TONSOKU is required for the maintenance of repressive chromatin modifications in Arabidopsis
Lin Wang,
Mande Xue,
Huairen Zhang,
Lijun Ma,
Danhua Jiang
Affiliations
Lin Wang
State Key Laboratory of Plant Genomics, Institute of Genetics and Developmental Biology, The Innovative Academy for Seed Design, Chinese Academy of Sciences, Beijing 100101, China; University of Chinese Academy of Sciences, Beijing 100049, China
Mande Xue
State Key Laboratory of Plant Genomics, Institute of Genetics and Developmental Biology, The Innovative Academy for Seed Design, Chinese Academy of Sciences, Beijing 100101, China; University of Chinese Academy of Sciences, Beijing 100049, China
Huairen Zhang
State Key Laboratory of Plant Genomics, Institute of Genetics and Developmental Biology, The Innovative Academy for Seed Design, Chinese Academy of Sciences, Beijing 100101, China
Lijun Ma
State Key Laboratory of Plant Genomics, Institute of Genetics and Developmental Biology, The Innovative Academy for Seed Design, Chinese Academy of Sciences, Beijing 100101, China; University of Chinese Academy of Sciences, Beijing 100049, China
Danhua Jiang
State Key Laboratory of Plant Genomics, Institute of Genetics and Developmental Biology, The Innovative Academy for Seed Design, Chinese Academy of Sciences, Beijing 100101, China; University of Chinese Academy of Sciences, Beijing 100049, China; Corresponding author
Summary: The stability of eukaryotic genomes relies on the faithful transmission of DNA sequences and the maintenance of chromatin states through DNA replication. Plant TONSOKU (TSK) and its animal ortholog TONSOKU-like (TONSL) act as readers for newly synthesized histones and preserve DNA integrity via facilitating DNA repair at post-replicative chromatin. However, whether TSK/TONSL regulate the maintenance of chromatin states remains elusive. Here, we show that TSK is dispensable for global histone and nucleosome accumulation but necessary for maintaining repressive chromatin modifications, including H3K9me2, H2A.W, H3K27me3, and DNA methylation. TSK physically interacts with H3K9 methyltransferases and Polycomb proteins. Moreover, TSK mutation strongly enhances defects in Polycomb pathway mutants. TSK is intended to only associate with nascent chromatin until it starts to mature. We propose that TSK ensures the preservation of chromatin states by supporting the recruitment of chromatin modifiers to post-replicative chromatin in a critical short window of time following DNA replication.
