Borukhov S, Sagitov V, Goldfarb A
Public Health Research Institute, New York, New York 10016.
Cell. 1993 Feb 12;72(3):459-66. doi: 10.1016/0092-8674(93)90121-6.
Two transcription elongation factors (GreA and GreB) related in primary sequence were isolated from E. coli. Each factor induced cleavage of the nascent transcript in artificially halted elongation complexes followed by the loss of the 3' proximal fragment and resumption of elongation from the new 3' terminus. GreA induced cleavages 2 or 3 nt behind the terminus while GreB released longer oligonucleotides up to 9 nt in length. The pattern of cleavages characteristically changed as the transcription complex advanced, supporting the "inchworm" model of RNA polymerase propagation. In addition to attacking artificially halted complexes, both factors antagonized the action of natural elongation-arresting sites that occasionally trap the advancing complex. GreB rescued the arrested complexes via the transcript cleavage and restart pathway while GreA acted by an unknown mechanism, preventing the arrest only if added before the polymerase reached the arresting site.
从大肠杆菌中分离出了两个在一级序列上相关的转录延伸因子(GreA和GreB)。每个因子都会在人工停滞的延伸复合物中诱导新生转录本的切割,随后3'近端片段丢失,并从新的3'末端恢复延伸。GreA在末端后2或3个核苷酸处诱导切割,而GreB释放长度达9个核苷酸的更长寡核苷酸。随着转录复合物的推进,切割模式发生特征性变化,这支持了RNA聚合酶延伸的“尺蠖”模型。除了攻击人工停滞的复合物外,这两个因子还拮抗天然延伸停滞位点的作用,这些位点偶尔会捕获前进的复合物。GreB通过转录本切割和重新启动途径拯救停滞的复合物,而GreA通过未知机制起作用,仅在聚合酶到达停滞位点之前添加时才防止停滞。