Crété P, Vaucheret H
Laboratoire de Biologie Cellulaire, INRA, Versailles, France.
Plant Mol Biol. 1999 Sep;41(1):105-14. doi: 10.1023/a:1006364323494.
We have previously reported that the introduction of a full-length tobacco nitrite reductase Nii1 cDNA under the control of the 35S promoter triggers co-suppression of endogenous Nii genes in 25% of tobacco transformants. Here we show that introduction of chimeric Nii1-uidA, uidA-Nii1 and Nii1-uidA-Nii1 transgenes carrying 186 bp of the 5' end and/or 241 bp of the 3' end of the Nii1 cDNA do not trigger co-suppression of endogenous Nii genes. In addition, we show that when introduced by crossing or transformation into co-suppressed transgenic tobacco lines carrying full-length Nii1 transgenes, these chimeric transgenes are not silenced. These results therefore suggest that the 5' and 3' ends of the Nii1 cDNA are not sufficient to trigger co-suppression and are not targets for homology-dependent RNA degradation. Surprisingly, co-suppression was released in a double transformant obtained by introduction of one of these constructs into the co-suppressed transgenic tobacco line 461-2.1 homozygous for a full-length Nii1 transgene, and in one plant regenerated from untransformed leaf discs (plant 461-2.1*). The reappearance of co-suppression at very low frequency (less than 10(-3)) in the F2 progeny of plant 461-2.1* and the apparent absence of structural modification of the transgene locus suggest a metastable epigenetic modification. The steady-state level of Nii mRNAs in the plant 461-2-.1* was higher than in wild-type plants but lower than in hemizygous plants 461-2.1 which never trigger silencing. These results therefore confirm that transcription of the transgene above a particular threshold is required to trigger co-suppression.
我们之前报道过,在35S启动子控制下引入全长烟草亚硝酸还原酶Nii1 cDNA会在25%的烟草转化体中引发内源Nii基因的共抑制。在此我们表明,引入携带Nii1 cDNA 5'端186 bp和/或3'端241 bp的嵌合Nii1-uidA、uidA-Nii1和Nii1-uidA-Nii1转基因不会引发内源Nii基因的共抑制。此外,我们还表明,当通过杂交或转化引入携带全长Nii1转基因的共抑制转基因烟草品系时,这些嵌合转基因不会被沉默。因此,这些结果表明Nii1 cDNA的5'端和3'端不足以引发共抑制,也不是同源依赖性RNA降解的靶标。令人惊讶的是,通过将这些构建体之一引入携带全长Nii1转基因的纯合共抑制转基因烟草品系461-2.1中获得的双转化体以及从未转化叶盘再生的一株植物(植物461-2.1*)中,共抑制被解除。在植物461-2.1的F2后代中,共抑制以非常低的频率(小于10(-3))再次出现,并且转基因位点明显没有结构修饰,这表明存在一种亚稳态的表观遗传修饰。植物461-2-.1中Nii mRNA的稳态水平高于野生型植物,但低于从不引发沉默的半合子植物461-2.1。因此,这些结果证实了转基因转录超过特定阈值是引发共抑制所必需的。