The Arabidopsis Homologs of Trithorax (ATX1) and Enhancer of Zeste (CLF) Establish ‘Bivalent Chromatin Marks’ at the Silent AGAMOUS Locus

Authors

Abdelaty Saleh, University of Nebraska-Lincoln
Ayed Al-Abdallat, University of Jordan
Ivan Ndamukong, University of Nebraska-Lincoln
Raul Alvarez-Venegas, Centro de Investigacion y de Estudios Avanzados-Unidad Irapuato
Zoya Avramova, University of Nebraska-LincolnFollow

Date of this Version

2007

Citation

Nucleic Acids Research 35:18 (2007), pp. 6290-6296.

doi: 10.1093/nar/gkm464

Comments

Copyright © 2007 Abdelaty Saleh, Ayed Al-Abdallat, Ivan Ndamukong, Raul Alvarez-Venegas, and Zoya Avramova.

See corrigendum in Additional Files.

Abstract

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.