzheimer's disease. 展开更多
关键词 Alzheimer’s disease DNA methylation epigenetic gene regulatory networks machine learning mitochondrial dysfunction multi-omics analysis nerve regeneration neuroinflammation
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Recent advances in the catalytic removal of gaseous methyl mercaptan 认领 引用
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作者 Xiaofeng Liu Dongling Liu +3 位作者 Litong Peng Yuqin Lu Jingjing Zhao Wangchuan Xiao 《Journal of Environmental Sciences》 SCIE EI CAS CSCD 2026年第6期676-695,共20页
Methyl mercaptan(CH3SH)is a malodorous and toxic gas commonly emitted from petrochemical,pharmaceutical,and wastewater treatment industries.Due to its low odor threshold and contribution to secondary atmospheric po... Methyl mercaptan(CH3SH)is a malodorous and toxic gas commonly emitted from petrochemical,pharmaceutical,and wastewater treatment industries.Due to its low odor threshold and contribution to secondary atmospheric pollution,its effective removal is essential.Traditional methods,such as adsorption,absorption,biodegradation,and non-thermal plasma,often suffer from limitations in efficiency and stability.Catalytic technologies have garnered increasing attention for their high removal efficiency,low energy consumption,and environmental compatibility.This review highlights recent advances in the gas-phase catalytic elimination of CH3SH,focusing on reaction mechanisms,catalyst design,and performance metrics.Special emphasis is placed on strategies such as oxygen vacancy engineering,modulation ofmetal oxidation states,and interface/defect tuning to enhance catalytic activity and durability.Key performance factors are discussed,and current challenges are critically evaluated.Finally,future research directions are proposed to support the development of efficient and sustainable CH3SH abatement technologies. 展开更多
关键词 Methyl mercaptan(CH3SH) Catalytic technologies Oxygen vacancy engineering Reaction mechanism Air pollutant removal
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Dimerization-induced conformational transitions of yeast iso-1 cytochrome c 认领 引用
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作者 Qianwen Wang Peng Sun +11 位作者 Qin Hu Mojie Duan Guangqing Zhang Jianhua Zhan Minghui Yang Qinjun Zhu Bin Yuan Bin Jiang Lichun He Maili Liu Xu Zhang Danyun Zeng 《Magnetic Resonance Letters》 EI CAS 2026年第3期61-74,共14页
Cytochrome c is a multifunctional protein involved in electron transport and apoptosis.However,its conformational landscape is complex and heterogeneous,which has obscured the functional understanding—particularly re... Cytochrome c is a multifunctional protein involved in electron transport and apoptosis.However,its conformational landscape is complex and heterogeneous,which has obscured the functional understanding—particularly regarding its long-observed dimerized state.In this study,we characterized the conformational distributions of yeast iso-1 cytochrome c(ycyt c)by exploiting the native trimethylated K72 residue(K72me3)as an NMR molecular probe.Our analysis revealed that C102-mediated dimerization disrupts the M80-heme iron coordination,shifting the equilibrium toward conformations featuring an exposed heme and enhanced peroxidase activity.Furthermore,molecular dynamics simulations suggest that the oxidized monomer samples an"open"conformation,which increases the active site accessibility,likely contributing to its elevated peroxidase activity.These findings shed light on the biological significance of C102 in ycyt c and propose a novel mechanism by which dimerization activates the protein as a peroxidase,potentially protecting cells against apoptosis or other oxidative damages. 展开更多
关键词 Cytochrome c Dimerization Conformational transitions Peroxidase activity Apoptosis Methyl selective NMR
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Dual-Direction of DNA Methylome Reprogramming During Rice Domestication 认领 引用
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作者 YU Xiaoman CHENG Xiang +8 位作者 LI Yilin YU Ruoqian LIU Jiajia YANG Lingwei HE Huiying WEI Hua SHANG Lianguang WANG Yuexing LIU Xiangpei 《Rice science》 SCIE CAS CSCD 2026年第3期287-291,I0153-I0170,共5页
Crop domestication has been attributed predominantly to selection on DNA sequence variation,yet the role of epigenetic factors remains largely unknown.Here,we conducted a genome-wide comparative methylome analysis of ... Crop domestication has been attributed predominantly to selection on DNA sequence variation,yet the role of epigenetic factors remains largely unknown.Here,we conducted a genome-wide comparative methylome analysis of African and Asian wild and cultivated rice species,revealing extensive methylation reprogramming during domestication. 展开更多
关键词 methylomeanalysis crop domestication dual direction methylome reprogramming rice domestication epigenetic factors genomewide sequencevariation methylation reprogramming comparative epigenetic factors
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Epigenetic landscape of gastrointestinal stromal tumors:Mechanistic insights and therapeutic opportunities 认领 引用
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作者 Stavros P Papadakos Georgios Mandrakis +4 位作者 Spyros I Siakavellas Nikolaos Memos Hara Gakiopoulou Dimitrios Schizas Stamatios Theocharis 《World Journal of Gastroenterology》 SCIE CAS 2026年第17期10-27,共18页
Gastrointestinal stromal tumors(GISTs)are the most common mesenchymal neoplasms of the gastrointestinal tract and are primarily driven by activating mutations in KIT or PDGFRA.A clinically important subset of KIT/PDGF... Gastrointestinal stromal tumors(GISTs)are the most common mesenchymal neoplasms of the gastrointestinal tract and are primarily driven by activating mutations in KIT or PDGFRA.A clinically important subset of KIT/PDGFRA wild-type GISTs harbors alterations affecting succinate dehydrogenase subunit genes,which are associated with distinct biology and epigenetic profiles.The introduction of tyrosine kinase inhibitors has transformed their management,yet resistance and recurrence remain major challenges.Increasing evidence indicates that epigenetic processes contribute to tumor initiation,progression,and therapeutic escape.Aberrant promoter methylation has been linked to silencing of tumor suppressor genes,histone modifications reshape transcriptional networks governing proliferation and apoptosis,and chromatin remodeling complexes influence lineage-specific transcription and resistance pathways.Clinical observations further demonstrate that alterations such as SETD2 loss,KDM6A downregulation,or PHH3 overexpression correlate with prognosis,while early-phase trials of histone deacetylase inhibitors illustrate therapeutic feasibility.This review synthesizes current preclinical and clinical evidence on epigenetic regulation in GIST,focusing on DNA methylation,histone modifications,and chromatin remodeling,and explores their translational implications for prognosis and therapy. 展开更多
关键词 Gastrointestinal stromal tumor Epigenetics DNA methylation Histone modifications Chromatin remodeling Therapeutic resistance Biomarkers
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Association between early-life submicron particulate matter exposure,inducible nitric oxide synthase methylation,and children's asthma/wheezing 认领 引用
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作者 Chaoqun Liu Ying Huang +7 位作者 Ying Zhong Yunyan Yang Jiaying Nie Wenen Su Xinqi Zhong Zhiqing Chen Siwen Yu Tao Liu 《Journal of Environmental Sciences》 SCIE EI CAS CSCD 2026年第8期669-681,共13页
The impact of PM1(particulate matter with aerodynamic diameter≤1μm)exposure on asthma risk during specific fetal lung development windows,and its potential mediation by DNA methylation,remains understudied.Thus,we c... The impact of PM1(particulate matter with aerodynamic diameter≤1μm)exposure on asthma risk during specific fetal lung development windows,and its potential mediation by DNA methylation,remains understudied.Thus,we conducted a nested case-control study from the Prenatal Environments and Offspring Health cohort with children having asthma/wheezing.The results revealed a positive correlation between average prenatal PM1 exposure and childhood asthma/wheezing risk(HR=1.39,95%CI:1.02,1.90),especially during the pseudoglandular period.PM1 exposure was negatively correlated with neonatal inducible nitric oxide synthase(iNOS)methylation(IQR(interquartile range)=4.44μg/m3,β=-1.19%,95%CI:-2.23%,-0.15%).Additionally,a 5.6%increase(the interquartile range)in neonatal iNOS methylation was associated with a reduced risk of childhood asthma/wheezing(OR=0.62,95%CI:0.43,0.88).In vitro studies showed PM1 treatment increased nitric oxide(NO)production and iNOS expression,and reduced iNOS methylation.Moreover,PM1 induced the accumulation of reactive oxygen species(ROS)and pro-inflammatory responses in human bronchial epithelial(HBE)cells,activating NOD-like receptor protein 3(NLRP3)inflammasomes and caspase-1 for inflammation,caspase-3and caspase-9 for apoptosis.NF-κB expression,crucial for NLRP3 synthesis,was also increased.In conclusion,maternal PM1 exposure was associated with childhood asthma/wheezing,especially during the pseudoglandular stage,and this effect may relate to iNOS hypomethylation as well as the exacerbation of oxidative stress and inflammation,possibly involving the iNOS/NLRP3/NF-κB signaling pathway. 展开更多
关键词 Submicron particulate matter iNOS methylation Asthma and wheezing Prenatal exposure Human bronchial epithelial cells(HBE cells)
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Catalpol ameliorates diabetic retinal vascular endothelial injury by suppressing NLRP3 inflammasome via targeting METTL3-m6A modification 认领 引用
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作者 Jing-Yu Liu Jun-Ya Zhu +3 位作者 Yi-Fang Xiao Yi-Rui Ge Feng Yan Qin Jiang 《International Journal of Ophthalmology(English edition)》 SCIE CAS 2026年第6期1038-1047,共10页
AIM:To investigate whether catalpol protects against diabetic retinal vascular endothelial injury by targeting the methyltransferase-like 3(METTL3)-m6A-thioredoxininteracting protein(TXNIP)axis and inhibiting nucle... AIM:To investigate whether catalpol protects against diabetic retinal vascular endothelial injury by targeting the methyltransferase-like 3(METTL3)-m6A-thioredoxininteracting protein(TXNIP)axis and inhibiting nucleotidebinding oligomerization domain(NOD)-like receptor family pyrin domain containing 3(NLRP3)inflammasome activation.METHODS:A streptozotocin-induced diabetic mouse model(n=20 per group)was used to assess retinal function via electroretinogram(ERG)and vascular integrity via Evans Blue leakage.Human retinal vascular endothelial cells(HRVECs)were exposed to high glucose(HG,30 mmol/L)with or without catalpol or the METTL3 inhibitor STM2457.NLRP3 inflammasome components(Western blot),oxidative stress(DCFH-DA probe),global m6A levels(Dot blot),and TXNIP expression were measured.The binding of catalpol to METTL3,NLRP3,TXNIP,and interleukin-1β(IL-1β)was analyzed via molecular docking and dynamics simulations.RESULTS:Catalpol treatment improved ERG amplitudes[a-wave,b-wave,oscillatory potentials(OPs)]and reduced vascular leakage in diabetic mice(P<0.05),while downregulating retinal vascular endothelial growth factor(VEGF),NLRP3,IL-1β,and IL-18 protein levels.In HGstimulated HRVECs,catalpol inhibited the NLRP3-apoptosisassociated speck-like protein containing a CARD(ASC)-caspase-1 inflammasome,reduced reactive oxygen species,and suppressed METTL3 expression and global m6A methylation(P<0.05).It also attenuated HG-induced TXNIP upregulation.METTL3 inhibition by STM2457 mimicked all protective effects of catalpol.Molecular simulations confirmed stable binding of catalpol to METTL3,NLRP3,TXNIP,and IL-1β.CONCLUSION:Catalpol alleviates diabetic retinal vascular endothelial injury by inhibiting the NLRP3 inflammasome.This effect is mediated,at least in part,through downregulating METTL3-dependent m6A RNA methylation of TXNIP. 展开更多
关键词 catalpol diabetic retinopathy NLRP3 inflammasome METTL3 m6A methylation
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