ABSTRACT
A plasma membrane receptor protein kinase, FERONIA (FER), regulates various aspects of plant reproductive and vegetative growth. In roots, binding of a peptide ligand to FER causes rapid suppression of cell elongation whereas in ovules, FER is involved in gametophyte interactions. Here, we examined the effect of a mutation that eliminates kinase activity, on both ovule fertilization and root growth, using the same batch of seeds containing a kinase-dead mutation. The kinase-dead mutation of FER reduced the ability to complement fer-4 knockout phenotypes, compared with wild-type sequence in root, but not in ovules. Our results support a model in which cell type-specific regulatory mechanisms, such as different interacting partners and/or downstream signaling events, lead to cell type-specific functions of FER.
