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A CEP Peptide Receptor-like Kinase Regulates Auxin Biosynthesis and Ethylene Signaling to Coordinate Root Growth and Symbiotic Nodulation in Medicago truncatula
背景回顧：Because of the high energy consumed during symbiotic nitrogen fixation, legumes must balance growth and symbiotic nodulation.
提出問題：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.
主要發現：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.
生長素合成：MtCEP1 peptides can activate MtCRA2 under N-starvation conditions, leading to a repression of MtYUC2auxin 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.
乙烯信號：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.
結論：Overall, by reducing auxin biosynthesis and inhibiting ethylene signaling, the MtCEP1/MtCRA2 pathway balances root and nodule development under low-N conditions.
Model for the action of MtCRA2 in coordinating root architecture and symbiotic nodulation under low-N conditions.因為共生固氮過程中需要消耗大量的能量，因此豆類植物必須平衡生長與共生結瘤之間的關係。側根和根瘤都在根系統中形成，然而這些器官之間在可利用氮資源減少後的發育協調還不清楚。本文中，作者發現蒺藜苜蓿的類受體激酶MtCRA2可以響應於低氮條件促進早期共生結瘤的起始，並抑制根的生長。MtCEP1多肽可以在氮飢餓條件下激活MtCRA2，導致生長素合成基因MtYUC2的表達抑制，從而抑制根的生長素響應。通過生長素處理或者過表達MtYUC2基因可以模擬cra2突變體緊湊的根結構表型；相反，通過YUC抑制劑處理或者是MtYUC2敲除能夠恢復cra2突變體根的表型。另外，MtCEP1激活的CRA2號會與乙烯信號通路組分MtEIN2互作，並在Ser643和Ser924磷酸化該蛋白，保護其不被切割，從而抑制乙烯響應，因此局部促進根對於根瘤菌的敏感性。而cra2突變體結瘤比較少的表型也能夠通過引入ein2突變所恢復。綜上，當蒺藜苜蓿生活在低氮條件下，MtCEP1/MtCRA2通路會通過減少生長素合成和抑制乙烯信號轉導，來平衡根與根瘤發育之間的平衡。
p.s. 乙烯信號組分EIN2正常定位於胞質的內質網膜上，在存在乙烯時，其C端被剪切入核，激活下遊的乙烯信號。
王 濤
個人簡介：
1986年，山東農業大學，學士；
1989年，中國農業大學，碩士；
1998年，中國農業大學，博士。
研究方向：豆科功能基因組研究和分子設計育種：
1. 苜蓿抗逆分子機制研究；
2. 苜蓿-根瘤菌共生固氮調控機制研究；
3. 分子育種技術創新和新品種培育。
doi: 10.1105/tpc.19.00428
Journal: Plant Cell
Published date: June 25, 2020