INACTIVATION OF MAIZE TRANSPOSON-MU SUPPRESSES A MUTANT PHENOTYPE BY ACTIVATING AN OUTWARD-READING PROMOTER NEAR THE END OF MU1
INACTIVATION OF MAIZE TRANSPOSON-MU SUPPRESSES A MUTANT PHENOTYPE BY ACTIVATING AN OUTWARD-READING PROMOTER NEAR THE END OF MU1
复制标题
DOI：
10.1073/pnas.88.8.3502
复制
发表时间：
1991-04-01
影响因子：
11.1
通讯作者：
MARTIENSSEN, RA
中科院分区：
文献类型：
--
作者：
BARKAN, A;MARTIENSSEN, RA
我们先前描述了玉米中的突变hcf 106，由Mu 1转座子插入引起。当Mu转座子系统处于活跃期时，hcf 106调节非光合作用的淡绿色表型。然而，当Mu系统失活时（与Mu元件的超甲基化相关的状态），尽管转座子在基因内持续存在，植物仍采用正常表型。现在已经研究了介导这种突变表型抑制的分子机制。我们在这里表明，Mu元件负责的HCF 106病变位于序列编码的HCF 106 mRNA的5 '-非翻译前导。当Mu转座子系统活跃时，这种插入干扰来自hcf 106等位基因的mRNA的积累。然而，当Mu失活时，与从正常等位基因转录的mRNA在大小和丰度上相似的mRNA积累。这些转录本起始于整个70个碱基对区域的许多位点，在穆尔插入内和紧接其下游。因此，跨越穆尔和Hcf 106之间的下游连接的不寻常的启动子取代正常的Hcf 106启动子，但仅当Mu失活时。在不同的器官和响应于光的mRNA积累的模式表明，该启动子的活性是有条件的，不仅在穆活动的阶段，但也在调节正常的Hcf 106启动子的信号。
We described previously a mutation in maize, hcf106, caused by the insertion of a Mu1 transposon. When the Mu transposon system is in an active phase, hcf106 conditions a nonphotosynthetic, pale green phenotype. However, when the Mu system is inactive (a state correlated with hypermethylation of Mu elements), the plant adopts a normal phenotype despite the continued presence of the transposon within the gene. The molecular mechanisms that mediate this suppression of the mutant phenotype have now been investigated. We show here that the Mu element responsible for the hcf106 lesion lies within sequences encoding the 5'-untranslated leader of the Hcf106 mRNA. When the Mu transposon system is active, this insertion interferes with the accumulation of mRNA from the hcf106 allele. However, when Mu is inactive, mRNA similar in size and abundance to that transcribed from the normal allele accumulates. These transcripts initiate at many sites throughout a 70-base-pair region, within and immediately downstream of the Mul insertion. Thus, an unusual promoter spanning the downstream junction between Mul and Hcf106 substitutes for the normal Hcf106 promoter but only when Mu is inactive. The pattern of mRNA accumulation in different organs and in response to light suggests that the activity of this promoter is conditional not only upon the phase of Mu activity, but also upon signals that regulate the normal Hcf106 promoter.