| Description: | A widely accepted hypothesis is that methylation of cytosines recruits histone deacetylases which, in turn, deacetylate local histones to repress genes. The hypothesis is supported by biochemical data which show that methyl binding proteins associate with histone deacetylases in large multi-protein complexes. The hypothesis is also supported by our studies of nucleolar dominance in hybrid plants showing that repressed ribosomal RNA genes can be derepressed by either aza-deoxycytosine (aza-dC; an inhibitor of cytosine methylation) or by trichostatin A (TSA; an inhibitor of histone deacetylation). In nucleolar dominance, there is no additive or synergistic affect when both aza-dC and TSA are used, implying that cytosine methylation and histone deacetylation are partners in the same gene silencing pathway. However, other evidence in our laboratory suggests that this is not true for all genes. Specifically, studies of silenced transgenes have shown that many respond to blocking cytosine methylation with aza-dC but do not respond in similar fashion when histone deacetylation is blocked with TSA. These data suggest that only a subset of genes are regulated in a manner in which cytosine methylation and histone deacetylation are partners in a simple linear pathway. Using microarray data we hope to further test this hypothesis. Specifically, we would like to compare the genome expression profiles for Arabidopsis thaliana Col-0 seedlings germinated and grown for 17 days on sterile media containing no chromatin modifying chemicals (control), or on media containing aza-dC, TSA, or both aza-dC and TSA. This design should allow us to determine the sets of genes that respond (both positively and negatively) to cytosine methylation and to TSA-induced histone deacetylation and to determine if there are synergistic or antagonistic responses when both processes are affected. |
NASCArrays Information at The BAR
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