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ABSTRACT

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.

Acknowledgments

We thank Makoto Hayashi for providing M. loti MAFF303099 expressing DsRED; Kazuko Ito for technical support. T.S. is supported by Grant-in-Aid for Scientific Research from the MEXT/JSPS (18H04773 and 19H03239), by JST ERATO (JPMJER1502), by the Cooperative Research Grant of the Plant Transgenic Design Initiative by Gene Research Center, University of Tsukuba.

Disclosure of Potential Conflicts of Interest

No potential conflicts of interest were disclosed.

Additional information

Funding

This work was supported by Grant-in-Aid for Scientific Research from the MEXT/JSPS (18H04773 and 19H03239), by JST ERATO (JPMJER1502), by the Cooperative Research Grant of the Plant Transgenic Design Initiative by Gene Research Center, University of Tsukuba..

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