Mutation of rescues the hypernodulation phenotype in , suggesting that a signaling pathway like CLV1/BAM in affects nodule number.

The unique evolutionary adaptation of legumes for nitrogen-fixing symbiosis leading to nodulation is tightly regulated by the host plant. The autoregulation of nodulation (AON) pathway negatively regulates the number of nodules formed in response to the carbon/nitrogen metabolic status of the shoot and root by long-distance signaling to and from the shoot and root. Central to AON signaling in the shoots of is SUNN, a leucine-rich repeat receptor-like kinase with high sequence similarity with CLAVATA1 (CLV1), part of a class of receptors in involved in regulating stem cell populations in the root and shoot. This class of receptors in includes the BARELY ANY MERISTEM family, which, like CLV1, binds to CLE peptides and interacts with CLV1 to regulate meristem development. contains five members of the family, but only and are highly expressed in the nodules 48 hours after inoculation. Plants carry mutations in individual s, and several double mutant combinations all displayed wild-type nodule number phenotypes. However, suppressed the hypernodulation phenotype and partially rescued the short root length phenotype of 5 when present in a background. Grafting determined that suppresses supernodulation from the roots, regardless of the status of the root. Overexpression of in wild-type plants increases nodule numbers, while overexpression of in some mutants rescues the hypernodulation phenotype, but not the hypernodulation phenotypes of AON mutant or . Relative expression measurements of the nodule transcription factor MtWOX5 downstream of the putative complex revealed disruption of meristem signaling; while both and influence expression, the expression changes are in different directions. We propose a genetic model wherein the specific root interactions of BAM2/SUNN are critical for signaling in nodule meristem cell homeostasis in .