A genetic screen for plant mutants with altered nodulation phenotypes in response to rhizobial glycan mutants.

摘要: Nodule primordia induced by rhizobial glycan mutants often remain uninfected. To identify processes involved in infection and organogenesis we used forward genetics to plant genes perception responses bacterial glycans. dissect the mechanisms underlying negative Mesorhizobium loti R7AexoU ML001cep mutants, a screen for genetic suppressors of nodulation phenotypes was performed on chemically mutagenized Lotus population. Two mutant lines formed infected nitrogen-fixing pink nodules, while five developed uninfected large white presumably altered controlling organogenesis. Genetic mapping identified mutation cytokinin receptor Lhk1 resulting an alanine valine substitution adjacent coiled-coil motif juxta-membrane region LHK1. This results spontaneous phenotype increased ethylene production. The allele renamed snf5, segregation studies snf5 together with complementation suggest that is gain-of-function allele. approach investigate role glycans pathway synchronizing shows combination opens new possibilities study plants as well identification alleles affecting nodule