Chromatin dynamics underlying cellular memory

通过这项研究，我们得到了以下结果：GAGA因子FACT复合体将染色质重塑复合体PBAP招募到Pc/trx应答元件，诱导染色质重塑，维持Hox基因的表达。GAGA因子- fact复合物结合白色基因下游的GA重复序列，诱导染色质重塑，用其变体H3.3取代组蛋白H3，并通过对抗异染色质扩散来维持白色基因的表达。通过Pc/trx应答元件转录非编码RNA调控Hox基因表达。超缠绕因子被MOF招募到组蛋白H4 K16乙酰化的染色质上，并通过与iswi的对抗参与X染色体的剂量补偿。Ash1基因敲除的小鼠是纯合子存活的，但显示出后体细胞的同型变异。SPT16敲除小鼠在纯合子中是胚胎致死的。其杂合子表现出IgG亚群水平的偏差。

We have obtained following results through this study.1. GAGA factor FACT complex recruits chromatin remodeling complex PBAP to Pc/trx response elements, induces chromatin remodeling, and maintains expression of Hox genes.2. GAGA factor-FACT complex binds to a GA repeat sequence downstream the white gene, induces chromatin remodeling, replaces histone H3 by its variant H3.3, and maintains white gene expression by counteracting the heterochromatin spreading.3. Transcription of non-coding RNA through Pc/trx response element regulates Hox gene expression.4. Supercoiling factor is recruited to chromatin acetylated at histone H4 K16 by MOF, and contributes dosage compensation of X chromosome through counteracting with ISWI.5. Ash1 knock-out mice are homozygous viable but show homeotic transformation of the back-one. SPT16 knock-out mice are embryonic lethal in homozygotes. Its heterozygotes show a deviation in the levels of IgG sublasses.