Journal of Biological Chemistry最新文献_第4页

APP family is a regulator of endo-lysosomal membrane vulnerability. APP家族是内溶酶体膜易损性的调节因子。

IF 4.8 2区生物学

Journal of Biological Chemistry Pub Date : 2025-09-27 DOI: 10.1016/j.jbc.2025.110774

Brianna Lundin,Natalia Wieckiewicz,Midori Yokomizo,Michael Sadek,Desmond Owusu Kwarteng,John R Dickson,Robert G R Sobolewski,Victoria Derosla,Gokce Armagan,Florian Perrin,Bradley T Hyman,Oksana Berezovska,Masato Maesako

{"title":"APP family is a regulator of endo-lysosomal membrane vulnerability.","authors":"Brianna Lundin,Natalia Wieckiewicz,Midori Yokomizo,Michael Sadek,Desmond Owusu Kwarteng,John R Dickson,Robert G R Sobolewski,Victoria Derosla,Gokce Armagan,Florian Perrin,Bradley T Hyman,Oksana Berezovska,Masato Maesako","doi":"10.1016/j.jbc.2025.110774","DOIUrl":"https://doi.org/10.1016/j.jbc.2025.110774","url":null,"abstract":"The amyloid precursor protein (APP) is cleaved by β- and γ-secretases, resulting in the generation of β-amyloid (Aβ). Aβ peptides accumulate in the brain of Alzheimer's disease (AD), and the removal of toxic Aβ species using antibodies slows the progression of the disease. However, the potential physiological function(s) of APP and its family members remains elusive. Various studies, including ours, reported that APP C99 is primarily processed by γ-secretase in the endo-lysosomal compartments. Here, we report using a series of complementary assays that the endo-lysosomal membrane in APP/APLP2-deficient mouse embryonic fibroblasts (MEFs) is more vulnerable to leakage caused by oxidative stress, adeno-associated virus (AAV), or tau incubation, compared to that in wild-type controls. The increased vulnerability of endo-lysosome membrane is, in part, rescued by APP overexpression, suggesting the contribution of both APP and APLP2. Mechanistically, we observed distinct lipid profiles, including increased cholesterol and Hex1Cer, between the membrane of APP/APLP2 knockout and that of WT MEF cells. Furthermore, we uncovered higher APP expression in primary neurons from the cerebellum of mouse embryos compared to those from the cortex, and the endo-lysosomal membrane in the cerebellum neurons is less vulnerable to leakage than that in the cortical neurons. Taken together, our findings suggest an unrecognized role of APP and its family members in the regulation of endo-lysosomal membrane vulnerability.","PeriodicalId":15140,"journal":{"name":"Journal of Biological Chemistry","volume":"201 1","pages":"110774"},"PeriodicalIF":4.8,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145188923","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Identification and Rescue of Congenital Hyperinsulinism-Associated ABCC8 Mutations that Impair K_ATP Channel Trafficking. 先天性高胰岛素相关ABCC8突变损害KATP通道运输的鉴定和抢救。

IF 4 2区生物学

Journal of Biological Chemistry Pub Date : 2025-09-27 DOI: 10.1016/j.jbc.2025.110779

Assmaa ElSheikh, Yi-Ying Kuo, Kara E Boodhansingh, Zhongying Yang, Charles A Stanley, Diva D De Leon, Show-Ling Shyng

{"title":"Identification and Rescue of Congenital Hyperinsulinism-Associated ABCC8 Mutations that Impair KATP Channel Trafficking.","authors":"Assmaa ElSheikh, Yi-Ying Kuo, Kara E Boodhansingh, Zhongying Yang, Charles A Stanley, Diva D De Leon, Show-Ling Shyng","doi":"10.1016/j.jbc.2025.110779","DOIUrl":"10.1016/j.jbc.2025.110779","url":null,"abstract":"KATP channels composed of Kir6.2 and sulfonylurea receptor 1 (SUR1) couple glucose metabolism with insulin secretion in pancreatic β-cells. Loss-of-function mutations in the large regulatory SUR1 subunit encoded by ABCC8 are the most common causes of severe persistent hypoglycemia in infants and children seen in the rare disease congenital hyperinsulinism (HI). The N-terminal transmembrane domain, TMD0, and the linker immediately C-terminal to TMD0, L0, of SUR1 (TMD0/L0) forms direct contact with Kir6.2 in KATP channels. Mutations in SUR1-TMD0/L0 often impair KATP channel trafficking to the plasma membrane, causing severe disease unresponsive to treatment by the KATP activator diazoxide; however, surface expression and function of many such mutant channels can be rescued by reversible KATP inhibitor pharmacochaperones. Here, we identified seven new SUR1 missense mutations in TMD0/L0 from HI patients unresponsive to diazoxide and investigated their effects on KATP channel expression, function, and response to pharmacochaperones. All seven mutations, N32K, Y124F, P133R, W143R, L171P, G228D, and Y230C, reduced channel function in Rb+ efflux assays. Further characterization by immunoblotting, immunostaining and electrophysiology revealed that Y124F primarily causes defective channel gating, while the others impair channel trafficking to different extents. The trafficking mutations showed varied response to surface expression and function rescue by the reversible KATP inhibitor pharmacochaperones, tolbutamide and Aekatperone. The study underscores the critical role of SUR1-TMD0/L0 in KATP expression and gating. It further highlights the importance of detailed biochemical and functional studies of mutant channels in understanding their pathogenic roles and response to potential pharmacological therapies.","PeriodicalId":15140,"journal":{"name":"Journal of Biological Chemistry","volume":" ","pages":"110779"},"PeriodicalIF":4.0,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145191712","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

NITAC-Mediated ISGylation of eIF4E2 Attenuates GSK3β Proline-Directed Kinase Activity, Conferring Cytoprotection. nitac介导的eIF4E2的isg酰化降低了GSK3β脯氨酸定向激酶的活性，赋予细胞保护作用。

IF 4.8 2区生物学

Journal of Biological Chemistry Pub Date : 2025-09-27 DOI: 10.1016/j.jbc.2025.110777

Lan Li,Jinjin Gong,Huiting Liang,Ying Yang,Yuanshun Wu,Ziyi Yin,Anni Wang,Shaoxiang Luo,Jian Chen,Min Zhang

{"title":"NITAC-Mediated ISGylation of eIF4E2 Attenuates GSK3β Proline-Directed Kinase Activity, Conferring Cytoprotection.","authors":"Lan Li,Jinjin Gong,Huiting Liang,Ying Yang,Yuanshun Wu,Ziyi Yin,Anni Wang,Shaoxiang Luo,Jian Chen,Min Zhang","doi":"10.1016/j.jbc.2025.110777","DOIUrl":"https://doi.org/10.1016/j.jbc.2025.110777","url":null,"abstract":"Eukaryotic translation initiation factor 4E family member 2 (eIF4E2) has recently been identified as an interacting protein of GSK3β and regulates its proline-directed kinase activity. eIF4E2 undergoes ISGylation at K134 and K222, a conserved post-translational modification mediated by interferon-stimulated gene 15 (ISG15). In this study, we engineered a novel NITAC (Nanobody-based ISGylation Targeting Chimera) tool to specifically activate eIF4E2 ISGylation and investigate its role in the eIF4E2-GSK3β signaling pathway. By integrating eIF4E2-specific nanobodies Nb.30C7 with the catalytic E3 ligase domain HECT from HERC5, we constructed the NITAC (Nb.30C7-HECT). This NITAC tool mediates site-specific ISGylation of eIF4E2, enhancing the eIF4E2-GSK3β interaction and unexpectedly suppressing proline-directed serine/threonine (S/T-P) phosphorylation across multiple crucial targets within the eIF4E2-GSK3β pathway. Importantly, NITAC treatment exerted cytoprotection against oxygen-glucose deprivation/reperfusion (OGD/R) stress, a commonly used in vitro model to simulate ischemic conditions in cell cultures. Furthermore, NITAC treatment reduced reactive oxygen species (ROS) in neurons and microglia and promoted an anti-inflammatory phenotype in microglia by suppressing S/T-P phosphorylation. In summary, we created a novel NITAC to specifically activate eIF4E2 ISGylation, which showed cytoprotective effects under OGD/R stress by inhibiting GSK3β proline-directed kinase activity.","PeriodicalId":15140,"journal":{"name":"Journal of Biological Chemistry","volume":"19 1","pages":"110777"},"PeriodicalIF":4.8,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145188837","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Widespread deployment of the human CD38 ADP-ribosyl cyclase fold in antibacterial and anti-eukaryotic polymorphic toxins. 人类CD38 adp -核糖素环化酶折叠在抗菌和抗真核多态毒素中的广泛部署。

IF 4.8 2区生物学

Journal of Biological Chemistry Pub Date : 2025-09-27 DOI: 10.1016/j.jbc.2025.110775

Julius Martinkus,Laurent Terradot,Dukas Jurėnas,Eric Cascales

{"title":"Widespread deployment of the human CD38 ADP-ribosyl cyclase fold in antibacterial and anti-eukaryotic polymorphic toxins.","authors":"Julius Martinkus,Laurent Terradot,Dukas Jurėnas,Eric Cascales","doi":"10.1016/j.jbc.2025.110775","DOIUrl":"https://doi.org/10.1016/j.jbc.2025.110775","url":null,"abstract":"Bacterial polymorphic toxins are modular weapons that mediate inter-microbial competition and host interactions by delivering diverse cytotoxic domains through specialized secretion systems. Here, we identify and characterize a novel toxin domain in Pantoea ananatis that displays remarkable structural and functional conservation with the human enzyme CD38. This bacterial toxin, fused to a type VI secretion system (T6SS) PAAR domain, harbors a C-terminal ADP-ribosyl cyclase (ARC) domain that hydrolyzes NAD+ and NADP+in vitro and in vivo, leading to growth inhibition in both bacterial and eukaryotic cells. The 1.6-Å resolution structure of ARC reveals that it adopts a globular fold nearly identical to the human CD38 ADP ribosyl cyclase, with key catalytic residues conserved. Comparative genomics reveals that CD38-like ARC domains are widespread in bacteria, fused to diverse delivery modules including T6SS, T7SS, and CDI systems. Functional assays demonstrate that these domains act as NAD-depleting toxins, with cross-immunity observed between non-cognate toxin-immunity pairs. Taken together, our findings identify a bacterial NAD+ hydrolase fold with strong similarity to human CD38 and define a novel class of metabolic toxins, expanding the functional scope of polymorphic effectors and illustrating how enzymes can be co-opted for microbial warfare.","PeriodicalId":15140,"journal":{"name":"Journal of Biological Chemistry","volume":"5 1","pages":"110775"},"PeriodicalIF":4.8,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145188925","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Nitric Oxide Regulates Cytochrome P450 2D6 and 3A4 Activity via Concentration-Dependent Modulation of Heme Loading. 一氧化氮通过血红素负荷浓度依赖性调节细胞色素P450 2D6和3A4活性。

IF 4.8 2区生物学

Journal of Biological Chemistry Pub Date : 2025-09-27 DOI: 10.1016/j.jbc.2025.110772

Priya Das Sinha,Sidra Islam,Pranjal Biswas,Dennis J Stuehr

{"title":"Nitric Oxide Regulates Cytochrome P450 2D6 and 3A4 Activity via Concentration-Dependent Modulation of Heme Loading.","authors":"Priya Das Sinha,Sidra Islam,Pranjal Biswas,Dennis J Stuehr","doi":"10.1016/j.jbc.2025.110772","DOIUrl":"https://doi.org/10.1016/j.jbc.2025.110772","url":null,"abstract":"Cytochrome P450 enzymes (CYP) play diverse roles in human health and disease, and although their activities depend on their heme contents, the cellular mechanisms governing CYP heme levels are unclear. Because CYP activities are influenced by biological nitric oxide (NO), we investigated how a range of NO exposures would impact the heme levels and activities of CYP2D6 and 3A4 expressed in CHO cells and in the human liver cell line HepG2. Following expression, both CYPs were present as a 60:40 mix of heme-free and heme-bound forms. A low range of NO concentrations (approximately 1-10 nM) generated in cultures by a chemical NO donor or by added activated macrophages caused cells to allocate heme into their heme-free CYP3A4 and 2D6 populations such that the levels of heme-replete and active CYPs increased by 2 to 3-fold. NO concentrations above this range (approximately 25-100 nM) gradually lost the positive effect and at the higher level caused heme loss from the CYPs and corresponding losses in activity. The positive or negative effects of NO began within the first 2 h of exposure and completed within 6 h. The NO-driven increase in CYP heme content relied on a GAPDH-heme complex forming and chaperone Hsp90 activity in the cells. Thus, NO can up- or down-regulate cellular CYP3A4 and 2D6 activities by exerting a concentration-dependent change in their heme contents. This may help explain how NO generation in disease or inflammation can change CYP activities and impact drug pharmacokinetics and the generation of immune-active metabolites.","PeriodicalId":15140,"journal":{"name":"Journal of Biological Chemistry","volume":"68 1","pages":"110772"},"PeriodicalIF":4.8,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145188929","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Apolipoprotein E (APOE) regulates the transport of monosialotetrahexosylganglioside (GM1). 载脂蛋白E （APOE）调节单唾液酸四己糖神经节苷脂（GM1）的转运。

IF 4.8 2区生物学

Journal of Biological Chemistry Pub Date : 2025-09-27 DOI: 10.1016/j.jbc.2025.110778

Dong Yan Zhang,Jian Wang,Gangtong Huang,Martin Dokholyan,Smaranda Willcox,Jack Griffith,Feng Ding,Nikolay V Dokholyan

{"title":"Apolipoprotein E (APOE) regulates the transport of monosialotetrahexosylganglioside (GM1).","authors":"Dong Yan Zhang,Jian Wang,Gangtong Huang,Martin Dokholyan,Smaranda Willcox,Jack Griffith,Feng Ding,Nikolay V Dokholyan","doi":"10.1016/j.jbc.2025.110778","DOIUrl":"https://doi.org/10.1016/j.jbc.2025.110778","url":null,"abstract":"Apolipoprotein E (APOE) is a key lipid transporter involved in the trafficking and clearance. The ε4 allele of APOE (APOE4) is the strongest genetic risk factor for late-onset Alzheimer's disease (AD), and certain lipids are closely linked to AD pathology. APOE may contribute to AD pathogenesis through its lipid transport function. Although cholesterol is a well-established cargo of APOE and has been associated with AD, its role as a mechanistic link between APOE and AD has not been demonstrated. Here, we demonstrate that monosialotetrahexosylganglioside (GM1), a membrane lipid implicated in AD, is a preferential binder of APOE. We have previously shown that GM1 promotes amyloid beta (Aβ) oligomer aggregation, which is a critical step in AD pathology. Here, we show that APOE binds GM1 with higher affinity than cholesterol and facilitates greater cellular uptake of GM1-containing lipid structures in a cell-type-dependent manner. Furthermore, GM1 alters the secondary structure of APOE and enhances its interaction with the low-density lipoprotein receptor (LDLR), thereby promoting the internalization of lipid assemblies. Using confocal imaging and discrete molecular dynamics simulations, we show that membranes containing 20% GM1 form stable stripe-like clusters, consistent with the formation of GM1-enriched lipid rafts that may serve as physiological platforms for APOE:GM1 interactions. These results reveal a reciprocal relationship in which APOE regulates GM1 transport, while GM1 modifies APOE function and localization. The competition between GM1 and cholesterol for APOE binding may contribute to cholesterol dysregulation in APOE4 carriers. Our results uncover a novel mechanistic link between APOE and AD pathogenesis through GM1-mediated promotion of Aβ aggregation.","PeriodicalId":15140,"journal":{"name":"Journal of Biological Chemistry","volume":"101 1","pages":"110778"},"PeriodicalIF":4.8,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145188928","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Leptin and G-protein coupled receptor (GPCR) Signaling: Therapeutic Potential in Obesity. 瘦素和g蛋白偶联受体（GPCR）信号传导：肥胖症的治疗潜力。

IF 4.8 2区生物学

Journal of Biological Chemistry Pub Date : 2025-09-26 DOI: 10.1016/j.jbc.2025.110768

Xun Sun,Lincoln Brueck,Dongming Yang,Patrick L Sheets,Baohua Zhou,Hongxia Ren

{"title":"Leptin and G-protein coupled receptor (GPCR) Signaling: Therapeutic Potential in Obesity.","authors":"Xun Sun,Lincoln Brueck,Dongming Yang,Patrick L Sheets,Baohua Zhou,Hongxia Ren","doi":"10.1016/j.jbc.2025.110768","DOIUrl":"https://doi.org/10.1016/j.jbc.2025.110768","url":null,"abstract":"Leptin, an adipocyte-derived hormone, plays a crucial role in regulating food intake and energy homeostasis. However, individuals with obesity exhibit hyperleptinemia and impaired leptin responsiveness, which contribute to greater food intake, reduced energy expenditure, and metabolic dysregulation, exacerbating weight gain and obesity-related complications. Leptin resistance remains a major challenge in obesity treatment, limiting the efficacy of leptin-based therapies. G-protein coupled receptors (GPCRs) are a large family of seven-transmembrane (7TM) receptors that respond to a variety of ligands, including neuropeptides, gastrointestinal hormones, and metabolites. GPCRs are central regulators of glucose metabolism and energy balance, which have emerged as key drug targets for diabetes and obesity. Combining leptin with GPCR-targeting therapies, such as gut peptides, shows promise in overcoming leptin resistance and improving metabolic outcomes. Understanding the molecular crosstalk between leptin and GPCRs provides valuable insights for expanding leptin's therapeutic potential and developing effective anti-obesity treatments. In this review, we highlight the therapeutic potential of combining molecules targeting GPCR signaling with leptin for obesity treatment.","PeriodicalId":15140,"journal":{"name":"Journal of Biological Chemistry","volume":"1 1","pages":"110768"},"PeriodicalIF":4.8,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145182707","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The necessity of multi-parameter normalization in cyanobacterial research: A case study of the PsbU in Synechocystis sp. PCC 6803 using CRISPRi. 蓝藻研究中多参数归一化的必要性——以CRISPRi技术对Synechocystis sp. PCC 6803中PsbU的研究为例

IF 4.8 2区生物学

Journal of Biological Chemistry Pub Date : 2025-09-24 DOI: 10.1016/j.jbc.2025.110763

Maria Christine Veit,Ron Stauder,Yu Bai,Ragini Gabhrani,Matthias Schmidt,Stephan Klähn,Bin Lai

{"title":"The necessity of multi-parameter normalization in cyanobacterial research: A case study of the PsbU in Synechocystis sp. PCC 6803 using CRISPRi.","authors":"Maria Christine Veit,Ron Stauder,Yu Bai,Ragini Gabhrani,Matthias Schmidt,Stephan Klähn,Bin Lai","doi":"10.1016/j.jbc.2025.110763","DOIUrl":"https://doi.org/10.1016/j.jbc.2025.110763","url":null,"abstract":"Photosystem II (PSII) is a multiprotein complex and plays a central role in oxygenic photosynthesis. PsbU, a 12 kDa subunit of PSII, is associated with thermotolerance and a structural stabilization of the oxygen-evolving complex in cyanobacteria. Corresponding knockout strains showed decreased oxygen evolution rates, although the growth was not impaired. In this study, we provide further insights into the consequences of PsbU perturbations and propose to revisit the impact of PsbU on cell physiology. We made use of CRISPRi to knock down the psbU gene in Synechocystis sp. PCC 6803, and assessed previously described effects referred to different biomass parameters including optical density, chlorophyll a content and cell number. After knocking down psbU, the growth rate was decreased by 15% based on counting the cell numbers, while this effect was not observed when monitoring optical density. Furthermore, the oxygen evolution rate per cell in the psbU knockdown strain did not show a significant difference compared to the control groups, which was probably due to its larger cell size and higher chlorophyll a content per cell. The decreased quantum efficiency of pigments was compensated by the increased pigment content on single cell level in the knockdown strain. Our results complement previous analyses and highlight the importance of evaluating cyanobacterial physiology based on different biomass quantitative units to avoid misinterpretation of the results.","PeriodicalId":15140,"journal":{"name":"Journal of Biological Chemistry","volume":"18 1","pages":"110763"},"PeriodicalIF":4.8,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145153496","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Omics Characteristics and Epigenetic Modifications of Adipose-Derived Stem Cells. 脂肪来源干细胞的组学特征和表观遗传修饰。

IF 4.8 2区生物学

Journal of Biological Chemistry Pub Date : 2025-09-24 DOI: 10.1016/j.jbc.2025.110758

Tiange Feng,Clifford J Rosen,Ziru Li

引用次数: 0

A shared basis for nutrient limitation response in cyanobacteria. 蓝藻中营养限制反应的共同基础。

IF 4.8 2区生物学

Journal of Biological Chemistry Pub Date : 2025-09-24 DOI: 10.1016/j.jbc.2025.110765

Hagit Zer,Stav Chen,David Rasin,Miguel Hernandez-Prieto,Nir Keren

{"title":"A shared basis for nutrient limitation response in cyanobacteria.","authors":"Hagit Zer,Stav Chen,David Rasin,Miguel Hernandez-Prieto,Nir Keren","doi":"10.1016/j.jbc.2025.110765","DOIUrl":"https://doi.org/10.1016/j.jbc.2025.110765","url":null,"abstract":"Cyanobacteria possess diverse regulatory mechanisms to adapt to nutrient limitation, yet the extent to which these responses are shared across different nutrient stresses remains unclear. Understanding these commonalities can reveal fundamental principles of cellular resource allocation and survival strategies. In this work, we investigated the transcriptional responses of Synechocystis sp. PCC 6803 to nitrogen, sulphur or phosphate limitation and found a core set of genes consistently regulated across all three conditions. This shared response includes repression of genes related to photosynthesis and respiratory electron transport, as well as genes encoding components of the Calvin-Benson cycle, ribosome function and cellular metabolism. Amongst the highest affected pathways is chlorophyll biosynthesis. A subset of regulatory genes, mostly kinases, are upregulated under all three limitation conditions. These results were further validated by a study of the composition and the function of the photosynthetic machinery. Chlorophyll accumulation was arrested immediately upon transition to limiting media, photosynthetic activities were reduced and protein complexes were degraded. Our findings reveal a conserved program in cyanobacteria that modulates cellular metabolism and photosynthesis in response to diverse nutrient limitations. Based on these findings, we suggest that chlorophyll biosynthesis is a key regulated pathway driving structural and physiological responses in photosynthesis.","PeriodicalId":15140,"journal":{"name":"Journal of Biological Chemistry","volume":"4 1","pages":"110765"},"PeriodicalIF":4.8,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145153500","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0