The MicroRNA390/TRANS-ACTING SHORT INTERFERING RNA3 Module Mediates Lateral Root Growth under Salt Stress via the Auxin Pathway

The MicroRNA390/TRANS-ACTING SHORT INTERFERING RNA3 Module Mediates Lateral Root Growth under Salt Stress via the Auxin Pathway
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MicroRNA390/反式短干扰RNA3模块通过生长素途径介导盐胁迫下侧根生长

DOI:
10.1104/pp.17.01559
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发表时间:
2018-06-01
期刊:
影响因子:
7.4
通讯作者:
Luo, Keming
Luo, Keming
中科院分区:
生物学1区
文献类型:
--
作者:
He, Fu;Xu, Changzheng;Luo, Keming

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盐诱导的植物根系发育可塑性强烈依赖于生长素信号。然而,这一过程背后的分子事件知之甚少。microRNA 390(miR 390)、trans-actin小干扰RNA(tasiRNA)和生长素应答因子(ARF)形成参与控制侧根(LR)生长的调节模块。在这里,我们发现,miR 390的表达强烈诱导暴露于盐在白杨(杨属)LR形成过程中。植物miR 390过表达刺激LR发育并增加耐盐性,而由短串联靶模拟物引起的miR 390敲低抑制LR生长并损害耐盐性。ARF3.1、ARF3.2和ARF 4的表达在盐的存在下被显著抑制,并且在miR 390过表达系中转录物丰度显著降低,但在miR 390敲低系中增加。ARF 4 m的组成型表达含有突变的反式作用小干扰性ARF结合位点,消除了miR 390过表达者的耐盐性。miR 390正调控生长素信号在LR遭受盐,但ARF 4抑制生长素信号。盐度稳定白杨Aux/IAA阻遏物吲哚-3-乙酸17.1,并且在盐存在下,生长素/盐抗性形式的该阻遏物的过表达抑制了miR 390过表达和ARF 4-RNA干扰系中的LR生长。因此,miR 390/TAS 3/ARFs模块是盐胁迫下白杨LR生长的关键调控因子,通过调节生长素途径发挥作用。
Salt-induced developmental plasticity in a plant root system strongly depends on auxin signaling. However, the molecular events underlying this process are poorly understood. MicroRNA390 (miR390), trans-actin small interfering RNAs (tasiRNAs), and AUXIN RESPONSE FACTORs (ARFs) form a regulatory module involved in controlling lateral root (LR) growth. Here, we found that miR390 expression was strongly induced by exposure to salt during LR formation in poplar (Populus spp.) plants. miR390 overexpression stimulated LR development and increased salt tolerance, whereas miR390 knockdown caused by a short tandem target mimic repressed LR growth and compromised salt resistance. ARF3.1, ARF3.2, and ARF4 expression was inhibited significantly by the presence of salt, and transcript abundance was decreased dramatically in the miR390-overexpressing line but increased in the miR390-knockdown line. Constitutive expression of ARF4m harboring mutated trans-acting small interfering ARF-binding sites removed the salt resistance of the miR390 overexpressors. miR390 positively regulated auxin signaling in LRs subjected to salt, but ARF4 inhibited auxin signaling. Salinity stabilized the poplar Aux/IAA repressor INDOLE-3-ACETIC ACID17.1, and overexpression of an auxin/salt-resistant form of this repressor suppressed LR growth in miR390-overexpressing and ARF4-RNA interfering lines in the presence of salt. Thus, the miR390/TAS3/ARFs module is a key regulator, via modulating the auxin pathway, of LR growth in poplar subjected to salt stress.