miRNAs trigger widespread epigenetically activated siRNAs from transposons in Arabidopsis.
miRNAs trigger widespread epigenetically activated siRNAs from transposons in Arabidopsis.
复制标题
miRNA触发了拟南芥中转座子的广泛表观遗传激活的siRNA。
作者：
在植物中，转录后基因沉默（PTGS）由DICER-LIKE 1（DCL 1）依赖性miRNA介导，其还通过RNA依赖性RNA聚合酶6（RDR 6）、DCL 4和Argonaute 1（AGO 1）触发21-nt二级siRNA，而转座子的转录基因沉默（TGS）由24-nt异染色质（het）siRNA RDR 2、DCL 3和AGO 4介导。转座子还可以在DNA甲基化减少1（ddm 1）和DNA甲基转移酶1（met 1）突变体中以及在花粉粒的营养核和去分化的植物细胞培养物中产生丰富的21-nt“表观遗传激活”小干扰RNA（siRNA）。在这里，我们表明，siRNA类似于二级siRNA，因为数千个转座子转录物被50多个miRNA特异性靶向，用于RDR 6的切割和加工。在ddm 1背景下，RDR 6、DCL 4或DCL 1的缺失导致21-nt siRNA的缺失和严重的不育，但24-nt hetsiRNA部分恢复，支持PTGS和TGS之间的拮抗关系。因此，miRNA指导的miRNA生物合成是一种特异性靶向转座子转录物的潜在机制，但仅当它们在种系重编程期间被表观遗传学重新激活时。这种古老的识别机制可能既被转座子保留以逃避长期异染色质沉默，也被其宿主保留以进行基因组防御。
In plants, post-transcriptional gene silencing (PTGS) is mediated by DICER-LIKE1 (DCL1)-dependent miRNAs, that also trigger 21-nt secondary siRNA via RNA DEPENDENT RNA POLYMERASE6 (RDR6), DCL4, and ARGONAUTE1 (AGO1), while transcriptional gene silencing (TGS) of transposons is mediated by 24-nt heterochromatic (het)siRNA RDR2, DCL3 and AGO4. Transposons can also give rise to abundant 21-nt “epigenetically activated” small interfering RNAs (easiRNAs) in DECREASE IN DNA METHYLATION1 (ddm1) and DNA METHYLTRANSFERASE1 (met1) mutants, as well as in the vegetative nucleus of pollen grains, and in dedifferentiated plant cell cultures. Here we show that easiRNAs resemble secondary siRNAs, in that thousands of transposon transcripts are specifically targeted by more than fifty miRNAs for cleavage and processing by RDR6. Loss of RDR6, DCL4 or DCL1 in a ddm1 background results in loss of 21-nt easiRNA, and severe infertility, but 24-nt hetsiRNA are partially restored, supporting an antagonistic relationship between PTGS and TGS. Thus miRNA-directed easiRNA biogenesis is a latent mechanism that specifically targets transposon transcripts, but only when they are epigenetically reactivated during reprogramming of the germline. This ancient recognition mechanism may have been retained both by transposons to evade long-term heterochromatic silencing, and by their hosts for genome defence.