bioRxiv preprint doi: https://doi.org/10.1101/2020.07.17.209098; this version posted July 17, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. Title: H3.1K27me1 maintains transcriptional silencing and genome stability by preventing GCN5-mediated histone acetylation Authors: Jie Dong1#, Chantal LeBlanc1#, Axel Poulet1#, Benoit Mermaz1, Gonzalo Villarino1, Kimberly M. Webb2, Valentin Joly1, Josefina Mendez1, Philipp Voigt2 and Yannick Jacob1* Affiliations: 1 Yale University, Department of Molecular, Cellular and Developmental Biology, Faculty of Arts and Sciences; 260 Whitney Avenue, New Haven, Connecticut 06511, United States. 2 Wellcome Centre for Cell Biology, School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3BF, United Kingdom. # These authors contributed equally to this manuscript. * To whom correspondence should be addressed. Email:
[email protected] 1 bioRxiv preprint doi: https://doi.org/10.1101/2020.07.17.209098; this version posted July 17, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. 1 Abstract 2 In plants, genome stability is maintained during DNA replication by the H3.1K27 3 methyltransferases ATXR5 and ATXR6, which catalyze the deposition of K27me1 on replication- 4 dependent H3.1 variants. Loss of H3.1K27me1 in atxr5 atxr6 double mutants leads to 5 heterochromatin defects, including transcriptional de-repression and genomic instability, but the 6 molecular mechanisms involved remain largely unknown.