以视黄素X受体基因γ(retinoid X receptor-gamma,RXRG)作为牛双胎性状的候选基因,运用测序法寻找牛RXRG基因SNPs,筛查到一个新的多态位点A1941G,该位点位于3′UTR。运用PCR-RFLP法验证并分析该位点在鲁西牛双胎群体和单胎群体及中国西...以视黄素X受体基因γ(retinoid X receptor-gamma,RXRG)作为牛双胎性状的候选基因,运用测序法寻找牛RXRG基因SNPs,筛查到一个新的多态位点A1941G,该位点位于3′UTR。运用PCR-RFLP法验证并分析该位点在鲁西牛双胎群体和单胎群体及中国西门塔尔牛、安格斯牛和西蒙杂交牛单胎群体间的多态性,结果表明,在鲁西牛双胎和单胎群体中分布A、B两个等位基因,处于中度多态。经χ2适合性检验,鲁西双胎牛群体在该位点未达到Hardy-Weinberg平衡状态(P<0.05)。将鲁西牛群体的A1941G位点的基因型效应与双胎性状进行关联分析,卡方独立性检测结果显示,基因型分布在鲁西单、双胎牛群体上差异达到极显著水平(P<0.01)。展开更多
The HIV-1 LTR controls the expression of HIV-1 viral genes and thus is critical for viral propagation and pathology. Numerous host factors have been shown to participate in the regulation of the LTR promoter. Among th...The HIV-1 LTR controls the expression of HIV-1 viral genes and thus is critical for viral propagation and pathology. Numerous host factors have been shown to participate in the regulation of the LTR promoter. Among them is the thyroid hormone (T3) receptor (TR). TR has been shown to bind to the critical region of the promoter that contain the NFbB and Sp1 binding sites. Interestingly, earlier transient transfection studies in tissue culture cells have yielded contradicting conclusions on the role of TR in LTR regulation, likely due to the use of different cell types and/or lack of proper chromatin organization. Here, using the frog oocyte as a model system that allows replication-coupled chromatin assembly, mimicking that in somatic cells, we demonstrate that unliganded heterodimers of TR and RXR (9-cis retinoic acid receptor) repress LTR while the addition of T3 relieves the repression and further activates the promoter. More importantly, we show that chromatin and unliganded TR/RXR synergize to repress the promoter in a histone deacetylase-dependent manner.展开更多
文摘以视黄素X受体基因γ(retinoid X receptor-gamma,RXRG)作为牛双胎性状的候选基因,运用测序法寻找牛RXRG基因SNPs,筛查到一个新的多态位点A1941G,该位点位于3′UTR。运用PCR-RFLP法验证并分析该位点在鲁西牛双胎群体和单胎群体及中国西门塔尔牛、安格斯牛和西蒙杂交牛单胎群体间的多态性,结果表明,在鲁西牛双胎和单胎群体中分布A、B两个等位基因,处于中度多态。经χ2适合性检验,鲁西双胎牛群体在该位点未达到Hardy-Weinberg平衡状态(P<0.05)。将鲁西牛群体的A1941G位点的基因型效应与双胎性状进行关联分析,卡方独立性检测结果显示,基因型分布在鲁西单、双胎牛群体上差异达到极显著水平(P<0.01)。
文摘The HIV-1 LTR controls the expression of HIV-1 viral genes and thus is critical for viral propagation and pathology. Numerous host factors have been shown to participate in the regulation of the LTR promoter. Among them is the thyroid hormone (T3) receptor (TR). TR has been shown to bind to the critical region of the promoter that contain the NFbB and Sp1 binding sites. Interestingly, earlier transient transfection studies in tissue culture cells have yielded contradicting conclusions on the role of TR in LTR regulation, likely due to the use of different cell types and/or lack of proper chromatin organization. Here, using the frog oocyte as a model system that allows replication-coupled chromatin assembly, mimicking that in somatic cells, we demonstrate that unliganded heterodimers of TR and RXR (9-cis retinoic acid receptor) repress LTR while the addition of T3 relieves the repression and further activates the promoter. More importantly, we show that chromatin and unliganded TR/RXR synergize to repress the promoter in a histone deacetylase-dependent manner.
