de Vegvar H E, Lund E, Dahlberg J E
Cell. 1986 Oct 24;47(2):259-66. doi: 10.1016/0092-8674(86)90448-4.
Promoters of small nuclear RNA (snRNA) genes are partly responsible for 3' end formation of snRNA precursors. In injected X. laevis oocytes, substitution of an mRNA promoter (HSV tk) for the snRNA promoter significantly reduces the utilization of a conserved snRNA 3' end signal and permits recognition of a downstream polyadenylation site. Neither the U1 enhancer nor the U1 coding region is essential for recognition of the snRNA 3' end signal. Deletion of the U1 3' end signal from genes with a U1 promoter results in utilization of "cryptic" signals resembling the consensus sequence. However, these snRNA gene-promoted transcripts are not polyadenylated, in spite of the functional polyadenylation signal they contain. Thus, the ability to recognize 3' end signals is determined during initiation, presumably by interaction of transcription complexes with specific processing or termination factors.
小核RNA(snRNA)基因的启动子部分负责snRNA前体3'端的形成。在注射的非洲爪蟾卵母细胞中,用mRNA启动子(单纯疱疹病毒胸苷激酶,HSV tk)替换snRNA启动子,会显著降低保守的snRNA 3'端信号的利用率,并允许识别下游的聚腺苷酸化位点。U1增强子和U1编码区对于snRNA 3'端信号的识别都不是必需的。从具有U1启动子的基因中删除U1 3'端信号,会导致利用类似于共有序列的“隐蔽”信号。然而,尽管这些由snRNA基因启动子驱动的转录本含有功能性的聚腺苷酸化信号,但它们不会被聚腺苷酸化。因此,识别3'端信号的能力在起始过程中就已确定,推测是通过转录复合物与特定加工或终止因子的相互作用实现的。