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Nucleic Acids Research Advance Access published online on September 18, 2007
Nucleic Acids Research, doi:10.1093/nar/gkm464
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© 2007 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Molecular Biology

The Arabidopsis homologs of trithorax (ATX1) and enhancer of zeste (CLF) establish ‘bivalent chromatin marks’ at the silent AGAMOUS locus

Abdelaty Saleh1, Ayed Al-Abdallat1,2, Ivan Ndamukong1, Raul Alvarez-Venegas1,3 and Zoya Avramova1,*

1School of Biological Sciences, UNL, Lincoln, NE 68588, USA, 2Faculty of Agriculture, University of Jordan, Amman 11942, Jordan and 3Department of Genetic Engineering, Centro de Investigacion y de Estudios Avanzados-Unidad Irapuato, México

*To whom Correspondence should be addressed. Tel: +402 472 3993; Fax: +402 472 2083; Email: zavramova2{at}unl.edu

Received April 17, 2007. Revised May 11, 2007. Accepted May 25, 2007.

Tightly balanced antagonism between the Polycomb group (PcG) and the Trithorax group (TrxG) complexes maintain Hox expression patterns in Drosophila and murine model systems. Factors belonging to the PcG/TrxG complexes control various processes in plants as well but whether they participate in mechanisms that antagonize, balance or maintain each other's effects at a particular gene locus is unknown. CURLY LEAF (CLF), an Arabidopsis homolog of enhancer of zeste (EZ) and the ARABIDOPSIS HOMOLOG OF TRITHORAX (ATX1) control the expression of the flower homeotic gene AGAMOUS (AG). Disrupted ATX1 or CLF function results in misexpression of AG, recognizable phenotypes and loss of H3K4me3 or H3K27me3 histone H3-tail marks, respectively. A novel idea suggested by our results here, is that PcG and TrxG complexes function as a specific pair generating bivalent chromatin marks at the silent AG locus. Simultaneous loss of ATX1 and CLF restored AG repression and normalized leaf phenotypes. At the molecular level, disrupted ATX1 and CLF functions did not lead to erasure of the CLF- and ATX1-generated epigenetic marks, as expected: instead, in the double mutants, H3K27me3 and H3K4me3 tags were partially restored. We demonstrate that ATX1 and CLF physically interact linking mechanistically the observed effects.


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