دورية أكاديمية
Crosstalk of MAP3K1 and EGFR signaling mediates gene-environment interactions that block developmental tissue closure.
| العنوان: | Crosstalk of MAP3K1 and EGFR signaling mediates gene-environment interactions that block developmental tissue closure. |
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| المؤلفون: | Wang J; Department of Environmental and Public Health Sciences, University of Cincinnati, College of Medicine, Cincinnati, Ohio, USA., Xiao B; Department of Environmental and Public Health Sciences, University of Cincinnati, College of Medicine, Cincinnati, Ohio, USA., Kimura E; Department of Environmental and Public Health Sciences, University of Cincinnati, College of Medicine, Cincinnati, Ohio, USA., Mongan M; Department of Environmental and Public Health Sciences, University of Cincinnati, College of Medicine, Cincinnati, Ohio, USA., Hsu WW; Department of Environmental and Public Health Sciences, University of Cincinnati, College of Medicine, Cincinnati, Ohio, USA., Medvedovic M; Department of Environmental and Public Health Sciences, University of Cincinnati, College of Medicine, Cincinnati, Ohio, USA., Puga A; Department of Environmental and Public Health Sciences, University of Cincinnati, College of Medicine, Cincinnati, Ohio, USA., Xia Y; Department of Environmental and Public Health Sciences, University of Cincinnati, College of Medicine, Cincinnati, Ohio, USA. Electronic address: ying.xia@uc.edu. |
| المصدر: | The Journal of biological chemistry [J Biol Chem] 2024 Jul; Vol. 300 (7), pp. 107486. Date of Electronic Publication: 2024 Jun 18. |
| نوع المنشور: | Journal Article |
| اللغة: | English |
| بيانات الدورية: | Publisher: Elsevier Inc. on behalf of American Society for Biochemistry and Molecular Biology Country of Publication: United States NLM ID: 2985121R Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1083-351X (Electronic) Linking ISSN: 00219258 NLM ISO Abbreviation: J Biol Chem Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: 2021- : [New York, NY] : Elsevier Inc. on behalf of American Society for Biochemistry and Molecular Biology Original Publication: Baltimore, MD : American Society for Biochemistry and Molecular Biology |
| مواضيع طبية MeSH: | Dioxins*/toxicity , ErbB Receptors*/metabolism , ErbB Receptors*/genetics , MAP Kinase Kinase Kinase 1*/metabolism , MAP Kinase Kinase Kinase 1*/genetics , Receptors, Aryl Hydrocarbon*/metabolism , Receptors, Aryl Hydrocarbon*/genetics, Animals ; Female ; Mice ; Basic Helix-Loop-Helix Transcription Factors/metabolism ; Basic Helix-Loop-Helix Transcription Factors/genetics ; Eyelids/metabolism ; Eyelids/abnormalities ; Gene-Environment Interaction ; JNK Mitogen-Activated Protein Kinases/metabolism ; JNK Mitogen-Activated Protein Kinases/genetics ; MAP Kinase Signaling System/drug effects ; Mice, Knockout ; Receptor Cross-Talk ; Signal Transduction/drug effects |
| مستخلص: | Aberrant regulation of signal transduction pathways can adversely derail biological processes for tissue development. One such process is the embryonic eyelid closure that is dependent on the mitogen-activated protein kinase kinase kinase 1 (MAP3K1). Map3k1 KO in mice results in defective eyelid closure and an autosomal recessive eye-open at birth phenotype. We have shown that in utero exposure to dioxin, a persistent environmental toxicant, induces the same eye defect in Map3k1 +/- heterozygous but not WT pups. Here, we explore the mechanisms of the Map3k1 (gene) and dioxin (environment) interactions (GxE) underlying defective eyelid closure. We show that, acting through the aryl hydrocarbon receptor, dioxin activates epidermal growth factor receptor signaling, which in turn depresses MAP3K1-dependent Jun N-terminal kinase (JNK) activity. The dioxin-mediated JNK repression is moderate but is exacerbated by Map3k1 heterozygosity. Therefore, dioxin exposed Map3k1 +/- embryonic eyelids have a marked reduction of JNK activity, accelerated differentiation and impeded polarization in the epithelial cells. Knocking out Ahr or Egfr in eyelid epithelium attenuates the open-eye defects in dioxin-treated Map3k1 +/- pups, whereas knockout of Jnk1 and S1pr that encodes the sphigosin-1-phosphate (S1P) receptors upstream of the MAP3K1-JNK pathway potentiates the dioxin toxicity. Our novel findings show that the crosstalk of aryl hydrocarbon receptor, epidermal growth factor receptor, and S1P-MAP3K1-JNK pathways determines the outcome of dioxin exposure. Thus, gene mutations targeting these pathways are potential risk factors for the toxicity of environmental chemicals. Competing Interests: Conflict of interest The authors declare that they have no conflicts of interest with the contents of this article. (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.) |
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| معلومات مُعتمدة: | P30 ES006096 United States ES NIEHS NIH HHS; R01 HD098106 United States HD NICHD NIH HHS |
| فهرسة مساهمة: | Keywords: AHR; EGFR; developmental tissue closure; dioxin; epithelial morphogenesis; gene-environment interactions; the S1PR-MAP3K1-JNK pathway |
| المشرفين على المادة: | 0 (Ahr protein, mouse) 0 (Basic Helix-Loop-Helix Transcription Factors) 0 (Dioxins) EC 2.7.10.1 (EGFR protein, mouse) EC 2.7.10.1 (ErbB Receptors) EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases) EC 2.7.11.25 (MAP Kinase Kinase Kinase 1) EC 2.7.11.25 (Map3k1 protein, mouse) 0 (Receptors, Aryl Hydrocarbon) |
| تواريخ الأحداث: | Date Created: 20240619 Date Completed: 20240725 Latest Revision: 20240804 |
| رمز التحديث: | 20240804 |
| مُعرف محوري في PubMed: | PMC11294703 |
| DOI: | 10.1016/j.jbc.2024.107486 |
| PMID: | 38897570 |
| قاعدة البيانات: | MEDLINE |
Full Text Finder | تدمد: | 1083-351X |
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| DOI: | 10.1016/j.jbc.2024.107486 |