The role of ATXR6 expression in modulating genome stability and transposable element repression in Arabidopsis
| Autor: | Magdalena E. Potok, Zhenhui Zhong, Colette L. Picard, Qikun Liu, Truman Do, Cassidy E. Jacobsen, Ocean Sakr, Bilguudei Naranbaatar, Ruwan Thilakaratne, Zhanna Khnkoyan, Megan Purl, Harrison Cheng, Helena Vervaet, Suhua Feng, Shima Rayatpisheh, James A. Wohlschlegel, Ronan C. O’Malley, Joseph R. Ecker, Steven E. Jacobsen |
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| Rok vydání: | 2022 |
| Předmět: |
Multidisciplinary
Arabidopsis Proteins histone methyltransferase Human Genome Arabidopsis H3K27me1 plant Methyltransferases Genomic Instability Histones Phenotype Genetic Gene Expression Regulation Heterochromatin Mutation DNA Transposable Elements Genetics 2.1 Biological and endogenous factors ATXR5/6 Aetiology Transcriptome Alleles Epigenesis Biotechnology |
| Zdroj: | Proceedings of the National Academy of Sciences of the United States of America, vol 119, iss 3 |
| ISSN: | 1091-6490 0027-8424 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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