RNA molecules such as small-interfering RNAs (siRNAs) and antisense RNAs 
(asRNAs) trigger chromatin silencing of target loci. In the model plant 
Arabidopsis, RNA-triggered chromatin silencing involves repressive histone 
modifications such as histone deacetylation, histone H3 lysine-9 methylation, 
and H3 lysine-27 monomethylation. Here, we report that two Arabidopsis homologs 
of the human histone-binding proteins Retinoblastoma-Associated Protein 46/48 
(RbAp46/48), known as MSI4 (or FVE) and MSI5, function in partial redundancy in 
chromatin silencing of various loci targeted by siRNAs or asRNAs. We show that 
MSI5 acts in partial redundancy with FVE to silence FLOWERING LOCUS C (FLC), 
which is a crucial floral repressor subject to asRNA-mediated silencing, FLC 
homologs, and other loci including transposable and repetitive elements which 
are targets of siRNA-directed DNA Methylation (RdDM). Both FVE and MSI5 
associate with HISTONE DEACETYLASE 6 (HDA6) to form complexes and directly 
interact with the target loci, leading to histone deacetylation and 
transcriptional silencing. In addition, these two genes function in de novo CHH 
(H = A, T, or C) methylation and maintenance of symmetric cytosine methylation 
(mainly CHG methylation) at endogenous RdDM target loci, and they are also 
required for establishment of cytosine methylation in the previously 
unmethylated sequences directed by the RdDM pathway. This reveals an important 
functional divergence of the plant RbAp46/48 relatives from animal counterparts.