Poster: Photomorphogenesis

Abs # 512: Activation-tagged suppressors of phyB-4: From transcription factors to brassinosteroid modulators.

Presenter:	Neff, Michael M, mneff@biology2.wustl.edu
Authors	Neff, Michael M (A)   Denzel, M  (A)   Fujioka, S  (B)   Seto, H  (B)   Shimada, Y  (B)   Stoll, E  (A)   Street, I  (A)   Takatsuto, S  (C)   Turk, E  (A)   Ward, J  (A)   Yoshida, S  (B)   Zhang, J.-Y.  (A)
Affiliations:	(A): Department of Biology, Washington University, Campus Box 1137, One Brookings Drive, St. Louis, MO 63130, USA (B): RIKEN (The Institute of Physical and Chemical Research), Wako-shi, Saitama 351-0198, Japan (C): Department of Chemistry, Joetsu University of Education, Joetsu-shi, Niigata 943-8512, Japan
Web Site:	http://dbbs.wustl.edu/RIB.Neff.html

Activation tagging, a gene-overexpression mutagenesis tool, has been used to identify extragenic suppressors of the long-hypocotyl phenotype conferred by the photoreceptor mutant phyB-4. This mutant screen allows us to cast a broad net in search of novel photomorphogenic signaling genes. Five of these sob-D mutants (suppressor of phyB- dominant) have been identified and cloned to date. The sob1-D mutant phenotype is caused by the over-expression of a nuclear-localized Dof transcription factor. sob1-RNAi transgenic plants demonstrate that this gene is involved in photomorphogenesis. The sob2-D, sob3-D/shq1-D, and sob5-D phenotypes are caused by the over-expression of predicted nuclear-localized and/or DNA interacting proteins. Analysis of null mutations or RNAi transgenic lines for each of these genes and potential redundant homologues addresses their role in photomorphogenesis. Further analysis includes: 1) examining changes in transcript accumulation in response to light; 2) exploring genetic and physical interactions with the phytochromes and cryptochromes; and 3) examining protein localization/accumulation in response to light via translational fusions with GUS and GFP reporters. The growth-promoting plant-steroid hormones, brassinosteroids, have been implicated in photomorphogenesis based on the characterization of a previously identified phyB activation-tagged suppressor, bas1-D (Neff et al. 1999 PNAS 96 15316). The bas1-D mutant phenotype is caused by the overexpression of a cytochrome P450, CYP72B1. Genetic and biochemical analysis demonstrates that CYP72B1 is a brassinosteroid-inactivating enzyme that regulates active brassinolide levels as a modulator of photomorphogenesis.