J-domain proteins stimulate PKL-mediated chromatin compaction at H3K4-hypomethylated genomic loci
- 1National Institute of Biological Sciences, Beijing, China
Abstract
Chromatin accessibility varies widely across distinct genomic regions in eukaryotes, yet the mechanisms governing these differential patterns remain poorly understood. Here, we identify a subfamily of functionally redundant J-domain proteins (JDPs) that assemble into a protein complex with PICKLE (PKL), an evolutionarily conserved CHD3-type chromatin remodeler, in Arabidopsis thaliana. JDPs are required not only for maintaining PKL protein stability but also for stimulating its nucleosome remodeling and ATPase activities. A previously uncharacterized histone-binding domain (HBD) within JDPs specifically recognizes the N-terminal tail of histone H3 when the H3K4me3 modification is absent. This interaction enhances PKL-mediated nucleosome sliding and ATPase activities in vitro, and promotes PKL-dependent chromatin compaction at H3K4me3-depleted genomic loci in vivo. The PKL-JDP complex drives chromatin compaction to repress developmentally regulated genes, thereby governing key developmental phase transitions, including the embryo-to-seedling transition and flowering. Collectively, these findings uncover a distinct mechanism by which the absence of H3K4me3 is sensed to initiate regional chromatin compaction, repress developmentally regulated genes, and facilitate key developmental transitions.
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BibTeX
@misc{guan2026jdomain,
title = {{J-domain proteins stimulate PKL-mediated chromatin compaction at H3K4-hypomethylated genomic loci}},
author = {B.-B. Guan and Z. Yan and P. Du and Y. Sia and D.-Y. Yuan and Y.-X. Luo and J.-X. Li and X.-M. Su and Y.-N. Su and J. Guo and Z.-Z. Liu and X.-Y. Liu and L. Li and S. Chen and Z. Chen and X.-J. He},
howpublished = {bioRxiv},
year = {2026},
month = sep,
doi = {10.64898/2026.09.14.751395},
url = {https://www.biorxiv.org/content/10.64898/2026.09.14.751395v1},
note = {CC BY},
}
RIS
TY - UNPB
TI - J-domain proteins stimulate PKL-mediated chromatin compaction at H3K4-hypomethylated genomic loci
AU - B.-B. Guan
AU - Z. Yan
AU - P. Du
AU - Y. Sia
AU - D.-Y. Yuan
AU - Y.-X. Luo
AU - J.-X. Li
AU - X.-M. Su
AU - Y.-N. Su
AU - J. Guo
AU - Z.-Z. Liu
AU - X.-Y. Liu
AU - L. Li
AU - S. Chen
AU - Z. Chen
AU - X.-J. He
PY - 2026
DA - 2026/09/14
PB - bioRxiv
DO - 10.64898/2026.09.14.751395
UR - https://www.biorxiv.org/content/10.64898/2026.09.14.751395v1
AB - Chromatin accessibility varies widely across distinct genomic regions in eukaryotes, yet the mechanisms governing these differential patterns remain poorly understood. Here, we identify a subfamily of functionally redundant J-domain proteins (JDPs) that assemble into a protein complex with PICKLE (PKL), an evolutionarily conserved CHD3-type chromatin remodeler, in Arabidopsis thaliana. JDPs are required not only for maintaining PKL protein stability but also for stimulating its nucleosome remodeling and ATPase activities. A previously uncharacterized histone-binding domain (HBD) within JDPs specifically recognizes the N-terminal tail of histone H3 when the H3K4me3 modification is absent. This interaction enhances PKL-mediated nucleosome sliding and ATPase activities in vitro, and promotes PKL-dependent chromatin compaction at H3K4me3-depleted genomic loci in vivo. The PKL-JDP complex drives chromatin compaction to repress developmentally regulated genes, thereby governing key developmental phase transitions, including the embryo-to-seedling transition and flowering. Collectively, these findings uncover a distinct mechanism by which the absence of H3K4me3 is sensed to initiate regional chromatin compaction, repress developmentally regulated genes, and facilitate key developmental transitions.
ER -