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Brassinosteroid (BR) is a class of polyhydroxysteroids plant hormones known to regulate shoot and root growth. Genetic and molecular analyses demonstrate that receptor kinase BRI1 protein acts as a perceiver for BR. One of the characteristics of bri1 mutant’s phenotypes is the complete BR insensitivity in the root. Biochemical evidences of the BRI1 protein complex indicates that somatic embryogenesis receptor kinase 1 (SERK1) and SERK3 participate in the BR pathway in Arabidopsis root. While only serk3 mutants show partial reduction to BR sensitivity, serk1 presents a normal BR penetration phenotype compared to the wild type. Interestingly, the double mutant serk1serk3 displays more, but not full resistance to BR in root length assay. In this study, we aimed to enhance the BR insensitivity of the double mutant serk1serk3 by crossing serk1 mutant allele with a strong serk3 and bri1 mutant alleles. In our study, by generating serk1-3serk3-2 double mutants, a complete insensitivity to BR that phenocopied bri1-301 mutant was recorded. However, we were unable to increase BR resistance in the root of serk1-3serk3-2 double mutant by crossing with bri1 mutant allele in the triple mutant serk1-3serk3-2bri1. As a result, all the BRI1 signaling in the root was mediated through the SERK1 and SERK3 co-receptors. Additionally, we established that based on conventional BR assays, the At1g27190 protein was also involved in BR signaling. Preliminary data indicated that the triple mutant serk1serk3-2At1g27190 showed a dwarfed phenotype. Whether or not this dwarfed phenotype is linked to BRI1 signaling impairment needs to be further investigated.

BRI1 Signaling in the Root is Mediated through the SERK1 and SERK3 Co-receptors