美國(guó)國(guó)立衛(wèi)生研究院（NIH）旗下的心肺血液研究所分子免疫學(xué)實(shí)驗(yàn)室，華盛頓大學(xué)生理系的科學(xué)家在組蛋白乙酰轉(zhuǎn)移酶和脫乙?；笇?duì)基因活化的研究上取得了新的進(jìn)展,，成果文章Genome-wide Mapping of HATs and HDACs Reveals Distinct Functions in Active and Inactive Genes發(fā)表在Cell在線版上。
組蛋白乙酰轉(zhuǎn)移酶（HAT）及脫乙?；福℉DAC）調(diào)節(jié)組蛋白和轉(zhuǎn)錄因子的乙?；剑瑥亩诳刂萍?xì)胞生命活動(dòng)中發(fā)揮著重要作用,。
乙?；墙M蛋白激活開(kāi)始轉(zhuǎn)錄的標(biāo)記，可以說(shuō)HATs是基因表達(dá)被激活的標(biāo)記,，而HDACs是基因表達(dá)失活的標(biāo)記,。
在本研究中，Zhao教授研究小組通過(guò)全基因組掃描的方式鑒定與乙?；M蛋白相關(guān)的活性基因,。研究結(jié)果表明，HATs和HDACs作用的靶位是活性基因的轉(zhuǎn)錄區(qū)域,。HDACs在人類基因組上的作用是消除活性基因的乙?；?，重新激活基因表達(dá)系統(tǒng)。
而無(wú)表達(dá)活性的基因則發(fā)生MLL介導(dǎo)的組蛋白H3K4甲基化進(jìn)入HAT/HDAC的乙?；兔撘阴,；难h(huán)周期，阻止Pol Ⅱ與基因結(jié)合,，確?；虿槐槐磉_(dá)。沉默的基因沒(méi)有H3K4甲基化信號(hào)則表明沒(méi)有與HDACs結(jié)合,。
這些數(shù)據(jù)表明,，HAT與HDAC在活性基因與沉默基因中發(fā)揮不同的功效。（生物谷Bioon.com）
生物谷推薦原始出處：
Cell, 20 August 2009 doi:10.1016/j.cell.2009.06.049
Genome-wide Mapping of HATs and HDACs Reveals Distinct Functions in Active and Inactive Genes
Zhibin Wang1,3,Chongzhi Zang2,3,Kairong Cui1,3,Dustin E. Schones1,Artem Barski1,Weiqun Peng2andKeji Zhao1,,
1 Laboratory of Molecular Immunology, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA
2 Department of Physics, The George Washington University, Washington D.C. 20052, USA
Histone acetyltransferases (HATs) and deacetylases (HDACs) function antagonistically to control histone acetylation. As acetylation is a histone mark for active transcription, HATs have been associated with active and HDACs with inactive genes. We describe here genome-wide mapping of HATs and HDACs binding on chromatin and find that both are found at active genes with acetylated histones. Our data provide evidence that HATs and HDACs are both targeted to transcribed regions of active genes by phosphorylated RNA Pol II. Furthermore, the majority of HDACs in the human genome function to reset chromatin by removing acetylation at active genes. Inactive genes that are primed by MLL-mediated histone H3K4 methylation are subject to a dynamic cycle of acetylation and deacetylation by transient HAT/HDAC binding, preventing Pol II from binding to these genes but poising them for future activation. Silent genes without any H3K4 methylation signal show no evidence of being bound by HDACs.
