Autoregulation of nodulation pathway is dispensable for nitrate-induced control of rhizobial infection
Autoregulation of nodulation pathway is dispensable for nitrate-induced control of rhizobial infection
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DOI：
10.1080/15592324.2020.1733814
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发表时间：
2020-02-27
影响因子：
2.9
通讯作者：
Suzaki, Takuya
中科院分区：
文献类型：
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作者：
Nishida, Hanna;Ito, Momoyo;Suzaki, Takuya
豆科植物具有自动调节结瘤（AON）途径，负责维持最佳根瘤数。在日本莲中，AON由CLE-HAR1-TML模块组成，该模块在根到枝到根的长距离信号传递中起着至关重要的作用。除了负调控根瘤菌数量的主要作用外，最近的一项研究揭示了AON在根瘤菌感染的系统性控制方面的另一个作用。硝酸盐还负调控豆科植物与根瘤菌共生的多效期，包括根瘤菌侵染和根瘤菌数量。硝酸盐信号最近被证明使用AON成分如CLE-RS2和HAR1来控制结节数。在这里，我们考虑了与硝酸盐有关的根瘤菌感染中CLE-RS1， -RS2和TML的功能丧失突变的作用。我们的结果与先前的研究结果一致，并支持了AON对根瘤菌感染的控制而不是硝酸盐诱导的控制所必需的假设。此外，我们证实tml突变体表现出不同于cle-rs2和har1的硝酸盐敏感性。因此，虽然硝酸盐诱导的根瘤数控制机制使用了AON成分，但在HAR1下游可能存在一种未知的硝酸盐特异性途径，与HAR1> TML途径平行作用。
Legumes possess the autoregulation of nodulation (AON) pathway which is responsible for maintaining optimal root nodule number. In Lotus japonicus, AON comprises the CLE-HAR1-TML module, which plays an essential role in transmitting signals via root-to-shoot-to-root long-distance signaling. In addition to AON's principal role of negatively regulating nodule number, a recent study revealed another in the systemic control of rhizobial infection. Nitrate also negatively regulates the pleiotropic phases of legume-Rhizobium symbioses, including rhizobial infection and nodule number. Nitrate signaling has recently been shown to use AON components such as CLE-RS2 and HAR1 to control nodule number. Here we consider the role of a loss-of-function mutation in CLE-RS1, -RS2 and TML in rhizobial infection in relation to nitrate. Our results agree with previous findings and support the hypothesis that AON is required for the control of rhizobial infection but not for its nitrate-induced control. Furthermore, we confirm that the tml mutants exhibit nitrate sensitivity that differs from that of cle-rs2 and har1. Hence, while the nitrate-induced control mechanism of nodule number uses AON components, an unknown pathway specific to nitrate may exist downstream of HAR1, acting in parallel with the HAR1> TML pathway.