The omics era: a nexus of untapped potential for Mendelian chromatinopathies

被引:10
作者
Nava, Aileen A. [1 ,2 ,3 ,4 ]
Arboleda, Valerie A. [1 ,2 ,3 ,4 ,5 ,6 ]
机构
[1] UCLA, David Geffen Sch Med, Dept Human Genet, Los Angeles, CA 90095 USA
[2] UCLA, David Geffen Sch Med, Dept Pathol & Lab Med, Los Angeles, CA 90095 USA
[3] UCLA, David Geffen Sch Med, Dept Computat Med, Los Angeles, CA 90095 USA
[4] Univ Calif Los Angeles, Broad Stem Cell Res Ctr, Los Angeles, CA 90095 USA
[5] Univ Calif Los Angeles, Mol Biol Inst, Los Angeles, CA 90095 USA
[6] Univ Calif Los Angeles, Jonsson Comprehens Canc Ctr, Los Angeles, CA 90095 USA
关键词
PLURIPOTENT STEM-CELLS; DNA METHYLATION; POSTTRANSLATIONAL MODIFICATIONS; HISTONE ACETYLTRANSFERASE; COMPREHENSIVE VIEW; ASXL1; MUTATIONS; HUMAN GENES; DISEASE; GENOME; MECHANISMS;
D O I
10.1007/s00439-023-02560-2
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
The OMICs cascade describes the hierarchical flow of information through biological systems. The epigenome sits at the apex of the cascade, thereby regulating the RNA and protein expression of the human genome and governs cellular identity and function. Genes that regulate the epigenome, termed epigenes, orchestrate complex biological signaling programs that drive human development. The broad expression patterns of epigenes during human development mean that pathogenic germline mutations in epigenes can lead to clinically significant multi-system malformations, developmental delay, intellectual disabilities, and stem cell dysfunction. In this review, we refer to germline developmental disorders caused by epigene mutation as "chromatinopathies". We curated the largest number of human chromatinopathies to date and our expanded approach more than doubled the number of established chromatinopathies to 179 disorders caused by 148 epigenes. Our study revealed that 20.6% (148/720) of epigenes cause at least one chromatinopathy. In this review, we highlight key examples in which OMICs approaches have been applied to chromatinopathy patient biospecimens to identify underlying disease pathogenesis. The rapidly evolving OMICs technologies that couple molecular biology with high-throughput sequencing or proteomics allow us to dissect out the causal mechanisms driving temporal-, cellular-, and tissue-specific expression. Using the full repertoire of data generated by the OMICs cascade to study chromatinopathies will provide invaluable insight into the developmental impact of these epigenes and point toward future precision targets for these rare disorders.
引用
收藏
页码:475 / 495
页数:21
相关论文
共 167 条
  • [1] Mass-spectrometric exploration of proteome structure and function
    Aebersold, Ruedi
    Mann, Matthias
    [J]. NATURE, 2016, 537 (7620) : 347 - 355
  • [2] iPSC-derived neurons of CREBBP- and EP300-mutated Rubinstein-Taybi syndrome patients show morphological alterations and hypoexcitability
    Alari, Valentina
    Russo, Silvia
    Terragni, Benedetta
    Ajmone, Paola Francesca
    Sironi, Alessandra
    Catusi, Ilaria
    Calzari, Luciano
    Concolino, Daniela
    Marotta, Rosa
    Milani, Donatella
    Giardino, Daniela
    Mantegazza, Massimo
    Gervasini, Cristina
    Finelli, Palma
    Larizza, Lidia
    [J]. STEM CELL RESEARCH, 2018, 30 : 130 - 140
  • [3] Next-generation proteomics: towards an integrative view of proteome dynamics
    Altelaar, A. F. Maarten
    Munoz, Javier
    Heck, Albert J. R.
    [J]. NATURE REVIEWS GENETICS, 2013, 14 (01) : 35 - 48
  • [4] Balancing serendipity and reproducibility: Pluripotent stem cells as experimental systems for intellectual and developmental disorders
    Anderson, Nickesha C.
    Chen, Pin-Fang
    Meganathan, Kesavan
    Saber, Wardiya Afshar
    Petersen, Andrew J.
    Bhattacharyya, Anita
    Kroll, Kristen L.
    Sahin, Mustafa
    [J]. STEM CELL REPORTS, 2021, 16 (06): : 1446 - 1457
  • [5] A Novel Small Molecule Supports the Survival of Cultured Dopamine Neurons and May Restore the Dopaminergic Innervation of the Brain in the MPTP Mouse Model of Parkinson's Disease
    Ardashov, Oleg V.
    Pavlova, Alla V.
    Mahato, Arun Kumar
    Sidorova, Yulia
    Morozova, Ekaterina A.
    Korchagina, Dina V.
    Salnikov, Georgi E.
    Genaev, Alexander M.
    Patrusheva, Oksana S.
    Li-Zhulanov, Nikolay S.
    Tolstikova, Tat'yana G.
    Volcho, Konstantin P.
    Salakhutdinov, Nariman. F.
    [J]. ACS CHEMICAL NEUROSCIENCE, 2019, 10 (10): : 4337 - 4349
  • [6] Homogenous 96-Plex PEA Immunoassay Exhibiting High Sensitivity, Specificity, and Excellent Scalability
    Assarsson, Erika
    Lundberg, Martin
    Holmquist, Goeran
    Bjoerkesten, Johan
    Thorsen, Stine Bucht
    Ekman, Daniel
    Eriksson, Anna
    Dickens, Emma Rennel
    Ohlsson, Sandra
    Edfeldt, Gabriella
    Andersson, Ann-Catrin
    Lindstedt, Patrik
    Stenvang, Jan
    Gullberg, Mats
    Fredriksson, Simon
    [J]. PLOS ONE, 2014, 9 (04):
  • [7] DNA methylation signature associated with Bohring-Opitz syndrome: a new tool for functional classification of variants in ASXL genes
    Awamleh, Zain
    Chater-Diehl, Eric
    Choufani, Sanaa
    Wei, Elizabeth
    Kianmahd, Rebecca R.
    Yu, Anna
    Chad, Lauren
    Costain, Gregory
    Tan, Wen-Hann
    Scherer, Stephen W.
    Arboleda, Valerie A.
    Russell, Bianca E.
    Weksberg, Rosanna
    [J]. EUROPEAN JOURNAL OF HUMAN GENETICS, 2022, 30 (06) : 695 - 702
  • [8] Mass Spectrometry for Neurobiomarker Discovery: The Relevance of Post-Translational Modifications
    Azevedo, Rita
    Jacquemin, Chloe
    Villain, Nicolas
    Fenaille, Francois
    Lamari, Foudil
    Becher, Francois
    [J]. CELLS, 2022, 11 (08)
  • [9] LIN28 alters cell fate succession and acts independently of the let-7 microRNA during neurogliogenesis in vitro
    Balzer, Erica
    Heine, Christian
    Jiang, Qiang
    Lee, Vivian M.
    Moss, Eric G.
    [J]. DEVELOPMENT, 2010, 137 (06): : 891 - 900
  • [10] Bantscheff M, 2012, ANAL BIOANAL CHEM, V404, P939, DOI 10.1007/s00216-012-6203-4