EPIGENETIC REPEAT-INDUCED GENE SILENCING (RIGS) IN ARABIDOPSIS
EPIGENETIC REPEAT-INDUCED GENE SILENCING (RIGS) IN ARABIDOPSIS
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DOI：
10.1007/bf00028978
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发表时间：
1993-09-01
影响因子：
5.1
通讯作者：
SIGNER, ER
中科院分区：
文献类型：
--
作者：
ASSAAD, FF;TUCKER, KL;SIGNER, ER
在一些植物系统中，当转基因构建体增加DNA序列的拷贝数时，结构完整的基因的表达可能在表观遗传学上被沉默。在这里，我们报告了表观遗传沉默在拟南芥系含有转基因插入定义的遗传结构，都在同一个基因组位点。这些包括等位基因系列，其包括携带重复的耐药性转基因的初级插入物的单拷贝，和一组其衍生物，其作为插入物内重组的结果携带不同数量和等位基因的耐药性基因。虽然耐药基因保持完整，但原代和一些重组株系仍然分离了许多由于沉默而部分或完全药物敏感的后代。与其他系统一样，沉默是可逆的，并且与稳态mRNA减少和DNA甲基化增加相关。每个不同数量和组合的基因，在相同或不同的（即，同源）染色体，条件自己的特质分离模式。引人注目的是，一个单一的基因线隔离只有少数轻微的药物敏感的后代，而多基因线隔离许多高度敏感的后代，表明在这个位点上的重复序列的沉默的依赖。这强烈反对基于反义RNA的解释，但与基于异位DNA配对的解释一致。一种可能性是沉默反映了配对的同源DNA与侧翼异源DNA的相互作用，其诱导染色质浓缩成不可转录的状态。
In several plant systems expression of structurally intact genes may be silenced epigenetically when a transgenic construct increases the copy number of DNA sequences. Here we report epigenetic silencing in Arabidopsis lines containing transgenic inserts of defined genetic structure, all at the same genomic locus. These comprise an allelic series that includes a single copy of the primary insert, which carries repeated drug resistance transgenes, and a set of its derivatives, which as a result of recombination within the insert carry different numbers and alleles of resistance genes. Although the drug resistance genes remained intact, both the primary and some recombinant lines nevertheless segregated many progeny that were partly or fully drug-sensitive because of silencing. As in other systems silencing was reversible, and correlated with decreased steady-state mRNA and increased DNA methylation. Each different number and combination of genes, on the same or different (i.e., homologous) chromosomes, conditioned its own idiosyncratic segregation pattern. Strikingly, lines with a single gene segregated only a few slightly drug-sensitive progeny whereas multi-gene lines segregated many highly sensitive progeny, indicating dependence of silencing at this locus on repeated sequences. This argues strongly against explanations based on antisense RNA, but is consistent with explanations based on ectopic DNA pairing. One possibility is that silencing reflects the interaction of paired homologous DNA with flanking heterologous DNA, which induces condensation of chromatin into a non-transcribable state.