A matrix protein silences transposons and repeats through interaction with retinoblastoma-associated proteins

Epigenetic regulation helps to maintain genomic integrity by suppressing transposable elements (TEs) and also controls key developmental processes, such as flowering time [1-3]. To prevent TEs from causing rearrangements and mutations, TE and TE-like repetitive DNA sequences are usually methylated, whereas histones are hypoacetylated and methylated on specific residues (e.g., H3 lysine 9 dimethylation [H3K9me2]) [4, 5]. TEs and repeats can also attenuate gene expression [2, 6-8]. However, how various histone modifiers are recruited to target loci is not well understood. Here we show that knockdown of the nuclear matrix protein with AT-hook DNA binding motifs [9-11] TRANSPOSABLE ELEMENT SILENCING VIA AT-HOOK (TEK) in Arabidopsis Landsberg erecta results in robust activation of various TEs, the TE-like repeat-containing floral repressor genes FLOWERING LOCUS C (FLC) and FWA [1, 2, 12]. This derepression is associated with chromatin conformational changes, increased histone acetylation, reduced H3K9me2, and even TE transposition. TEK directly binds to an FLC-repressive regulatory region and the silencing repeats of FWA and associates with Arabidopsis homologs of the Retinoblastoma-associated protein 46/48, FVE and MSI5, which mediate histone deacetylation [13, 14]. We propose that the nuclear matrix protein TEK acts in the maintenance of genome integrity by silencing TE and repeat-containing genes.