| 词条 | Trithorax-group proteins | ||||||||||||||||||||||||||||||||||||||||||||||||||
| 释义 |
Trithorax Group (TrxG) proteins are a heterogeneous collection of proteins whose main action is to maintain gene expression. They can be categorized into 3 general classes based on molecular function:
plus other TrxG proteins not categorized in the first three classes.[1] DiscoveryThe founding member of TrxG Proteins, trithorax (trx), was discovered ~1978 by P.W. Ingham as part of his doctoral thesis while a graduate student in the laboratory of J.R.S. Whittle at the University of Sussex.[2] Myeloid/lymphoid or mixed-lineage Leukemia (MLL) is the human homolog of trx.[2]
The table contains names of Drosophila TrxG members. Homologs in other species may have different names. FunctionTrithorax Group (TrxG) proteins typically function in large complexes formed with other proteins. The complexes formed by TrxG proteins are divided into 2 groups: Histone-modifying complexes and ATP-dependent chromatin-remodeling complexes. The main function of TrxG proteins, along with polycomb group (PcG) proteins, is regulating gene expression. Whereas, PcG proteins are typically associated with gene silencing, TrxG proteins are most commonly linked to gene activation. The Trithorax complex activates gene transcription by inducing trimethylation of lysine 4 of histone H3 (H3K4me3) at specific sites in chromatin recognized by the complex.[1] Ash1 domain is involved in H3K36 methylation. Trithorax complex also interacts with CBP (CREB binding protein) which is an acteyltransferase to acetylate H3K27[3]. This gene activation is reinforced by acetylation of histone H4. The actions of TrxG proteins are often described as 'antagonistic' of PcG proteins function.[4] Aside from gene regulation, evidence suggests TrxG proteins are also involved in other processes including apoptosis, cancer, and stress responses.[5][6][7] Role in developmentDuring development, TrxG proteins maintain activation of required genes, particularly the Hox genes, after maternal factors are depleted.[8] This is accomplished by preserving the epigenetic marks, specifically H3K4me3, established by maternally-supplied factors.[9] TrxG proteins are also implicated in X-chromosome inactivation, which occurs during early embryogenesis.[10] {{as of|2011}} it is unclear whether TrxG activity is required in every cell during the entire development of an organism or only during certain stages in certain cell types.[11] See also
References1. ^1 {{cite journal | vauthors = Schuettengruber B, Chourrout D, Vervoort M, Leblanc B, Cavalli G | title = Genome regulation by polycomb and trithorax proteins | journal = Cell | volume = 128 | issue = 4 | pages = 735–45 |date=February 2007 | pmid = 17320510 | doi = 10.1016/j.cell.2007.02.009 }} 2. ^1 {{cite journal | author = Ingham PW | title = trithorax and the regulation of homeotic gene expression in Drosophila: a historical perspective | journal = Int. J. Dev. Biol. | volume = 42 | issue = 3 | pages = 423–9 | year = 1998 | pmid = 9654027 | doi = }} 3. ^{{Cite journal|last=Geisler|first=Sarah J.|last2=Paro|first2=Renato|date=2015-09-01|title=Trithorax and Polycomb group-dependent regulation: a tale of opposing activities|url=http://dev.biologists.org/content/142/17/2876|journal=Development|language=en|volume=142|issue=17|pages=2876–2887|doi=10.1242/dev.120030|issn=0950-1991|pmid=26329598}} 4. ^{{cite journal | vauthors = Grimaud C, Nègre N, Cavalli G | title = From genetics to epigenetics: the tale of Polycomb group and trithorax group genes | journal = Chromosome Res. | volume = 14 | issue = 4 | pages = 363–75 | year = 2006 | pmid = 16821133 | doi = 10.1007/s10577-006-1069-y }} 5. ^{{cite journal | vauthors = Tyagi S, Herr W | title = E2F1 mediates DNA damage and apoptosis through HCF-1 and the MLL family of histone methyltransferases | journal = EMBO J. | volume = 28 | issue = 20 | pages = 3185–95 |date=October 2009 | pmid = 19763085 | pmc = 2771094 | doi = 10.1038/emboj.2009.258 }} 6. ^{{cite journal | vauthors = Siebold AP, Banerjee R, Tie F, Kiss DL, Moskowitz J, Harte PJ | title = Polycomb Repressive Complex 2 and Trithorax modulate Drosophila longevity and stress resistance | journal = Proc. Natl. Acad. Sci. U.S.A. | volume = 107 | issue = 1 | pages = 169–74 |date=January 2010 | pmid = 20018689 | pmc = 2806727 | doi = 10.1073/pnas.0907739107 }} 7. ^{{cite journal | vauthors = Bagchi A, Papazoglu C, Wu Y, Capurso D, Brodt M, Francis D, Bredel M, Vogel H, Mills AA | title = CHD5 is a tumor suppressor at human 1p36 | journal = Cell | volume = 128 | issue = 3 | pages = 459–75 |date=February 2007 | pmid = 17289567 | doi = 10.1016/j.cell.2006.11.052 }} 8. ^{{cite journal | vauthors = Brock HW, Fisher CL | title = Maintenance of gene expression patterns | journal = Dev. Dyn. | volume = 232 | issue = 3 | pages = 633–55 |date=March 2005 | pmid = 15704101 | doi = 10.1002/dvdy.20298 }} 9. ^{{cite journal | author = Soshnikova N | title = Dynamics of Polycomb and Trithorax activities during development | journal = Birth Defects Res. Part A Clin. Mol. Teratol. | volume = 91 | issue = 8 | pages = 781–7 |date=August 2011 | pmid = 21290568 | doi = 10.1002/bdra.20774 }} 10. ^{{cite journal | vauthors = Pullirsch D, Härtel R, Kishimoto H, Leeb M, Steiner G, Wutz A | title = The Trithorax group protein Ash2l and Saf-A are recruited to the inactive X chromosome at the onset of stable X inactivation | journal = Development | volume = 137 | issue = 6 | pages = 935–43 |date=March 2010 | pmid = 20150277 | pmc = 2834461 | doi = 10.1242/dev.035956 }} 11. ^{{cite journal | vauthors = Schuettengruber B, Martinez AM, Iovino N, Cavalli G | title = Trithorax group proteins: switching genes on and keeping them active | journal = Nat. Rev. Mol. Cell Biol. | volume = 12 | issue = 12 | pages = 799–814 |date=December 2011 | pmid = 22108599 | doi = 10.1038/nrm3230 }} External links
3 : DNA-binding proteins|Molecular genetics|Drosophila melanogaster genes |
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