MuDR转座子末端反向重复包含一个复杂的植物启动子,指导不同的体细胞和生发程序。

M. Raizada, M. Benito, V. Walbot
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引用次数: 49

摘要

玉米Mu转座子受到严格的发育控制。元件在末梢分裂的体细胞中以高频率切除,但在分生组织中则不然。生发细胞中的Mu元素在不切除的情况下扩增,并插入整个基因组。所有的活性都需要MuDR,它编码两个基因,mudrA和mudrB,其几乎相同的启动子位于转座子末端倒置重复序列(TIR)。我们将mudrB基因的216 bp TIR与GUS和荧光素酶报告基因融合。我们证明TIRB程序在不同的分生体细胞中报告表达,矛盾的是在那些Mu切除被抑制的细胞中。在生发细胞、未成熟的雄穗和成熟的花粉中,报告基因的表达比叶片增加了20倍。通过RNA印迹杂交,我们发现内源mudrB和mudrA转录本在成熟花粉中显著增加;序列比较表明,MuDR TIRs包含植物细胞周期增强子基序和功能定义的花粉增强子。因此,MuDR TIR启动子在体细胞和生发组织中都受到发育调控。由于数据库序列分析表明,MuDR TIR增强子应该在单子体和双子体中都有功能,我们建议使用原生MuDR启动子来尝试将Mu转位的独特行为转移到异源宿主。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The MuDR transposon terminal inverted repeat contains a complex plant promoter directing distinct somatic and germinal programs.
The Mu transposons of maize are under stringent developmental control. Elements excise at high frequencies in terminally dividing somatic cells, but not in meristems. Mu elements in germinal cells amplify, without excision, and insert throughout the genome. All activities require MuDR, which encodes two genes, mudrA and mudrB, whose near-identical promoters are located in the transposon terminal inverted repeats (TIR). We have fused the 216 bp TIR of the mudrB gene to GUS and luciferase reporters. We demonstrate that TIRB programs reporter expression in diverse, meristematic somatic cells, paradoxically in those cells in which Mu excisions are repressed. In germinal cells, immature tassel and mature pollen, reporter expression increases up to 20-fold compared to leaf. By RNA blot hybridization, we demonstrate that endogenous mudrB and mudrA transcripts increase significantly in mature pollen; sequence comparisons demonstrate that the MuDR TIRs contain plant cell-cycle enhancer motifs and functionally defined pollen enhancers. Therefore, the MuDR TIR promoters are developmentally regulated in both somatic and germinal tissues. Because database sequence analysis suggests that the MuDR TIR enhancers should be functional in both monocots and dicots, we suggest that the native MuDR promoter be used in attempts to transfer the unique behavior of Mu transposition to heterologous hosts.
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