MicroRNA156 conditions auxin sensitivity to enable growth plasticity in response to environmental changes in Arabidopsis (miRNA-Seq). MicroRNA156 conditions auxin sensitivity to enable growth plasticity in response to environmental changes in Arabidopsis (miRNA-Seq)

MicroRNAs (miRNAs) play diverse roles in plant development, but whether and how miRNAs participate in thermomorphogenesis remains ambiguous. Here we show that HYPONASTIC LEAVES1 (HYL1) – a key component of microRNA biogenesis – acts downstream of the thermal regulator PHYTOCHROME INTERACTING FACTOR 4 in temperature-dependent plasticity of hypocotyl growth in Arabidopsis. A hyl1-2 suppressor screen identified a dominant dicer-like1 (dcl1) allele, dcl1-24, which rescues hyl1-2’s defects in miRNA biosynthesis and warm temperature-induced hypocotyl elongation. Genome-wide miRNA and transcriptome analysis reveal microRNA156 (miR156) and its target SQUAMOSA PROMOTER-BINDING-LIKE 9 (SPL9) as critical regulators of thermomorphogenesis. Surprisingly, perturbation of the miR156/SPL9 module disengages seedling responsiveness to warm temperatures by impeding auxin sensitivity. Moreover, the miR156-dependent auxin sensitivity also operates in the shade avoidance response at lower temperatures. Thus, these results unveil the miRNA156/SPL9 module as a previously-uncharacterized genetic circuitry that enables plant growth plasticity in response to environmental temperature and light changes. Overall design: We compared global miRNA levels in 4-d-old Col-0, hyl1-2 and dcl1-24/hyl1-2 seedlings grown in 50 umol m-2 s-1 red light at either 21 C or 27 C.

微RNA（microRNAs, miRNAs）在植物发育过程中发挥多样化调控功能，但miRNAs是否参与以及如何参与温度形态建成（thermomorphogenesis）仍不明确。本研究证实，微RNA生物发生的关键组分偏上性叶1（HYPONASTIC LEAVES1, HYL1）在拟南芥下胚轴生长的温度依赖性可塑性调控中，位于温度调控因子光敏色素互作因子4（PHYTOCHROME INTERACTING FACTOR 4, PIF4）的下游。通过对hyl1-2突变体的抑制子筛选，我们获得了一个显性的类Dicer核糖核酸酶1（dicer-like1, DCL1）等位基因dcl1-24，该等位基因可恢复hyl1-2在miRNA生物合成以及温暖温度诱导的下胚轴伸长中的缺陷表型。全基因组miRNA与转录组分析显示，微RNA156（microRNA156, miR156）及其靶基因SQUAMOSA启动子结合蛋白样9（SQUAMOSA PROMOTER-BINDING-LIKE 9, SPL9）是温度形态建成的关键调控因子。令人意外的是，miR156/SPL9模块的扰动会通过削弱生长素敏感性，使幼苗丧失对温暖温度的响应能力。此外，依赖于miR156的生长素敏感性在低温环境下的避荫响应中同样发挥调控作用。综上，本研究揭示miR156/SPL9模块作为一种此前未被表征的遗传调控通路，可介导植物响应环境温度与光照变化的生长可塑性。整体实验设计：我们比较了在50 μmol·m⁻²·s⁻¹红光光照条件下，分别于21℃与27℃培养的4日龄Col-0、hyl1-2以及dcl1-24/hyl1-2幼苗的全局miRNA表达水平。