Depletion of hCINAP by RNA interference causes defects in Cajal body formation, histone transcription, and cell viability
Depletion of hCINAP by RNA interference causes defects in Cajal body formation, histone transcription, and cell viability
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RNA 干扰消除 hCINAP 会导致卡哈尔体形成、组蛋白转录和细胞活力缺陷
DOI：
10.1007/s00018-010-0301-2
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发表时间：
2010-06-01
影响因子：
8
通讯作者：
Zheng, Xiaofeng
中科院分区：
文献类型：
--
作者：
Zhang, Jinfang;Zhang, Feiyun;Zheng, Xiaofeng
hCINAP是一种在真核生物中高度保守且普遍表达的蛋白，其过表达可减少具有多种核功能的Cajal小体（CBs）的平均数量。在这里，我们报道hCINAP与CBs的重要组成部分有关。RNA干扰导致hCINAP耗损导致CB形成缺陷，并破坏其组分的亚细胞定位，包括线圈蛋白、存活运动神经元蛋白、剪接体小核核糖核蛋白和核蛋白失调性毛细血管扩张。此外，敲低hCINAP表达导致组蛋白转录显著减少，U小核rna （U1, U2， U4和U5）水平降低，细胞活力丧失。在hcinap缺失的细胞中检测到caspase-3活性增加，表明细胞凋亡是丧失生存能力的原因之一。总之，这些数据表明hCINAP对于典型CBs的形成、组蛋白转录和细胞活力至关重要。
hCINAP is a highly conserved and ubiquitously expressed protein in eukaryotic organisms and its overexpression decreases the average number of Cajal bodies (CBs) with diverse nuclear functions. Here, we report that hCINAP is associated with important components of CBs. Depletion of hCINAP by RNA interference causes defects in CB formation and disrupts subcellular localizations of its components including coilin, survival motor neurons protein, spliceosomal small nuclear ribonucleoproteins, and nuclear protein ataxia-telangiectasia. Moreover, knockdown of hCINAP expression results in marked reduction of histone transcription, lower levels of U small nuclear RNAs (U1, U2, U4, and U5), and a loss of cell viability. Detection of increased caspase-3 activities in hCINAP-depleted cells indicate that apoptosis is one of the reasons for the loss of viability. Altogether, these data suggest that hCINAP is essential for the formation of canonical CBs, histone transcription, and cell viability.