ABSTRACT
Recently, we have identified circadian clock genes as targets of Histone Monoubiquitination1 (HUB1) in Arabidopsis from a transcriptome comparison between the hub1-1 mutant and HUB1 overexpression lines. HUB1 affected the amplitudes of the circadian clock gene expression profiles in the hub1-1 mutant that coincided with reduced monoubiquitination of histone H2B at their coding regions. Here we showed that parameters for plant fitness are altered in HUB1 mutant and overexpression lines, suggesting that the histone H2B monoubiquitination status affects plant fitness.
Subject(s)
Arabidopsis Proteins/metabolism , Arabidopsis/metabolism , Arabidopsis/physiology , Ubiquitin-Protein Ligases/metabolism , Arabidopsis/genetics , Arabidopsis Proteins/genetics , Chloroplasts/metabolism , Chloroplasts/physiology , Gene Expression Regulation, Plant , Plants, Genetically Modified/genetics , Plants, Genetically Modified/metabolism , Plants, Genetically Modified/physiology , Ubiquitin-Protein Ligases/genetics , UbiquitinationABSTRACT
Chromatin modification and transcriptional activation are novel roles for E3 ubiquitin ligase proteins that have been mainly associated with ubiquitin-dependent proteolysis. We identified HISTONE MONOUBIQUITINATION1 (HUB1) (and its homolog HUB2) in Arabidopsis thaliana as RING E3 ligase proteins with a function in organ growth. We show that HUB1 is a functional homolog of the human and yeast BRE1 proteins because it monoubiquitinated histone H2B in an in vitro assay. Hub knockdown mutants had pale leaf coloration, modified leaf shape, reduced rosette biomass, and inhibited primary root growth. One of the alleles had been designated previously as ang4-1. Kinematic analysis of leaf and root growth together with flow cytometry revealed defects in cell cycle activities. The hub1-1 (ang4-1) mutation increased cell cycle duration in young leaves and caused an early entry into the endocycles. Transcript profiling of shoot apical tissues of hub1-1 (ang4-1) indicated that key regulators of the G2-to-M transition were misexpressed. Based on the mutant characterization, we postulate that HUB1 mediates gene activation and cell cycle regulation probably through chromatin modifications.