Because of the high energy consumed during symbiotic nitrogen fixation, legumes must balance growth and symbiotic nodulation. Both lateral roots and nodules form on the root system and the developmental coordination of these organs according to reduced nitrogen (N) availability remains elusive. We show that the Compact Root Architecture 2 (MtCRA2) receptor-like kinase is essential to promote the initiation of early symbiotic nodulation and to inhibit root growth in response to low-N. MtCEP1 peptides can activate MtCRA2 under N-starvation conditions, leading to a repression of MtYUC2 auxin biosynthesis gene expression, and therefore of auxin root responses. Accordingly, the compact root architecture phenotype of cra2 can be mimicked by an auxin treatment or by over-expressing MtYUC2, and conversely, a treatment with YUC inhibitors or a MtYUC2 knock-out rescues the cra2 root phenotype. The MtCEP1-activated CRA2 can additionally interact with and phosphorylate the MtEIN2 ethylene signaling component at Ser643 and Ser924, preventing its cleavage and therefore repressing ethylene responses, thus locally promoting the root susceptibility to rhizobia. In agreement, the cra2 low nodulation phenotype is rescued by an ein2 mutation. Overall, by reducing auxin biosynthesis and inhibiting ethylene signaling, the MtCEP1/MtCRA2 pathway balances root and nodule development under low-N conditions.

由于共生固氮过程中消耗大量能量，豆科植物必须平衡生长和共生结瘤。侧根和根瘤均在根系上形成，并且这些器官根据氮 (N) 利用率减少的发育协调仍然难以捉摸。我们发现，紧凑根结构 2 (MtCRA2) 受体样激酶对于促进早期共生结瘤的启动和抑制响应低氮的根生长至关重要。 MtCEP1 肽可以在氮饥饿条件下激活 MtCRA2，从而抑制 MtYUC2 生长素生物合成基因表达，从而抑制生长素根反应。因此，cra2 的紧凑根结构表型可以通过生长素处理或通过过表达 MtYUC2 来模拟，相反，用 YUC 抑制剂处理或 MtYUC2 敲除可以挽救 cra2 根表型。 MtCEP1 激活的 CRA2 还可以与 MtEIN2 乙烯信号成分 Ser643 和 Ser924 相互作用并磷酸化，防止其裂解，从而抑制乙烯反应，从而局部促进根部对根瘤菌的敏感性。一致认为，cra2 低结瘤表型是由 ein2 突变拯救的。总体而言，通过减少生长素生物合成和抑制乙烯信号传导，MtCEP1/MtCRA2 途径在低氮条件下平衡根和根瘤的发育。