期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2022
卷号：119
期号：3
DOI：10.1073/pnas.2115570119
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：Significance
The plant-specific H3K27me1 methyltransferases ATXR5 and ATXR6 play integral roles connecting epigenetic silencing with genomic stability. However, how H3K27me1 relates to these processes is poorly understood. In this study, we performed a comprehensive transcriptome analysis of tissue- and ploidy-specific expression in a hypomorphic
atxr5/6 mutant and revealed that the tissue-specific defects correlate with residual
ATXR6 expression. We also determined that ATXR5/6 function is essential for female germline development. Furthermore, we provide a comprehensive analysis of H3K27me1 changes in relation to other epigenetic marks. We also determined that some previously reported suppressors of
atxr5/6 may act by restoring the levels of H3K27me1, such as through up-regulation of the
ATXR6 transcript in the
atxr6 hypomorphic promoter allele.
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.
