DMI3 (mutated the autophosphorylated threonine 271 to alanine)
Symbiotic Phenotype Brief
Nod+
Phenotype Detail
DMI3 T271A activated ENOD11-GUS in the absence of Nod factor indicating gain-of-function activities. Unlike the deletion constructs, DMI3 T271A was able to complement dmi3-1 and formed bacterial infected nodules, indicating that the gain-of-function mutant was also fully functional proteins. Authors predicted that DMI3 T271A and DMI3 T271D would also lead to spontaneous nodulation if expressed from the native promoter.
Single gene targeted?
yes
Extra Information
The construct is driven by the 35S promoter.
Mutagenesis Method
Site-directed Mutagenesis
Mutant Class
Nod+Fix+
Allelism
The earliest development stage known to be affected
N/A
Wildtype Line
Jemalong J5
References:
Authors
Year
Title
Locator
Gleason C, Chaudhuri S, Yang T, Munoz A, Poovaiah BW and Oldroyd GE
2006
Nodulation independent of rhizobia induced by a calcium-activated kinase lacking autoinhibition
