Plant Cell|福建农林陈栩教授团队揭示了GmPIN依赖的生长素极性运输参与了大豆根瘤的发育
为了克服氮缺乏症，豆科植物的根系与固氮的根瘤菌建立共生的相互作用，这种相互作用在专门的器官(结节)中培育。与其他器官类似，根瘤的形成是由植物激素在原基部位的局部最大值决定的。然而，生长素如何调节节瘤发育仍然知之甚少。在这里，我们发现在大豆(Glycine max)中，PIN-FORMED (PIN)转运体 GmPIN1驱动的生长素动态转运参与了根瘤原基的形成。GmPIN1在结节原基细胞中有特异性表达，并且在这些细胞中极性定位。两种结瘤调节剂，即异黄酮类化合物，促使 GmPIN1b 向根皮层细胞扩散，细胞分裂素重排 GmPIN1b 的极性。利用 CRISPR-Cas9产生的 Gmpin1abc 三重突变体显示，在根瘤分生组织中生长素最大值的建立受到损害，在根瘤原基细胞中发生异常分裂。此外，GmPIN1的过度表达抑制了小瘤原基的发生。GmPIN9d 是拟南芥 PIN2的同源基因，在结节发育后期与 GmPIN1一起作用，在维管束中顶端运输生长素，微调生长素供应以促进结节增大。我们的研究结果揭示了依赖于 pin 的生长素转运如何调节大豆根瘤发育的不同方面，并表明建立生长素梯度是豆类和根瘤菌之间适当相互作用的先决条件。
To overcome nitrogen deficiency, legume roots establish symbiotic interactions with nitrogen-fixing rhizobia that is fostered in specialized organs (nodules). Similar to other organs, nodule formation is determined by a local maximum of the phytohormone auxin at the primordium site. However, how auxin regulates nodule development remains poorly understood. Here, we found that in soybean, (Glycine max), dynamic auxin transport driven by PIN-FORMED (PIN) transporter GmPIN1 is involved in nodule primordium formation. GmPIN1 was specifically expressed in nodule primordium cells and GmPIN1 was polarly localized in these cells. Two nodulation regulators, (iso)flavonoids trigger expanded distribution of GmPIN1b to root cortical cells, and cytokinin rearranges GmPIN1b polarity. Gmpin1abc triple mutants generated with CRISPR-Cas9 showed impaired establishment of auxin maxima in nodule meristems and aberrant divisions in the nodule primordium cells. Moreover, overexpression of GmPIN1 suppressed nodule primordium initiation. GmPIN9d, an ortholog of Arabidopsis thaliana PIN2, acts together with GmPIN1 later in nodule development to acropetally transport auxin in vascular bundles, fine-tuning the auxin supply for nodule enlargement. Our findings reveal how PIN-dependent auxin transport modulates different aspects of soybean nodule development and suggest that establishment of auxin gradient is a prerequisite for the proper interaction between legumes and rhizobia.
https://doi.org/10.1093/plcell/koab183
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