January 15-19, 2005
Town & Country Convention Center
San Diego, CA
Arief Indrasumunar1 , Peter M. Gresshoff1 , Artem E. Men2
The early stages of the Rhizobium-legume association involve a complex of signalling events. Recently, the Nod-factor receptor gene (LjNFR1) was cloned in Lotus japonicus. This gene consists of 12 exons and encodes a LysM-type serine/threonine receptor kinase. Nod49 (induced) and rj1 (naturally occurring) are allelic non-nodulation, root-controlled, recessive, Mendelian soybean mutants. Nod49 forms symbioses with mycorrhizal fungus, but fails to deform or curl root hairs and has no actual infections. Some cell divisions in the subepidermal cortex are seen. Inoculation with high Bradyrhizobium titres results in “occasional” nodulation. These are formed with proper infection threads. Two genomic sequences with high similarity (85%) to LjNFR1 (and 90% to each other) were isolated from soybean and called GmNFR1a and GmNFR1b. BAC fingerprinting revealed two genomic environments. DNA sequence comparisons between wild type (Bragg and Clark) and their mutant (nod49 and rj1) showed a mutation of GmNFR1b in both mutants. GmNFR1a has a 300 bp deletion in one of its introns, but otherwise seems to be able to form a normal protein (ESTs were detected). The leaky mutant phenotype and ability to be suppressed by high inoculum may suggest functional redundancy, in which the GmNFR1b protein is the high affinity Nod factor receptor needed for hair curling and infection, while GmNFR1a sufficies to recognize the signal for cortical cell proliferation. If this is correct, one suspects that infection is needed to increase the dose of the Nod factor for continued proliferation and nodule initiation. Complementation and expression studies are in progress.