| The cell wall is essential for plants. In an elongating cell, the cellulose microfibrils are wrapped transversely around the cell, thus allowing longitudinal expansion but restricting lateral expansion. The signaling pathways that regulate cell wall biosynthesis in response to developmental and environmental cues are still poorly understood. I describe the cloning and characterization of two Arabidopsis thaliana LRR receptor-like kinases, FEI1 and FEI2, that act as positive regulators of cell wall biosynthesis. Mutations in FEI1 and FEI2 disrupt anisotropic expansion and the synthesis of cell wall polymers, and act additively with inhibitors or mutations disrupting cellulose biosynthesis. In addition, I demonstrate that FEI1 is an active protein kinase however, a kinase-inactive version of FEI1 was able to fully complement the fei1 fei2 mutant, suggesting intrinsic kinase activity is not required for FEI function in roots. The expansion defect in fei1 fei2 roots was suppressed by inhibition of ACC synthase, an enzyme that converts Ado-Met to ACC in ethylene biosynthesis, but not by disruption of the ethylene response pathway. Furthermore, the FEI proteins interact directly with ACC synthase. These results suggest that the FEI proteins define a novel signaling pathway that regulates cell wall function, likely via an ACC-mediated signal. To further our understanding of the FEI pathway in mediating cell wall biosynthesis, a suppressor screen was carried out and nine suppressors (shou1-shou8) which represent mutation in eight different genes or complementation groups have been identified. Two suppressors have been further studied. shou1 was mapped to bottom arm of chromosome 5 and found to encode a pentatricopeptide repeat protein. In addition, two alleles of shou2 have been identified and mapped to a 47kb region on the upper arm of chromosome 1. Paradoxically, shou2 also inhibits root hair elongation. These studies have uncovered a novel signaling pathway regulating cell wall biosynthesis. |
