SUVR2 is involved in transcriptional gene silencing by associating with SNF2-related chromatin-remodeling proteins in Arabidopsis.

Yong-Feng Han,Tao Cai,Huan-Wei Huang,Su-Wei Zhang,She Chen,Kun Dou,Lin Li,Jian-Kang Zhu,Xin-Jian He,Ze-Yang Ma

doi:10.1038/cr.2014.156

Abstract

The SU(VAR)3-9-like histone methyltransferases usually catalyze repressive histone H3K9 methylation and are involved in transcriptional gene silencing in eukaryotic organisms. We identified a putative SU(VAR)3-9-like histone methyltransferase SUVR2 by a forward genetic screen and demonstrated that it is involved in transcriptional gene silencing at genomic loci targeted by RNA-directed DNA methylation (RdDM). We found that SUVR2 has no histone methyltransferase activity and the conserved catalytic sites of SUVR2 are dispensable for the function of SUVR2 in transcriptional silencing. SUVR2 forms a complex with its close homolog SUVR1 and associate with three previously uncharacterized SNF2-related chromatin-remodeling proteins CHR19, CHR27, and CHR28. SUVR2 was previously thought to be a component in the RdDM pathway. We demonstrated that SUVR2 contributes to transcriptional gene silencing not only at a subset of RdDM target loci but also at many RdDM-independent target loci. Our study suggests that the involvement of SUVR2 in transcriptional gene silencing is related to nucleosome positioning mediated by its associated chromatin-remodeling proteins.

Highlights

DNA methylation, histone H3K9 methylation and other repressive histone marks are involved in transcriptional silencing of transposable elements (TEs) and other DNA repeats [1,2,3]
SUVR1, SUVR2, and SUVR5 have no histone methyltransferase activity as determined by in vitro assays (Figure 5G) [28, 30], even though SUVR5 is involved in histone H3K9 methylation in vivo [28, 30]
Previous structural and biochemical studies suggest that some conserved residues in the SET domains of the SU(VAR)3-9 homologs are directly responsible for the binding of the substrate histone H3 and the methyl group donor SAM [20, 64]

Summary

Introduction

DNA methylation, histone H3K9 methylation and other repressive histone marks are involved in transcriptional silencing of transposable elements (TEs) and other DNA repeats [1,2,3]. Two atypical DNA-dependent RNA polymerases IV and V (Pol IV and Pol V) are responsible for producing 24-nt small interfering RNAs (siRNAs) and long noncoding RNAs, respectively, in the RdDM pathway [6]. The double-stranded RNAs are cleaved by Dicer Like 3 (DCL3) into 24-nt siRNAs, which are loaded onto AGO4 (Argonaute 4) in the cytoplasm and subsequently transported into the nucleus for the assembly of RdDM effector complex [7,8,9,10]. Pol V generates long noncoding scaffold RNAs to recruit the RdDM effector complex [11, 12]. DRM2 is recruited to RdDM target loci by associating with the AGO4-siRNA complex and mediates de novo DNA methylation [17]

Methods

Results

Conclusion