Silencing of an aleurone-specific gene in transgenic rice is caused by a rearranged transgene.
Silencing of an aleurone-specific gene in transgenic rice is caused by a rearranged transgene.
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转基因水稻中糊粉特异性基因的沉默是由重排的转基因引起的。
DOI：
10.1046/j.1365-313x.1999.00373.x
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发表时间：
1999
期刊：
影响因子：
--
通讯作者：
K. Shimamoto
中科院分区：
文献类型：
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作者：
Kazuko Morino;O. Olsen;K. Shimamoto
在水稻中，糊粉层特异性Ltp 2-gus转基因的沉默，导致容易检测到的染色模式的粮食表面上，提供了一个方便的工具，研究在单子叶植物中的基因沉默的定量方面。本文分析了沉默的表型、发生、遗传和环境效应。我们还报告了转基因的克隆，其结构的测定和分析从转基因位点的成绩单。结果表明，在R2代出现了多种沉默模式，大多数转基因在R2代成为纯合的，并且它们遗传了五代。从L3.3转基因株系中克隆出两个转基因位点：一个是完整的Ltp 2-gus基因，另一个是重排的gus基因，其中部分基因处于反义方向。gus转录物的分析表明，来自重排的转基因的部分反义RNA是存在于沉默线，是聚腺苷酸化，但它是不存在的非沉默线。RNA分析表明，在糊粉层Ltp 2-gus沉默是转录后的，它可能是由部分反义gus转录本与正常的正义转录本的相互作用。反义转录物可能参与转录后沉默进行了讨论。
In rice, silencing of the aleurone-specific Ltp2-gus transgene, causing easily detectable staining patterns on the grain surface, offers a convenient tool to study quantitative aspects of gene silencing in monocots. In this paper we analyzed phenotypes, occurrence, inheritance and environmental effects on the silencing. We also report on the cloning of transgenes, determination of their structure and analysis of transcripts from the transgene loci. The results show that various patterns of silencing appeared in the R2 generation at which most of the transgenes became homozygous and that they were inherited for five generations. In addition, silencing independently occurred in three generations and reversion to full expression was also found. Cloning of transgenes from a silenced L3.3 line demonstrated that this line carried two transgene loci: one carried an intact Ltp2-gus gene and the other carried a rearranged transgene in which part of the gus gene was in the antisense orientation. Analysis of gus transcripts indicated that partial antisense RNA derived from the rearranged transgene was present in silenced lines and was polyadenylated but that it was absent in non-silenced lines. RNA analyses suggested that the Ltp2-gus silencing in the aleurone layer was post-transcriptional and that it may be caused by interaction of partial antisense gus transcripts with normal sense transcripts. Possible involvement of antisense transcripts in post-transcriptional silencing is discussed.