RECOMBINATION BETWEEN SATELLITE RNAS OF TURNIP CRINKLE VIRUS

RECOMBINATION BETWEEN SATELLITE RNAS OF TURNIP CRINKLE VIRUS
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DOI:
10.1002/j.1460-2075.1990.tb08294.x
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发表时间:
1990-06-01
期刊:
影响因子:
11.4
通讯作者:
SIMON, AE
SIMON, AE
中科院分区:
生物学1区
文献类型:
--
作者:
CASCONE, PJ;CARPENTER, CD;SIMON, AE

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芜菁皱缩病毒(TCV)与卫星(sat)RNA(sat-RNA D、sat-RNA F)、缺陷型干扰(DI)RNA(DI RNA G、DI 1 RNA)和一种具有sat-RNA和DI RNA特性的RNA(sat-RNA C)相关。当植物接种TCV,sat-RNA D和在体外sat-RNA C转录物含有非活性突变的5“结构域,重组sat-RNA回收。这些重组子由位于5“端的sat-RNA D和位于3”端的sat-RNA AC序列组成。对20个独立的重组连接点的分析表明,在植物中两个sat-RNA之间的序列相似区域发生了不相等的交换,导致3-16个核苷酸的重复。30%的sat-RNA重组体还在交叉连接处插入了1至3个额外的核苷酸,这些核苷酸不对应于sat-RNA C或sat-RNA D序列。重组连接的右侧总是从sat-RNA C的三个连续核苷酸中的一个开始。基于卫星RNA C的该序列、DI RNA G的右侧连接和TCV的5“末端之间的相似性,以及DI 1 RNA和卫星RNA C的右侧连接和卫星RNA的5”末端之间的序列相似性,提出了复制酶驱动的拷贝选择机制。复制酶在复制病毒或亚病毒负链时,可以与新生正链一起沿着从模板解离,并在相同或不同模板上的两个内部复制酶识别序列之一处重新启动合成,从而产生重组sat-RNA或DI RNA。
Turnip crinkle virus (TCV) is associated with satellite (sat) RNAs (sat-RNA D, sat-RNA F), defective interfering (DI) RNAs (DI RNA G, DI1 RNA), and one RNA with properties of both sat-RNAs and DI RNAs (sat-RNA C). When plants were inoculated with TCV, sat-RNA D and in vitro sat-RNA C transcripts containing non-viable mutation in the 5'' domain, recombinant sat-RNAs were recovered. These recombinants were composed of sat-RNA D at the 5'' end and sat-RNAC sequences at the 3'' end. Analysis of 20 independent recombination junctions revealed that unequal crossing-over had occurred in plants in a region of sequence similarity between the two sat-RNAs which resulted in the duplication of 3-16 nucleotides. Thirty percent of the sat-RNA recombinants also had one to three additional nucleotides inserted at the crossover junctions which did not correspond to either sat-RNA C or sat-RNA D sequence. The right side of the recombination junctions always began with one of three consecutive nucleotides of sat-RNA C. Based on the similarity between this sequence of sat-RNA C, the right side junction of DI RNA G and the 5'' end of TCV, as well as the sequence similarity between right side junctions of DI1 RNA and sat-RNA C and the 5'' end of the sat-RNAs, a replicase-driven copy choice mechanism is proposed. The replicase, while replicating viral or subviral minus strands, can dissociate from the template along with the nascent plus strand and reinitiate synthesis at one of two internal replicase recognition sequences on the same or different template thus generating recombinant sat-RNAs or DI RNAs.