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The role of ATXR6 expression in modulating genome stability and transposable element repression in Arabidopsis.

  • Author(s): Potok, Magdalena E;
  • Zhong, Zhenhui;
  • Picard, Colette L;
  • Liu, Qikun;
  • Do, Truman;
  • Jacobsen, Cassidy E;
  • Sakr, Ocean;
  • Naranbaatar, Bilguudei;
  • Thilakaratne, Ruwan;
  • Khnkoyan, Zhanna;
  • Purl, Megan;
  • Cheng, Harrison;
  • Vervaet, Helena;
  • Feng, Suhua;
  • Rayatpisheh, Shima;
  • Wohlschlegel, James A;
  • O'Malley, Ronan C;
  • Ecker, Joseph R;
  • Jacobsen, Steven E
  • et al.
Abstract

ARABIDOPSIS TRITHORAX-RELATED PROTEIN 5 (ATXR5) AND ATXR6 are required for the deposition of H3K27me1 and for maintaining genomic stability in Arabidopsis 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 atxr5/6 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 atxr5/6 mutant correlated with residual ATXR6 expression from the hypomorphic ATXR6 allele. However, up-regulation of DNA damage genes occurred regardless of ATXR6 levels and thus appears to be a separable process. We also isolated an atxr6-null allele which showed that ATXR5 and ATXR6 are required for female germline development. Finally, we characterize three previously reported suppressors of the hypomorphic atxr5/6 mutant and show that these rescue atxr5/6 via distinct mechanisms, two of which involve increasing H3K27me1 levels.

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