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Plant Cell Advance Online Publication
Published on February 28, 2007; 10.1105/tpc.106.049221


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Received November 28, 2006
Returned for revision January 19, 2007
Accepted February 6, 2007

The Absence of Histone H2B Monoubiquitination in the Arabidopsis hub1 (rdo4) Mutant Reveals a Role for Chromatin Remodeling in Seed Dormancy

Yongxiu Liu 1, Maarten Koornneef 2, and Wim J.J. Soppe 1*

1 Department of Plant Breeding and Genetics, Max Planck Institute for Plant Breeding Research, 50829 Cologne, Germany
2 Department of Plant Breeding and Genetics, Max Planck Institute for Plant Breeding Research, 50829 Cologne, Germany; Laboratory of Genetics, Wageningen University, 6703 BD Wageningen, The Netherlands

* To whom correspondence should be addressed. E-mail: soppe{at}mpiz-koeln.mpg.de.

Seed dormancy is defined as the failure of a viable seed to germinate under favorable conditions. Besides playing an adaptive role in nature by optimizing germination to the most suitable time, a tight control of dormancy is important in crop plants. Extensive genetic and physiological studies have identified the involvement of several factors, but the molecular mechanisms underlying this process are still largely unknown. We cloned the HISTONE MONOUBIQUITINATION1 (HUB1) gene, of which the mutant (previously identified as reduced dormancy4) has reduced seed dormancy and several pleiotropic phenotypes. HUB1 encodes a C3HC4 RING finger protein. The Arabidopsis thaliana genome contains one HUB1 homolog, which we named HUB2. The hub2 mutant also has reduced seed dormancy and is not redundant with hub1. Homologs of HUB1 and HUB2 in other species are required for histone H2B monoubiquitination. In agreement with this, the ubiquitinated form of histone H2B could not be detected in the hub1 and hub2 mutants. In yeast and human cells, histone H2B monoubiquitination is associated with actively transcribed genes. The hub1 mutant showed altered expression levels for several dormancy-related genes. We propose a role for chromatin remodeling in seed dormancy by H2B monoubiquitination through HUB1 and HUB2.




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