JBP2是一种类似于SWI2/SNF2的蛋白质，它在布氏锥虫的血流形式中调节端粒DNA的从头糖基化。
JBP2, a SWI2/SNF2-like protein, regulates de novo telomeric DNA glycosylation in bloodstream form Trypanosoma brucei.
作者信息
Kieft Rudo, Brand Verena, Ekanayake Dilrukshi K, Sweeney Kate, DiPaolo Courtney, Reznikoff William S, Sabatini Robert
机构信息
Department of Biochemistry and Molecular Biology, University of Georgia, Athens, GA, USA.
出版信息
Mol Biochem Parasitol. 2007 Nov;156(1):24-31. doi: 10.1016/j.molbiopara.2007.06.010. Epub 2007 Jun 28.
Abstract
Synthesis of the modified thymine base, beta-d-glucosyl-hydroxymethyluracil or J, within telomeric DNA of Trypanosoma brucei correlates with the bloodstream form specific epigenetic silencing of telomeric variant surface glycoprotein genes involved in antigenic variation. In order to analyze the function of base J in the regulation of antigenic variation, we are characterizing the regulatory mechanism of J biosynthesis. We have recently proposed a model in which chromatin remodeling by a SWI2/SNF2-like protein (JBP2) regulates the developmental and de novo site-specific localization of J synthesis within bloodstream form trypanosome DNA. Consistent with this model, we now show that JBP2 (-/-) bloodstream form trypanosomes contain five-fold less base J and are unable to stimulate de novo J synthesis in newly generated telomeric arrays.
摘要
在布氏锥虫的端粒DNA中，修饰胸腺嘧啶碱基β - d - 葡糖基羟甲基尿嘧啶（即J）的合成与参与抗原变异的端粒可变表面糖蛋白基因的血流形式特异性表观遗传沉默相关。为了分析碱基J在抗原变异调控中的功能，我们正在对J生物合成的调控机制进行表征。我们最近提出了一个模型，其中一种类似SWI2/SNF2的蛋白（JBP2）介导的染色质重塑调节了血流形式锥虫DNA中J合成的发育和从头位点特异性定位。与该模型一致，我们现在表明JBP2（-/-）血流形式锥虫中的碱基J含量减少了五倍，并且无法刺激新生成的端粒阵列中的J从头合成。
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本文引用的文献
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Repression of polymerase I-mediated gene expression at Trypanosoma brucei telomeres.
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J-binding protein increases the level and retention of the unusual base J in trypanosome DNA.
Mol Microbiol. 2002 Oct;46(1):37-47. doi: 10.1046/j.1365-2958.2002.03144.x.
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Expression of the human DNA glycosylase hSMUG1 in Trypanosoma brucei causes DNA damage and interferes with J biosynthesis.
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