January 15-19, 2005
Town & Country Convention Center
San Diego, CA
Lucinda Smith2 , Elise Schnabel1 , Arijit Mukherjee1 , Sharon Long2 , Julia Frugoli1
With the development of legume model systems such as L. japonicus and M. truncatula, a molecular understanding of nodulation is emerging. Non-nodulating mutants appear to affect rhizobial recognition and response steps of the symbiosis, while supernodulation mutants affect genes controlling the extent of symbiotic development. We present three independent supernodulation mutants of Medicago truncatula, two of which (sn-1 and sunn) demonstrate intergenic non-complementation. The phenotype of sn-1 is almost indistinguishable from the phenotype of sunn, a previously characterized supernodulator resulting from a mutation in a LRR-receptor kinase. Crossing sn-1 with sunn demonstrated that the two mutations do not complement each other in the F1. However several lines of evidence indicate that sn-1 is a separate gene from sunn. Sequencing of the SUNN gene in sn-1 plants revealed no lesion in SUNN, its promoter sequence or 150 bases past the poly A site. The expression of the SUNN gene product as determined by Real Time RT-PCR is normal in sn-1 plants. Finally, wild type plants segregate in the F2 of the sunn/sn-1 cross. Shoot grafting experiments show that supernodulation in sn-1 and sunn is a shoot-controlled phenotype. A third recently isolated supernodulation mutant is distinct from sunn and sn-1, in that it complements the sunn mutation in the F1 and demonstrates root control of nodule number in grafting experiments. These three mutants will allow us to begin to construct a genetic pathway governing the control of nodule number.