Different Pathways Act Downstream of the CEP Peptide Receptor CRA2 to Regulate Lateral Root and Nodule Development
Different Pathways Act Downstream of the CEP Peptide Receptor CRA2 to Regulate Lateral Root and Nodule Development
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DOI：
10.1104/pp.16.00113
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发表时间：
2016-08-01
期刊：
影响因子：
7.4
通讯作者：
Djordjevic, Michael A.
中科院分区：
文献类型：
--
作者：
Mohd-Radzman, Nadiatul A.;Laffont, Carole;Djordjevic, Michael A.
c -末端编码肽（cep）以非细胞自主的方式控制根系结构。在短根紫花苜蓿中，MtCEP1通过未知途径增加根瘤形成和抑制侧根出苗来影响根发育。在这里，我们发现MtCEP1肽依赖性的结瘤增加需要共生信号通路和乙烯不敏感2 (EIN2)/镰状细胞（SKL），但独立于SUPER NUMERIC结节。mtcep1依赖性的侧根发育抑制是通过ein2不依赖的机制起作用的。MtCEP1通过促进根瘤菌感染、根形成根瘤的发育能力、融合根瘤的形成以及在原韧皮部极开始的根瘤发育频率的增加来促进根瘤的形成。这些表型与ein2/skl突变体相似，支持MtCEP1调节ein2依赖性共生反应。因此，MtCEP1抵消了乙烯前体浓度增加引起的结瘤减少，乙烯合成抑制剂处理拮抗MtCEP1根表型。MtCEP1也抑制ein2依赖性假结节形成的发展。最后，影响与拟南芥CEP受体密切相关的COMPACT ROOT ARCHITECTURE2 （CRA2）受体的突变体对MtCEP1对侧根和根瘤形成的影响没有反应，这表明CRA2是一个介导这两个器官发生程序的CEP肽受体。此外，乙烯抑制剂处理抵消了cra2结瘤表型。这些结果表明，MtCEP1及其可能的受体CRA2通过不同的途径介导根瘤和侧根的发育。
C-TERMINALLY ENCODED PEPTIDEs (CEPs) control root system architecture in a non-cell-autonomous manner. In Medicago truncatula, MtCEP1 affects root development by increasing nodule formation and inhibiting lateral root emergence by unknown pathways. Here, we show that the MtCEP1 peptide-dependent increase in nodulation requires the symbiotic signaling pathway and ETHYLENE INSENSITIVE2 (EIN2)/SICKLE (SKL), but acts independently of SUPER NUMERIC NODULES. MtCEP1-dependent inhibition of lateral root development acts through an EIN2-independent mechanism. MtCEP1 increases nodulation by promoting rhizobial infections, the developmental competency of roots for nodulation, the formation of fused nodules, and an increase in frequency of nodule development that initiates at proto-phloem poles. These phenotypes are similar to those of the ein2/skl mutant and support that MtCEP1 modulates EIN2-dependent symbiotic responses. Accordingly, MtCEP1 counteracts the reduction in nodulation induced by increasing ethylene precursor concentrations, and an ethylene synthesis inhibitor treatment antagonizes MtCEP1 root phenotypes. MtCEP1 also inhibits the development of EIN2-dependent pseudonodule formation. Finally, mutants affecting the COMPACT ROOT ARCHITECTURE2 (CRA2) receptor, which is closely related to the Arabidopsis CEP Receptor1, are unresponsive to MtCEP1 effects on lateral root and nodule formation, suggesting that CRA2 is a CEP peptide receptor mediating both organogenesis programs. In addition, an ethylene inhibitor treatment counteracts the cra2 nodulation phenotype. These results indicate that MtCEP1 and its likely receptor, CRA2, mediate nodulation and lateral root development through different pathways.