The role of ATXR6 expression in modulating genome stability and transposable element repression in <i>Arabidopsis</i>

Abstract

ARABIDOPSIS TRITHORAX-RELATED PROTEIN 5 (ATXR5) AND ATXR6 are required for the deposition of H3K27me1 and for maintaining genomic stability in <i>Arabidopsis</i> Reduction of ATXR5/6 activity results in activation of DNA damage response genes, along with tissue-specific derepression of transposable elements (TEs), chromocenter decompaction, and genomic instability characterized by accumulation of excess DNA from heterochromatin. How loss of ATXR5/6 and H3K27me1 leads to these phenotypes remains unclear. Here we provide extensive characterization of the <i>atxr5/6</i> hypomorphic mutant by comprehensively examining gene expression and epigenetic changes in the mutant. We found that the tissue-specific phenotypes of TE derepression and excessive DNA in this <i>atxr5/6</i> mutant correlated with residual <i>ATXR6</i> expression from the hypomorphic <i>ATXR6</i> allele. However, up-regulation of DNA damage genes occurred regardless of <i>ATXR6</i> levels and thus appears to be a separable process. We also isolated an <i>atxr6</i>-null allele which showed that ATXR5 and ATXR6 are required for female germline development. Finally, we characterize three previously reported suppressors of the hypomorphic <i>atxr5/6</i> mutant and show that these rescue <i>atxr5/6</i> via distinct mechanisms, two of which involve increasing H3K27me1 levels.