HAR1 mediates systemic regulation of symbiotic organ development

Abstract

Symbiotic root nodules are beneficial to leguminous host plants; however, excessive nodulation damages the host because it interferes with the distribution of nutrients in the plant. To keep a steady balance, the nodulation programme is regulated systemically in leguminous hosts. Leguminous mutants that have lost this ability display a hypernodulating phenotype. Through the use of reciprocal and self-grafting studies using Lotus japonicus hypernodulating mutants, har1 (also known as sym78), we show that the shoot genotype is responsible for the negative regulation of nodule development. A map-based cloning strategy revealed that HAR1 encodes a protein with a relative molecular mass of 108,000, which contains 21 leucine-rich repeats, a single transmembrane domain and serine/threonine kinase domains. The har1 mutant phenotype was rescued by transfection of the HAR1 gene. In a comparison of Arabidopsis receptor-like kinases, HAR1 showed the highest level of similarity with CLAVATA1 (CLV1). CLV1 negatively regulates formation of the shoot and floral meristems through cell-cell communication involving the CLV3 peptide. Identification of hypernodulation genes thus indicates that genes in leguminous plants bearing a close resemblance to CLV1 regulate nodule development systemically, by means of organ-organ communication.

Community shifts of soybean stem-associated bacteria responding to different nodulation phenotypes and N levels

“…Mutations in En 1314 and En 1282 soybeans were found in the NFR1 gene, which is known to be responsible for a LysM-type receptor kinase for Nod factor recognition (Radutoiu et al, 2003 Masaki Hayashi (National Institute of Agrobiological Sciences, Tsukuba, Japan), personal communication). A mutation in En 6500 was found in the GmNARK (NTS1) gene (Nishimura et al, 2002), which mediates systemic autoregulation of nodulation (Searle et al, 2003), and Sakukei 4 is a descendant with a hypernodulating phenotype that was derived from En 6500 (Matsunami et al, 2004).…”

Isolation of a novel root-determined hypernodulation mutantrdh1ofLotus japonicus

“…The position mapped for OL2168 was the same as that of har1 (Nishimura et al 2002a). OL2168 developed shorter taproots and a large number of lateral roots.…”

“…In the known mutants of hypernodulation, several peculiar non-symbiotic characteristics were found that differed from the wild-type plant. The har1 plant develops a greater number of lateral roots than the wild-type plant (Kawaguchi et al 2002;Nishimura et al 2002a), whereas the mutant clavier is a dwarf with delayed flowering and a different morphology of leaf veins (Oka-Kira et al 2005). The mutant astray exhibits characteristics that are associated with defects in light and gravity responses (Nishimura et al 2002b).…”

“…Three different hypernodulation mutants have been reported for L. japonicus. In Har1 and clavier mutants, hypernodulation was related to the shoot-derived signaling system (Krusell et al 2002;Nishimura et al 2002a; Oka-Kira and Kawaguchi 2006; Oka- Kira et al 2005). The mutant astray forms approximately twice as many nodules as the wild-type plant, and is reported to have a deficiency in nodule suppression through light signaling (Nishimura et al 2002b).…”

“…In peas, a root-regulated mutant, nod3, was found (Sagan and Duc 1996), while in the model legume Lotus japonicus and Medicago truncatula, similar hypernodulation mutants were isolated, and the generality of a shoot-derived signaling system has been confirmed (Kawaguchi et al 2002;Penmetsa and Cook 1997;Schauser et al 1998;Szczyglowski et al 1998;Wopereis et al 2000). The responsible genes har1 of L. japonicus and nark (nts1) of Glycine max have been determined by positional cloning, and encode receptor-like kinase containing leucinerich repeats (LRRs), a single transmembrane domain and a serine/threonine kinase domain (Krusell et al 2002;Nishimura et al 2002a;Searle et al 2003).…”