title: Genetic suppressors of the Lotus japonicus har1-1 hypernodulation phenotype.
abstract: Lotus japonicus har1 mutants respond to inoculation with Mesorhizobium loti by forming an excessive number of nodules due to genetic lesions in the HAR1 autoregulatory receptor kinase gene. In order to expand the repertoire of mutants available for the genetic dissection of the root nodule symbiosis (RNS), a screen for suppressors of the L. japonicus har1-1 hypernodulation phenotype was performed. Of 150,000 M2 plants analyzed, 61 stable L. japonicus double-mutant lines were isolated. In the context of the har1-1 mutation, 26 mutant lines were unable to form RNS, whereas the remaining 35 mutant lines carried more subtle symbiotic phenotypes, either forming white ineffective nodules or showing reduced nodulation capacity. When challenged with Glomus intraradices, 18 of the 61 suppressor lines were unable to establish a symbiosis with this arbuscular mycorrhiza fungus. Using a combined approach of genetic mapping, targeting induced local lesions in genomics, and sequencing, all non-nodulating mutant lines were characterized and shown to represent new alleles of at least nine independent symbiotic loci. The class of mutants with reduced nodulation capacity was of particular interest because some of them may specify novel plant functions that regulate nodule development in L. japonicus. To facilitate mapping of the latter class of mutants, an introgression line, in which the har1-1 allele was introduced into a polymorphic background of L. japonicus ecotype MG20, was constructed.
authors.affiliation: Agriculture and Agri-Food Canada, Southern Crop Protection and Food Research Centre, 1391 Sandford Street, London, Ontario N5V 4T3, Canada.
authors.forename: Jeremy
authors.initials: J
authors.lastname: Murray
authors.forename: Bogumil
authors.initials: B
authors.lastname: Karas
authors.forename: Loretta
authors.initials: L
authors.lastname: Ross
authors.forename: Andreas
authors.initials: A
authors.lastname: Brachmann
authors.forename: Cameron
authors.initials: C
authors.lastname: Wagg
authors.forename: Ryan
authors.initials: R
authors.lastname: Geil
authors.forename: Jillian
authors.initials: J
authors.lastname: Perry
authors.forename: Katarzyna
authors.initials: K
authors.lastname: Nowakowski
authors.forename: Mandy
authors.initials: M
authors.lastname: MacGillivary
authors.forename: Mark
authors.initials: M
authors.lastname: Held
authors.forename: Jens
authors.initials: J
authors.lastname: Stougaard
authors.forename: Larry
authors.initials: L
authors.lastname: Peterson
authors.forename: Martin
authors.initials: M
authors.lastname: Parniske
authors.forename: Krzysztof
authors.initials: K
authors.lastname: Szczyglowski
mesh_terms: D000483:Alleles; D020561:Alphaproteobacteria / Q000502:physiology; D002874:Chromosome Mapping; D005819:Genetic Markers; D000070116:Lotus / Q000033:anatomy & histology / Q000235:genetics* / Q000382:microbiology; D018895:Microsatellite Repeats; D009154:Mutation; D038821:Mycorrhizae / Q000502:physiology; D010641:Phenotype; D010770:Phosphotransferases / Q000235:genetics* / Q000502:physiology; D010940:Plant Proteins / Q000235:genetics* / Q000502:physiology; D018517:Plant Roots / Q000033:anatomy & histology / Q000235:genetics / Q000382:microbiology; D017422:Sequence Analysis, DNA; D013489:Suppression, Genetic; D013559:Symbiosis / Q000235:genetics
chemical_list: D005819:Genetic Markers; D010940:Plant Proteins; D010770:Phosphotransferases