دورية أكاديمية

Yin Yang 1 regulates cohesin complex protein SMC3 in mouse hematopoietic stem cells.

التفاصيل البيبلوغرافية
العنوان: Yin Yang 1 regulates cohesin complex protein SMC3 in mouse hematopoietic stem cells.
المؤلفون: Lu Z; Department of Medical Sciences, School of Veterinary Medicine, University of Wisconsin, Madison, WI.; Carbone Cancer Center, University of Wisconsin, Madison, WI.; Wisconsin Blood Cancer Research Institute, University of Wisconsin, Madison, WI., Wang Y; Department of Medical Sciences, School of Veterinary Medicine, University of Wisconsin, Madison, WI.; Carbone Cancer Center, University of Wisconsin, Madison, WI.; Wisconsin Blood Cancer Research Institute, University of Wisconsin, Madison, WI., Assumpção ALFV; Department of Medical Sciences, School of Veterinary Medicine, University of Wisconsin, Madison, WI.; Carbone Cancer Center, University of Wisconsin, Madison, WI.; Wisconsin Blood Cancer Research Institute, University of Wisconsin, Madison, WI., Liu P; Carbone Cancer Center, University of Wisconsin, Madison, WI.; Department of Biostatistics and Medical Informatics, University of Wisconsin School of Medicine and Public Health, Madison, WI., Kopp A; Wisconsin Blood Cancer Research Institute, University of Wisconsin, Madison, WI.; Department of Cell and Regenerative Biology, University of Wisconsin School of Medicine and Public Health, Madison, WI., Saka S; Department of Medical Sciences, School of Veterinary Medicine, University of Wisconsin, Madison, WI.; Carbone Cancer Center, University of Wisconsin, Madison, WI.; Wisconsin Blood Cancer Research Institute, University of Wisconsin, Madison, WI., Mcilwain SJ; Carbone Cancer Center, University of Wisconsin, Madison, WI.; Department of Biostatistics and Medical Informatics, University of Wisconsin School of Medicine and Public Health, Madison, WI., Viny AD; Division of Hematology & Oncology, Department of Medicine, Columbia University Irving Medical Center, New York, NY.; Columbia Stem Cell Initiative, Columbia University Irving Medical Center, New York, NY.; Department of Genetics & Development, Columbia University Irving Medical Center, New York, NY., Brand M; Wisconsin Blood Cancer Research Institute, University of Wisconsin, Madison, WI.; Department of Cell and Regenerative Biology, University of Wisconsin School of Medicine and Public Health, Madison, WI., Pan X; Department of Medical Sciences, School of Veterinary Medicine, University of Wisconsin, Madison, WI.; Carbone Cancer Center, University of Wisconsin, Madison, WI.; Wisconsin Blood Cancer Research Institute, University of Wisconsin, Madison, WI.
المصدر: Blood advances [Blood Adv] 2024 Jun 25; Vol. 8 (12), pp. 3076-3091.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: American Society of Hematology Country of Publication: United States NLM ID: 101698425 Publication Model: Print Cited Medium: Internet ISSN: 2473-9537 (Electronic) Linking ISSN: 24739529 NLM ISO Abbreviation: Blood Adv Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Washington, DC : American Society of Hematology, [2016]-
مواضيع طبية MeSH: Cell Cycle Proteins*/metabolism , Cell Cycle Proteins*/genetics , Chromosomal Proteins, Non-Histone*/metabolism , Chromosomal Proteins, Non-Histone*/genetics , Hematopoietic Stem Cells*/metabolism , Hematopoietic Stem Cells*/cytology , YY1 Transcription Factor*/metabolism , YY1 Transcription Factor*/genetics, Animals ; Mice ; Cohesins ; Gene Expression Regulation ; Hematopoiesis ; Mice, Knockout ; Promoter Regions, Genetic
مستخلص: Abstract: Yin Yang 1 (YY1) and structural maintenance of chromosomes 3 (SMC3) are 2 critical chromatin structural factors that mediate long-distance enhancer-promoter interactions and promote developmentally regulated changes in chromatin architecture in hematopoietic stem/progenitor cells (HSPCs). Although YY1 has critical functions in promoting hematopoietic stem cell (HSC) self-renewal and maintaining HSC quiescence, SMC3 is required for proper myeloid lineage differentiation. However, many questions remain unanswered regarding how YY1 and SMC3 interact with each other and affect hematopoiesis. We found that YY1 physically interacts with SMC3 and cooccupies with SMC3 at a large cohort of promoters genome wide, and YY1 deficiency deregulates the genetic network governing cell metabolism. YY1 occupies the Smc3 promoter and represses SMC3 expression in HSPCs. Although deletion of 1 Smc3 allele partially restores HSC numbers and quiescence in YY1 knockout mice, Yy1-/-Smc3+/- HSCs fail to reconstitute blood after bone marrow transplant. YY1 regulates HSC metabolic pathways and maintains proper intracellular reactive oxygen species levels in HSCs, and this regulation is independent of the YY1-SMC3 axis. Our results establish a distinct YY1-SMC3 axis and its impact on HSC quiescence and metabolism.
(© 2024 by The American Society of Hematology. Licensed under Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0), permitting only noncommercial, nonderivative use with attribution. All other rights reserved.)
معلومات مُعتمدة: K08 CA215317 United States CA NCI NIH HHS
المشرفين على المادة: 0 (Cell Cycle Proteins)
0 (Chromosomal Proteins, Non-Histone)
0 (Cohesins)
0 (Yy1 protein, mouse)
0 (YY1 Transcription Factor)
تواريخ الأحداث: Date Created: 20240326 Date Completed: 20240614 Latest Revision: 20240627
رمز التحديث: 20240628
DOI: 10.1182/bloodadvances.2023011411
PMID: 38531064
قاعدة البيانات: MEDLINE
الوصف
تدمد:2473-9537
DOI:10.1182/bloodadvances.2023011411