دورية أكاديمية
أعرض في EDS

Erosion of human X chromosome inactivation causes major remodeling of the iPSC proteome.

التفاصيل البيبلوغرافية
العنوان: Erosion of human X chromosome inactivation causes major remodeling of the iPSC proteome.
المؤلفون: Brenes AJ; Centre for Gene Regulation and Expression, School of Life Sciences, University of Dundee, Dow St., Dundee DD1 5EH, UK; Cell Signalling & Immunology, School of Life Sciences, University of Dundee, Dow St., Dundee DD1 5EH, UK. Electronic address: ajbrenesmurillo@dundee.ac.uk., Yoshikawa H; Centre for Gene Regulation and Expression, School of Life Sciences, University of Dundee, Dow St., Dundee DD1 5EH, UK; Division of Cell Signalling, Fujii Memorial Institute of Medical Sciences, Institute of Advanced Medical Sciences, Tokushima University, 3-18-15 Kuramoto, Tokushima 770-8503, Japan., Bensaddek D; Centre for Gene Regulation and Expression, School of Life Sciences, University of Dundee, Dow St., Dundee DD1 5EH, UK; Biosciences Core Labs, Proteomics, King Abdullah University of Science and Technology, Thuwal 23955-6900, Saudi Arabia., Mirauta B; European Molecular Biology Laboratory, European Bioinformatics Institute, Wellcome Genome Campus, Hinxton CB10 1SD, UK., Seaton D; European Molecular Biology Laboratory, European Bioinformatics Institute, Wellcome Genome Campus, Hinxton CB10 1SD, UK., Hukelmann JL; Centre for Gene Regulation and Expression, School of Life Sciences, University of Dundee, Dow St., Dundee DD1 5EH, UK; Immatics Biotechnologies, Paul-Ehrlich-Str. 15, Tuebingen 72076, Germany., Jiang H; Centre for Gene Regulation and Expression, School of Life Sciences, University of Dundee, Dow St., Dundee DD1 5EH, UK., Stegle O; European Molecular Biology Laboratory, European Bioinformatics Institute, Wellcome Genome Campus, Hinxton CB10 1SD, UK; European Molecular Biology Laboratory, Genome Biology Unit, Heidelberg, Germany; Division of Computational Genomics and Systems Genetic, German Cancer Research Center, Heidelberg, Germany., Lamond AI; Centre for Gene Regulation and Expression, School of Life Sciences, University of Dundee, Dow St., Dundee DD1 5EH, UK. Electronic address: a.i.lamond@dundee.ac.uk.
المصدر: Cell reports [Cell Rep] 2021 Apr 27; Vol. 35 (4), pp. 109032.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Cell Press Country of Publication: United States NLM ID: 101573691 Publication Model: Print Cited Medium: Internet ISSN: 2211-1247 (Electronic) NLM ISO Abbreviation: Cell Rep Subsets: MEDLINE
أسماء مطبوعة: Original Publication: [Cambridge, MA] : Cell Press, c 2012-
مواضيع طبية MeSH: Induced Pluripotent Stem Cells/*metabolism , Proteome/*metabolism , X Chromosome Inactivation/*genetics, Female ; Humans
مستخلص: X chromosome inactivation (XCI) is a dosage compensation mechanism in female mammals whereby transcription from one X chromosome is repressed. Analysis of human induced pluripotent stem cells (iPSCs) derived from female donors identified that low levels of XIST RNA correlated strongly with erosion of XCI. Proteomic analysis, RNA sequencing (RNA-seq), and polysome profiling showed that XCI erosion resulted in amplified RNA and protein expression from X-linked genes, providing a proteomic characterization of skewed dosage compensation. Increased protein expression was also detected from autosomal genes without an mRNA increase, thus altering the protein-RNA correlation between the X chromosome and autosomes. XCI-eroded lines display an ∼13% increase in total cell protein content, with increased ribosomal proteins, ribosome biogenesis and translation factors, and polysome levels. We conclude that XCI erosion in iPSCs causes a remodeling of the proteome, affecting the expression of a much wider range of proteins and disease-linked loci than previously realized.
Competing Interests: Declaration of interests D.S. now works for GSK.
(Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.)
References: Oncogene. 2017 Apr 20;36(16):2255-2264. (PMID: 27748766)
Nat Biotechnol. 2008 Dec;26(12):1367-72. (PMID: 19029910)
Bioinformatics. 2019 Apr 15;35(8):1441-1442. (PMID: 30239567)
Bioinformatics. 2010 Jan 1;26(1):139-40. (PMID: 19910308)
Nucleic Acids Res. 2019 Jan 8;47(D1):D442-D450. (PMID: 30395289)
Mol Cell Proteomics. 2019 Oct;18(10):1967-1980. (PMID: 31332098)
Nucleic Acids Res. 2016 Jan 4;44(D1):D447-56. (PMID: 26527722)
PLoS Genet. 2017 Oct 9;13(10):e1007050. (PMID: 28991910)
Elife. 2014 Jan 01;3:e01630. (PMID: 24596151)
Nature. 2017 Jun 15;546(7658):370-375. (PMID: 28489815)
Hum Reprod Update. 2017 Sep 1;23(5):520-532. (PMID: 28582519)
Bioinformatics. 2014 Apr 1;30(7):923-30. (PMID: 24227677)
Cell Stem Cell. 2012 Jul 6;11(1):75-90. (PMID: 22770242)
Trends Cell Biol. 2013 May;23(5):242-50. (PMID: 23375955)
Cell. 2006 Aug 25;126(4):663-76. (PMID: 16904174)
Nucleic Acids Res. 2017 Jan 4;45(D1):D183-D189. (PMID: 27899595)
Hum Mol Genet. 2017 Apr 1;26(7):1219-1229. (PMID: 28369266)
Cancer. 2010 Apr 1;116(7):1629-37. (PMID: 20151426)
Curr Biol. 2008 Sep 9;18(17):1269-77. (PMID: 18722121)
Nat Struct Mol Biol. 2017 Mar;24(3):226-233. (PMID: 28134930)
Nature. 1996 Jan 11;379(6561):131-7. (PMID: 8538762)
Mol Cell Biol. 2003 Mar;23(6):2083-95. (PMID: 12612080)
Nat Methods. 2006 Aug;3(8):637-46. (PMID: 16862139)
Mol Syst Biol. 2010 Dec 21;6:450. (PMID: 21179022)
Nucleic Acids Res. 2020 Jan 8;48(D1):D70-D76. (PMID: 31722421)
Nucleic Acids Res. 2015 Apr 20;43(7):e47. (PMID: 25605792)
Nucleic Acids Res. 2018 Jan 4;46(D1):D1202-D1209. (PMID: 28981707)
Stem Cell Reports. 2019 Feb 12;12(2):333-350. (PMID: 30639215)
Nature. 2005 Feb 3;433(7025):477-80. (PMID: 15690031)
Elife. 2020 Aug 10;9:. (PMID: 32773033)
Nat Rev Genet. 2011 Jun;12(6):429-42. (PMID: 21587299)
Oncogene. 2019 Mar;38(13):2223-2240. (PMID: 30487597)
Nucleic Acids Res. 2017 Jan 4;45(D1):D158-D169. (PMID: 27899622)
Nat Struct Mol Biol. 2017 Sep 7;24(9):689-699. (PMID: 28880863)
Cell. 2016 Apr 21;165(3):535-50. (PMID: 27104977)
Mol Cell Proteomics. 2014 Dec;13(12):3497-506. (PMID: 25225357)
Annu Rev Genet. 2018 Nov 23;52:535-566. (PMID: 30256677)
PLoS Comput Biol. 2007 Mar 23;3(3):e57. (PMID: 17381238)
Cell Stem Cell. 2012 Jul 6;11(1):9-15. (PMID: 22770238)
Wiley Interdiscip Rev RNA. 2019 Jan;10(1):e1516. (PMID: 30406965)
Mol Syst Biol. 2016 Oct 20;12(10):883. (PMID: 27951527)
Bioinformatics. 2009 May 1;25(9):1189-91. (PMID: 19151095)
Nat Protoc. 2016 Dec;11(12):2301-2319. (PMID: 27809316)
Mol Biol Evol. 2013 Dec;30(12):2588-601. (PMID: 24023392)
Cell Stem Cell. 2017 May 4;20(5):706-719.e7. (PMID: 28366588)
J Neurodev Disord. 2016 Jun 09;8:22. (PMID: 27303449)
Bioinformatics. 2013 Jan 1;29(1):15-21. (PMID: 23104886)
Heredity (Edinb). 2012 Jan;108(1):50-8. (PMID: 22086077)
Nucleic Acids Res. 2018 Jan 4;46(D1):D754-D761. (PMID: 29155950)
Nature. 2020 Feb;578(7795):455-460. (PMID: 32025035)
Proc Natl Acad Sci U S A. 2016 Apr 5;113(14):E2029-38. (PMID: 27001848)
Genes Dev. 1997 Jan 15;11(2):156-66. (PMID: 9009199)
Elife. 2018 Aug 10;7:. (PMID: 30095066)
J Biol Chem. 2007 May 11;282(19):14056-64. (PMID: 17360704)
Mol Cell Proteomics. 2017 May;16(5):873-890. (PMID: 28325852)
Cell. 2007 Nov 30;131(5):861-72. (PMID: 18035408)
Development. 2017 Aug 1;144(15):2784-2797. (PMID: 28684628)
J Biol Chem. 2015 Oct 2;290(40):24091-9. (PMID: 26324716)
Nucleic Acids Res. 2000 Jan 1;28(1):27-30. (PMID: 10592173)
Cell. 2012 Oct 26;151(3):476-82. (PMID: 23101621)
Nat Rev Genet. 2015 May;16(5):261-75. (PMID: 25732612)
Nat Methods. 2017 Apr;14(4):417-419. (PMID: 28263959)
Cell Stem Cell. 2017 Jan 5;20(1):102-111. (PMID: 27989768)
Cell. 2012 Oct 26;151(3):671-83. (PMID: 23101633)
Nat Rev Mol Cell Biol. 2010 Feb;11(2):113-27. (PMID: 20094052)
Nature. 2016 Jul 28;535(7613):575-9. (PMID: 27437574)
Cell Stem Cell. 2012 May 4;10(5):595-609. (PMID: 22560080)
Development. 1990 May;109(1):189-201. (PMID: 2209464)
Nat Rev Genet. 2016 Jan;17(1):33-46. (PMID: 26616198)
Nucleic Acids Res. 2016 Sep 6;44(15):7441-56. (PMID: 27325746)
Science. 2007 Dec 21;318(5858):1917-20. (PMID: 18029452)
Trends Genet. 2016 Jun;32(6):348-359. (PMID: 27103486)
معلومات مُعتمدة: 105024/Z/14/Z United Kingdom WT_ Wellcome Trust; 098503/E/12/Z United Kingdom WT_ Wellcome Trust; United Kingdom MRC_ Medical Research Council; 073980/Z/03/Z United Kingdom WT_ Wellcome Trust; United Kingdom WT_ Wellcome Trust
فهرسة مساهمة: Keywords: RNA-seq; X chromosome inactivation; dosage compensation; erosion of X chromosome inactivation; gene expression; iPSC; mass spectrometry; proteome; proteomics; transcriptome
المشرفين على المادة: 0 (Proteome)
تواريخ الأحداث: Date Created: 20210428 Date Completed: 20220208 Latest Revision: 20240810
رمز التحديث: 20240812
مُعرف محوري في PubMed: PMC8097692
DOI: 10.1016/j.celrep.2021.109032
PMID: 33910018
قاعدة البيانات: MEDLINE
الوصف
تدمد:2211-1247
DOI:10.1016/j.celrep.2021.109032