Institute for Horticultural Plants, China Agricultural University, No. 2 Yuanmingyuan West Rd, Beijing, 100193, China.
Sci Rep. 2017 Oct 27;7(1):14223. doi: 10.1038/s41598-017-14671-8.
In higher plants, miR156 regulates the vegetative phase change via the target SBP/SPL genes. The regulation of miR156 during ontogenetic processes is not fully understood. In the apple genome, of 31 putative MdMIR156 genes that encode pre-miR156, seven were dominantly expressed. However, the transcript levels of only MdMIR156a5 and MdMIR156a12 decreased significantly during the vegetative phase change, which was consistent with the mature miR156 level, indicating that miR156 is under transcriptional regulation. Leaf HO content was higher in the adult phase than in the juvenile phase because of excess HO accumulation in chloroplasts. When in vitro shoots were treated with menadione, diphenyleneiodonium, L-2-oxothiazolidine-4-carboxylic acid or buthionine sulphoximine, the expressions of MdMIR156a5, MdMIR156a12, and as well miR156 were coordinated with reduced glutathione (GSH) contents and glutathione/glutathione disulfide ratio but not HO contents. Alteration of miR156 expression level by MdMIR156a6-overexpressing or miR156-mimetic transgenic Nicotiana benthamiana did not cause a corresponding change in reactive oxygen species or GSH status. Collectively, the results indicate that the vegetative phase change in apple is controlled by the MdMIR156a5 and MdMIR156a12 transcriptional regulatory network in response to the plastid-nucleus redox signals, such as GSH.
在高等植物中，miR156 通过靶标 SBP/SPL 基因调控营养生长向生殖生长的转变。miR156 在个体发育过程中的调控机制尚不完全清楚。在苹果基因组中，31 个假定的 MdMIR156 基因中，有 7 个基因编码 pre-miR156。然而，只有 MdMIR156a5 和 MdMIR156a12 的转录本水平在营养生长向生殖生长转变过程中显著下降，这与成熟 miR156 水平一致，表明 miR156 受到转录调控。由于叶绿体中 HO 的过量积累，成年期叶片的 HO 含量高于幼年期。当体外芽被 menadione、二苯乙烯碘二酮、L-2-氧代噻唑烷-4-羧酸或丁硫氨酸亚砜处理时，MdMIR156a5、MdMIR156a12 的表达以及 miR156 的表达与还原型谷胱甘肽 (GSH) 含量和谷胱甘肽/谷胱甘肽二硫化物比值的降低相协调，但与 HO 含量无关。过表达 MdMIR156a6 或 miR156 模拟物转基因烟草中 miR156 表达水平的改变并没有导致活性氧或 GSH 状态的相应变化。综上所述，这些结果表明，苹果的营养生长向生殖生长的转变是由 MdMIR156a5 和 MdMIR156a12 转录调控网络响应质体-核氧化还原信号（如 GSH）来控制的。
