Department of Immunology, Duke University Medical Center, Durham, NC 27710, USA.
J Immunol. 2011 Mar 15;186(6):3556-62. doi: 10.4049/jimmunol.1003164. Epub 2011 Feb 11.
In CD4(-)CD8(-) double-negative thymocytes, the murine Tcrb locus is composed of alternating blocks of active and inactive chromatin containing Tcrb gene segments and trypsinogen genes, respectively. Although chromatin structure is appreciated to be critical for regulated recombination and expression of Tcrb gene segments, the molecular mechanisms that maintain the integrity of these differentially regulated Tcrb locus chromatin domains are not understood. We localized a boundary between active and inactive chromatin by mapping chromatin modifications across the interval extending from Prss2 (the most 3' trypsinogen gene) to D(β)1. This boundary, located 6 kb upstream of D(β)1, is characterized by a transition from repressive (histone H3 lysine 9 dimethylation [H3K9me2]) to active (histone H3 acetylation [H3ac]) chromatin and is marked by a peak of histone H3 lysine 4 dimethylation (H3K4me2) that colocalizes with a retroviral long terminal repeat (LTR). Histone H3 lysine 4 dimethylation is retained and histone H3 lysine 9 dimethylation fails to spread past the LTR even on alleles lacking the Tcrb enhancer (E(β)) suggesting that these features may be determined by the local DNA sequence. Notably, we found that LTR-containing DNA functions as a barrier-type insulator that can protect a transgene from negative chromosomal position effects. We propose that, in vivo, the LTR blocks the spread of heterochromatin, and thereby helps to maintain the integrity of the E(β)-regulated chromatin domain. We also identified low-abundance, E(β)-dependent transcripts that initiate at the border of the LTR and an adjacent long interspersed element. We speculate that this transcription, which extends across D(β), J(β) and C(β) gene segments, may play an additional role promoting initial opening of the E(β)-regulated chromatin domain.
在 CD4(-)CD8(-) 双阴性胸腺细胞中,鼠 Tcrb 基因座由交替的活跃和不活跃染色质块组成,分别包含 Tcrb 基因片段和胰蛋白酶原基因。尽管染色质结构对于 Tcrb 基因片段的调控重组和表达至关重要,但维持这些差异调控 Tcrb 基因座染色质结构域完整性的分子机制尚不清楚。我们通过绘制从 Prss2(最 3' 的胰蛋白酶原基因)延伸到 D(β)1 的间隔内的染色质修饰图谱,定位了活跃和不活跃染色质之间的边界。该边界位于 D(β)1 的上游 6 kb 处,其特征是从抑制性(组蛋白 H3 赖氨酸 9 二甲基化 [H3K9me2])到活性(组蛋白 H3 乙酰化 [H3ac])染色质的转变,并以组蛋白 H3 赖氨酸 4 二甲基化(H3K4me2)的峰值为特征,该峰值与逆转录病毒长末端重复序列(LTR)共定位。组蛋白 H3 赖氨酸 4 二甲基化被保留,而组蛋白 H3 赖氨酸 9 二甲基化未能在缺乏 Tcrb 增强子(E(β))的等位基因上扩散超过 LTR,这表明这些特征可能由局部 DNA 序列决定。值得注意的是,我们发现含有 LTR 的 DNA 作为一种屏障型绝缘子发挥作用,可以保护转基因免受负染色体位置效应的影响。我们提出,在体内,LTR 阻止异染色质的扩散,从而有助于维持 E(β)调控染色质结构域的完整性。我们还鉴定了低丰度、E(β)依赖性转录本,它们在 LTR 边界和相邻的长散布元件处起始。我们推测,这种横跨 D(β)、J(β)和 C(β)基因片段延伸的转录可能在促进 E(β)调控染色质结构域的初始开放中发挥额外作用。