Department of Botany and Plant Sciences and Institute of Integrative Genome Biology, University of California, Riverside, CA, 92506, USA.
University of Freiburg, Faculty of Biology; BIOSS Centre for Biological Signaling Studies and ZBSA Centre for Biosystems Studies, Schänzlestr. 1, 79104, Freiburg, Germany.
Nat Commun. 2018 Jun 11;9(1):2262. doi: 10.1038/s41467-018-04708-5.
The ancient morphoregulatory hormone auxin dynamically realigns dedicated cellular processes that shape plant growth under prevailing environmental conditions. However, the nature of the stress-responsive signal altering auxin homeostasis remains elusive. Here we establish that the evolutionarily conserved plastidial retrograde signaling metabolite methylerythritol cyclodiphosphate (MEcPP) controls adaptive growth by dual transcriptional and post-translational regulatory inputs that modulate auxin levels and distribution patterns in response to stress. We demonstrate that in vivo accumulation or exogenous application of MEcPP alters the expression of two auxin reporters, DR5:GFP and DII-VENUS, and reduces the abundance of the auxin-efflux carrier PIN-FORMED1 (PIN1) at the plasma membrane. However, pharmacological intervention with clathrin-mediated endocytosis blocks the PIN1 reduction. This study provides insight into the interplay between these two indispensable signaling metabolites by establishing the mode of MEcPP action in altering auxin homeostasis, and as such, positioning plastidial function as the primary driver of adaptive growth.
古老的形态调节激素生长素在流行的环境条件下动态地重新排列专门的细胞过程，从而塑造植物的生长。然而，改变生长素动态平衡的应激响应信号的性质仍然难以捉摸。在这里，我们确定了进化上保守的质体逆行信号代谢物甲基赤藓醇环二磷酸（MEcPP）通过双重转录和翻译后调节输入来控制适应性生长，该输入调节生长素水平和分布模式以响应应激。我们证明，体内积累或外源施加 MEcPP 会改变两种生长素报告基因 DR5:GFP 和 DII-VENUS 的表达，并降低质膜上生长素外排载体 PIN-FORMED1（PIN1）的丰度。然而，用网格蛋白介导的内吞作用进行药理学干预会阻止 PIN1 的减少。这项研究通过确定 MEcPP 作用改变生长素动态平衡的模式，深入了解这两种不可或缺的信号代谢物之间的相互作用，并将质体功能定位为适应性生长的主要驱动因素。
