Session 9: Light-Regulated Development
Chair: Joanne Chory, Salk Institute, La Jolla, USA
email:joanne_chory@qm.salk.edu
New receptors and circadian cycling dominated the talks in the session on light-regulated development. The cloning of two new putative receptors was announced. Joanne Chory (Salk Institute) spoke about the cloning of the BRI1 gene, which encodes a putative leucine-rich repeat receptor kinase involved in brassinosteroid signal transduction. While direct binding of brassinosteroids to this putative receptor has not been shown yet, the cloning of the receptor opens the way for studying the complex interactions between light and hormone signalling which were also touched upon during this talk.Eva Huala (The Carnegie Institute) described the cloning of the putative receptor for phototropism encoded by the NPH1 gene. This gene encodes a protein that is predicted to be a serine/threonine protein kinase which also contains a putative redox-sensing regulatory domain. Protein kinase activity for the phototropism photoreceptor was predicted earlier from biochemical experiments, and, as such, the identification of the NPH1 gene as a protein kinase is satisfying. The NPH1 gene represents another new class of regulatory photoreceptor used by higher plants.
Steve Kay (Scripps Institute) gave an overview of the interactions between phototransduction pathways and the circadian clock in controlling plant growth and development. Studies from his lab using cab-luciferase transgenic lines crossed into various photoreceptor mutant backgrounds underscored the importance of studying complex signalling networks in real time. Kay showed elegantly the precise contribution of individual photoreceptors and signalling components to light and clock-regulated responses in Arabidopsis. Kay's talk nicely set the stage for two talks identifying a new class of myb-type transcription factors that play a role in light- and clock-regulated gene expression. George Coupland (John Innes Centre) reported on the identification and cloning of one of these genes, LHY. Overexpression of LHY causes late-flowering, a long hypocotyl, and leaf movements and circadian regulated gene expression to become arrhythmic. Likewise, Zhi-Yong Wang (UCLA) reported new studies on the Arabidopsis CCA1 gene. CCA1 was identified as an activator of CAB gene transcription in response to phytochrome action. As with LHY, overexpression of CCA1 causes increased hypocotyl length and substantially delayed flowering, and CAB gene expression and leaf movements to become arrhythmic. Thus, this new class of transcription factors, currently represented by CCA1 and LHY, may prove to be key regulators in the phototransduction and circadian clock transduction pathways.
The session was closed by Keiko Torii (Yale) who discussed the functional dissection of the COP1 protein which has been proposed to be a negative regulator in the light signalling pathways. Her studies showed that the 3 predicted domains of COP1-a ring finger, WD40 repeats, and a coiled-coil domain-were all essential for COP1 activity. Future biochemical studies with COP1 should help to elucidate the mechanism by which it represses photomorphogenetic development.