Nod Factor/Nitrate-Induced CLE Genes that Drive HAR1-Mediated Systemic Regulation of Nodulation
Nod Factor/Nitrate-Induced CLE Genes that Drive HAR1-Mediated Systemic Regulation of Nodulation
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DOI：
10.1093/pcp/pcn194
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发表时间：
2009-01-01
影响因子：
4.9
通讯作者：
Kawaguchi, Masayoshi
中科院分区：
文献类型：
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作者：
Okamoto, Satoru;Ohnishi, Erika;Kawaguchi, Masayoshi
寄主豆科植物通过感知外部和内部信号来控制根瘤数量。一个主要的外部线索是土壤硝酸盐，而反馈调节系统，早期形成的结核抑制进一步通过主根通信是一个重要的内部线索。后者被称为植物生长的自动调节（autoregulation of prophylation，AUT），被认为是由两个长距离信号组成：一个是在受感染的根中产生并传递到芽的根源信号;一个是系统性抑制植物生长的芽源信号。在百脉根中，富含亮氨酸的重复序列受体样激酶，即超结性异常根形成1（HAR 1），介导AUT和硝酸盐对结瘤的抑制，并被假设识别根源性信号。在这里，我们确定L。RjCLE-Root信号1（LjCLE-RS 1）和LjCLE-RS 2作为根源信号的强候选。毛状根转化研究表明，过表达LjCLE-RS 1和-RS 2抑制系统性的生长，而且，系统性抑制依赖于HAR 1。此外，LjCLE-RS 2的表达强烈上调根硝酸盐添加。基于这些发现，我们提出了一个简单的模型，AUT和硝酸盐抑制由LjCLE-RS 1，-RS 2肽和HAR 1受体样激酶介导的凝血。
Host legumes control root nodule numbers by sensing external and internal cues. A major external cue is soil nitrate, whereas a feedback regulatory system in which earlier formed nodules suppress further nodulation through shootroot communication is an important internal cue. The latter is known as autoregulation of nodulation (AUT), and is believed to consist of two long-distance signals: a root-derived signal that is generated in infected roots and transmitted to the shoot; and a shoot-derived signal that systemically inhibits nodulation. In Lotus japonicus, the leucine-rich repeat receptor-like kinase, HYPERNODULATION ABERRANT ROOT FORMATION 1 (HAR1), mediates AUT and nitrate inhibition of nodulation, and is hypothesized to recognize the root-derived signal. Here we identify L. japonicus CLE-Root Signal 1 (LjCLE-RS1) and LjCLE-RS2 as strong candidates for the root-derived signal. A hairy root transformation study shows that overexpressing LjCLE-RS1 and -RS2 inhibits nodulation systemically and, furthermore, that the systemic suppression depends on HAR1. Moreover, LjCLE-RS2 expression is strongly up-regulated in roots by nitrate addition. Based on these findings, we propose a simple model for AUT and nitrate inhibition of nodulation mediated by LjCLE-RS1, -RS2 peptides and the HAR1 receptor-like kinase.