CELL STRESS AND TRANSLATIONAL INHIBITORS TRANSIENTLY INCREASE THE ABUNDANCE OF MAMMALIAN SINE TRANSCRIPTS
CELL STRESS AND TRANSLATIONAL INHIBITORS TRANSIENTLY INCREASE THE ABUNDANCE OF MAMMALIAN SINE TRANSCRIPTS
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DOI：
10.1093/nar/23.10.1758
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发表时间：
1995-05-25
影响因子：
14.9
通讯作者：
SCHMID, CW
中科院分区：
文献类型：
--
作者：
LIU, WM;CHU, WM;SCHMID, CW
在人细胞系中，Alu RNA的丰度通过热休克而瞬时增加，这种效应对于Pol III转录基因中的Alu重复是特异性的，因为7SL、7SK、5S和U6 RNA的丰度基本上不受热休克的影响。Alu表达的快速诱导先于泛素和HSP 70热休克基因的mRNA的热休克诱导，热休克模拟物也瞬时诱导Alu表达，表明Alu表达增加是一般的细胞应激反应。放线菌酮处理快速且瞬时地增加Alu RNA的丰度。再次，与Pol III转录的其他基因相比，这种增加是Alu特异性的，然而，与细胞应激反应不同，放线菌酮不诱导HSP 70和泛素mRNA的表达。嘌呤霉素还增加Alu表达，表明这种反应通常由翻译抑制引起。哺乳动物西内斯对细胞应激和翻译抑制的反应不限于作为Alu同系物的西内斯。热休克和放线菌酮各自瞬时诱导小鼠细胞中的B1和B2 RNA以及兔细胞中的C元件RNA的Pol III定向表达。总之，这三个物种取代了胎盘哺乳动物的已知SINE组成，表明哺乳动物西内斯受到类似的调节，并且可能具有共同的功能。
The abundance of Alu RNA is transiently increased by heat shock in human cell lines, This effect is specific to Alu repeats among Pol III transcribed genes, since the abundance of 7SL, 7SK, 5S and U6 RNAs is essentially unaffected by heat shock, The rapid induction of Alu expression precedes the heat shock induction of mRNAs for the ubiquitin and HSP 70 heat shock genes, Heat shock mimetics also transiently induce Alu expression indicating that increased Alu expression is a general cell-stress response, Cycloheximide treatment rapidly and transiently increases the abundance of Alu RNA, Again, compared with other genes transcribed by Pol III, this increase is specific to Alu, However, as distinguished from the cell stress response, cycloheximide does not induce expression of HSP 70 and ubiquitin mRNAs. Puromycin also increases Alu expression, suggesting that this response is generally caused by translational inhibition, The response of mammalian SINEs to cell stress and translational inhibition is not limited to SINEs which are Alu homologues. Heat shock and cycloheximide each transiently induce Pol III directed expression of B1 and B2 RNAs in mouse cells and C-element RNA in rabbit cells, Together, these three species exemplify the known SINE composition of placental mammals, suggesting that mammalian SINEs are similarly regulated and may serve a common function.