Ke Meiyu, Ma Zhiming, Wang Deyan, Sun Yanbiao, Wen Chenjin, Huang Dingquan, Chen Zichen, Yang Liang, Tan Shutang, Li Ruixi, Friml Jiří, Miao Yansong, Chen Xu
College of Life Science and Fujian Provincial Key Laboratory of Haixia Applied Plant Systems Biology, Fujian Agriculture and Forestry University, Fuzhou, 350002, China.
Haixia Institute of Science and Technology, Horticultural Plant Biology and Metabolomics Centre, Fujian Agriculture and Forestry University, Fuzhou, 350002, China.
New Phytol. 2021 Jan;229(2):963-978. doi: 10.1111/nph.16915. Epub 2020 Sep 30.
To adapt to the diverse array of biotic and abiotic cues, plants have evolved sophisticated mechanisms to sense changes in environmental conditions and modulate their growth. Growth-promoting hormones and defence signalling fine tune plant development antagonistically. During host-pathogen interactions, this defence-growth trade-off is mediated by the counteractive effects of the defence hormone salicylic acid (SA) and the growth hormone auxin. Here we revealed an underlying mechanism of SA regulating auxin signalling by constraining the plasma membrane dynamics of PIN2 auxin efflux transporter in Arabidopsis thaliana roots. The lateral diffusion of PIN2 proteins is constrained by SA signalling, during which PIN2 proteins are condensed into hyperclusters depending on REM1.2-mediated nanodomain compartmentalisation. Furthermore, membrane nanodomain compartmentalisation by SA or Remorin (REM) assembly significantly suppressed clathrin-mediated endocytosis. Consequently, SA-induced heterogeneous surface condensation disrupted asymmetric auxin distribution and the resultant gravitropic response. Our results demonstrated a defence-growth trade-off mechanism by which SA signalling crosstalked with auxin transport by concentrating membrane-resident PIN2 into heterogeneous compartments.
为了适应各种各样的生物和非生物信号，植物进化出了复杂的机制来感知环境条件的变化并调节自身生长。促进生长的激素和防御信号以拮抗方式精细调节植物发育。在宿主与病原体相互作用期间，这种防御与生长的权衡由防御激素水杨酸（SA）和生长激素生长素的拮抗作用介导。在这里，我们揭示了拟南芥根中SA通过限制PIN2生长素外流转运蛋白的质膜动力学来调节生长素信号传导的潜在机制。SA信号传导限制了PIN2蛋白的侧向扩散，在此过程中，PIN2蛋白根据REM1.2介导的纳米结构域分隔浓缩成超簇。此外，SA或Remorin（REM）组装引起的膜纳米结构域分隔显著抑制了网格蛋白介导的内吞作用。因此，SA诱导的异质表面凝聚破坏了生长素的不对称分布以及由此产生的向重力性反应。我们的结果证明了一种防御与生长的权衡机制，即SA信号通过将膜驻留的PIN2集中到异质区室中与生长素运输发生串扰。
