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Published on December 8, 2006; 10.1104/pp.106.092320


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Received October 30, 2006
Accepted November 23, 2006

Repression of the LEC1-B3 Regulatory Network in Plant Embryo Development by the VAL B3 Genes

Masaharu Suzuki *, Heidi H.-Y. Wang , and Donald R. McCarty

Plant Molecular and Cellular Biology Program, Horticultural Sciences Department, University of Florida, Gainesville, FL 32611

* Corresponding author; email: masaharu{at} ufl.edu.

Plant embryo development is regulated by a network of transcription factors that include LEAFY COTYLEDON 1 (LEC1), LEC1-LIKE (L1L); and B3 domain factors, LEAFY COTYLEDON 2 (LEC2), FUSCA3 (FUS3), and ABSCISIC ACID INSENSITIVE 3 (ABI3) of Arabidopsis thaliana. Interactions of these genes result in a temporal progression of over-lapping B3 gene expression culminating in maturation and desiccation of the seed. Three VP1/ABI3-LIKE (VAL) genes encode B3 proteins that include PHD-like and CW domains associated with chromatin factors. Whereas, the val monogenic mutants have phenotypes similar to wild type, val1 val2 double mutant seedlings form no leaves and develop embryo-like proliferations in root and apical meristem regions. In a val1 background val2 and val3 condition a dominant variegated leaf phenotype revealing a VAL function in vegetative development. Reminiscent of pickle (pkl) mutant, inhibition of gibberellin biosynthesis during germination induces embryonic phenotypes in val1 seedlings. Consistent with the embryonic seedling phenotype, LEC1, L1L, ABI3 and FUS3 are up-regulated in val1 val2 seedlings in association with a global shift in gene expression to a profile resembling late torpedo stage embryogenesis. Hence, the VAL factors function as global repressors of the LEC1-B3 gene system. The consensus binding site of the ABI3/FUS3/LEC2 B3 DNA binding domain (Sph/RY) is strongly enriched in the promoters and first introns of VAL repressed genes including the early-acting LEC1 and L1L genes. We suggest that VAL targets Sph/RY containing genes in the network for chromatin mediated repression in conjunction with the PKL-related CHD3 chromatin remodeling factors.




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