Abstract: The combination of mutation-based genetics and functional genomics has allowed a detailed dissection of the nodulation-induction and autoregulation of nodulation (AON) pathways of soybean. Applicable to all legumes, nodulation is induced by Rhizobium/Bradyrhizobium-produced lipopolysaccharides (Nod factors), perceived by Nod factor receptors (NFR1/NFR5 dimers), leading to cortical and pericycle cell divisions. These induce the production of Clavata3-like (CLE) peptides, which travel in the xylem to the shoot, where they are perceived by a receptor complex including a leucine-rich repeat (LRR) receptor kinase, encoded by GmNARK, LjHAR1, MtSUNN and closely related receptors in other legumes like Phaseolus vulgaris (common bean), Pisum sativum (pea), and Glycine soja. The activated receptor complex negatively regulates by phosphorylation of the constitutive synthesis of miR2111 in the shoot. This is normally is translocated via the phloem to the entire plant body, initiating suppression of a root-expressed Kelch repeat-containing F-box protein "Too Much Love (TML)," which in turn suppresses the nodule initiation cascade. Nodulation is therefore permitted during a developmental window between the induction and progress of the nodulation/cell division/infection cascade during the first few days after inoculation and the functional "readiness" of the AON cascade, delayed by the root–shoot–root loop. Loss-of-function mutations in GmNARK and LjTML result in excessive nodulation (supernodulation/hypernodulation/supernummary nodulation) as well as localized tolerance to externally applied nitrate. Recent analyses have indicated an interaction of the AON with lateral root formation as well as with the autoregulation of mycorrhization (AOM). Further details of the parallel functions of key points in this regulatory loop remain to be elucidated.

Key words: autoregulation of nodulation, legumes, soybean, symbiotic nodulation