Location: Plant Gene Expression Center Albany_CA
Title: The SAND domain protein ULTRAPETALA1 acts as a trithorax group factor to regulate cell fate in plants Authors
|Carles, Cristel -|
Submitted to: Genes and Development
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: October 14, 2009
Publication Date: December 1, 2009
Repository URL: http://genesdev.cshlp.org/content/23/23/2723.full.pdf+html
Citation: Carles, C.C., Fletcher, J.C. 2009. The SAND domain protein ULTRAPETALA1 acts as a trithorax group factor to regulate cell fate in plants. Genes and Development. 23(23)2723-2728. Interpretive Summary: This article reports the molecular function of the ULTRAPETALA1 (ULT1) gene that is required to regulate stem cell activity during Arabidopsis flower development. We show that ULT1 has opposite effects on plant growth and gene expression as a gene called CURLY LEAF (CLF), which has been shown to maintain key flower genes in a repressed state during vegetative growth. We demonstrate that in flower stem cells ULT1 antagonizes the activity of CLF and activates the expression of the flower regulatory gene AGAMOUS (AG) by changing its chromatin into a more open configuration. Our findings identify a novel mechanism that operates to turn genes from an “off” state to an “on” state in flower stem cells at the appropriate time during plant development.
Technical Abstract: During development, trithorax group (trxG) chromatin remodeling complexes counteract repression by Polycomb group (PcG) complexes to sustain active expression of key regulatory genes. Although PcG complexes are well characterized in plants, little is known about trxG activities. Here we demonstrate that the Arabidopsis SAND (Sp100, AIRE-1, NucP41/75, DEAF-1) domain protein ULTRAPETALA1 (ULT1) functions as a trxG factor that counteracts the PcG-repressive activity of CURLY LEAF. In floral stem cells, ULT1 protein associates directly with the master homeotic locus AGAMOUS, inducing its expression by regulating its histone methylation status. Our analysis introduces a novel mechanism that mediates epigenetic switches controlling post-embryonic stem cell fates in plants.