Abstract
GLYCOGEN SYNTHASE KINASE3 (GSK3) is a highly conserved serine/threonine kinase involved in a variety of developmental signaling processes. The Arabidopsis (Arabidopsis thaliana) genome encodes 10 GSK3-like kinases that are clustered into four groups. Forward genetic screens have so far uncovered eight mutants, all of which carry gain-of-function mutations in BRASSINOSTEROID-INSENSITIVE2 (BIN2), one of the three members in group II. Genetic and biochemical studies have implicated a negative regulatory role for BIN2 in brassinosteroid (BR) signaling. Here, we report the identification of eight ethyl methanesulfonate-mutagenized loss-of-function bin2 alleles and one T-DNA insertional mutation each for BIN2 and its two closest homologs, BIN2-Like1 and BIN2-Like2. Our genetic, biochemical, and physiological assays revealed that despite functional redundancy, BIN2 plays a dominant role among the three group II members in regulating BR signaling. Surprisingly, the bin2bil1bil2 triple T-DNA insertional mutant still responds to BR and accumulates a more phosphorylated form of a BIN2 substrate than the wild-type plant. Using the specific GSK3 inhibitor lithium chloride, we have provided strong circumstantial evidence for the involvement of other Arabidopsis GSK3-like kinases in BR signaling. Interestingly, lithium chloride treatment was able to suppress the gain-of-function bin2-1 mutation but had a much weaker effect on a strong BR receptor mutant, suggesting the presence of a BIN2-independent regulatory step downstream of BR receptor activation.
Highlights
GLYCOGEN SYNTHASE KINASE3 (GSK3) is a highly conserved serine/threonine kinase involved in a variety of developmental signaling processes
It remains unknown why no single gain-of-function mutation in the two BIN2 homologs was discovered in the forward genetic screens and if other Arabidopsis GSK3-like kinases might participate in BR signaling
Unlike BRI1, which was discovered through recessive loss-of-function mutants, all of the bin2 mutants uncovered from forward genetic screens carry semidominant gain-of-function alleles (Peng and Li, 2003)
Summary
GLYCOGEN SYNTHASE KINASE3 (GSK3) is a highly conserved serine/threonine kinase involved in a variety of developmental signaling processes. GSK3 Kinase in Brassinosteroid Signaling and Chory, 2006), as well as dimerization and transphosphorylation with BAK1, a suspected BRI1 coreceptor (Li et al, 2002; Nam and Li, 2002; Russinova et al, 2004; Wang et al, 2005, 2008) These membrane events lead to BIN2 inhibition, via protein degradation (Peng et al, 2008) and/or some yet to be discovered biochemical mechanisms, relieving its inhibitory effects on BES1 and BZR1 that regulate the expression of BR-responsive genes (Li and Jin, 2007). A recent study using T-DNA insertional mutants of BIN2 and its two closest homologs concluded that the three group II AtSKs function redundantly in BR signaling (Vert and Chory, 2006) It remains unknown why no single gain-of-function mutation in the two BIN2 homologs was discovered in the forward genetic screens and if other Arabidopsis GSK3-like kinases might participate in BR signaling
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
