SU(VAR)3-9 like histone methyltransferases control heterochromatic domains in eukaryotes. In Arabidopsis, 10 SUVH genes encode SU(VAR)3-9 homologues where SUVH1, SUVH2 and SUVH4 (KRYPTONITE) represent distinct subgroups of SUVH genes. Loss of SUVH1 and SUVH4 causes weak reduction of heterochromatic histone H3K9 dimethylation, whereas in SUVH2 null plants monoand dimethyl H3K9, mono-and dimethyl H3K27, and monomethyl H4K20, the histone methylation marks of Arabidopsis heterochromatin are significantly reduced. Like animal SU(VAR)3-9 proteins SUVH2 displays strong dosage-dependent effects. Loss of function suppresses, whereas overexpression enhances, gene silencing, causes ectopic heterochromatization and significant growth defects. Furthermore, modification of transgene silencing by SUVH2 is partially transmitted to the offspring plants. This epigenetic stability correlates with heritable changes in DNA methylation. Mutational dissection of SUVH2 indicates an implication of its N-terminus and YDG domain in directing DNA methylation to target sequences, a prerequisite for consecutive histone methylation. Gene silencing by SUVH2 depends on MET1 and DDM1, but not CMT3. In Arabidopsis, SUVH2 with its histone H3K9 and H4K20 methylation activity has a central role in heterochromatic gene silencing.

DNA repair associated with DNA replication is important for the conservation of genomic sequence information, whereas reconstitution of chromatin after replication sustains epigenetic information. We have isolated and characterized mutations in the BRU1 gene of Arabidopsis that suggest a novel link between these underlying maintenance mechanisms. Bru1 plants are highly sensitive to genotoxic stress and show stochastic release of transcriptional gene silencing. They also show increased intrachromosomal homologous recombination and constitutively activated expression of poly (ADP-ribose) polymerase-2 (AtPARP-2), the induction of which is associated with elevated DNA damage. Bru1 mutations affect the stability of heterochromatin organization but do not interfere with genome-wide DNA methylation. BRU1 encodes a novel nuclear protein with two predicted protein-protein interaction domains. The developmental abnormalities characteristic of bru1 mutant plants resemble those triggered by mutations in genes encoding subunits of chromatin assembly factor (CAF-1), the condensin complex, or MRE11. Comparison of bru1 with these mutants indicates cooperative roles in the replication and stabilization of chromatin structure, providing a novel link between chromatin replication, epigenetic inheritance, S-phase DNA damage checkpoints, and the regulation of meristem development. A dynamic chromatin structure contributes to the regulation of repair and transcription of DNA templates. Chromatin components involved in both processes have been described that imply shared molecular mechanisms modulating DNA accessibility for repair and transcription (Green and Almouzni 2002). The first molecular link between transcription and DNA repair was revealed during characterization of transcription factor IIH (TFIIH), which is required for initiation of RNA synthesis by RNA polymerase II and for efficient repair of DNA through nucleotide excision (Feaver et al. 1993;Schaeffer et al. 1993;Drapkin et al. 1994;Wang et al. 1994).Accessibility is determined by compaction of chromatin, which consists of loosely packaged, transcriptionally active euchromatin, and heterochromatin, which is condensed and transcriptionally silent and consists mainly of transposable elements and repetitive sequences. Chromatin states are inherited during DNA replication, providing a scaffold for epigenetic information that influences transcriptional gene regulation.Several chromatin components determining heritable features of chromatin also have an influence on epigenetic regulation of gene activity and efficiency of DNA repair or genome stability. For example, SIR proteins in yeast mediate formation of a compact chromatin structure similar to heterochromatin in multicellular eukaryotes (Gross 2001) and are required for transcriptional gene silencing (TGS) and for suppression of homologous recombination of rDNA repeats (Guarente 2000). They

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