bioRxiv · 10.64898/2026.09.14.751395
J-domain proteins stimulate PKL-mediated chromatin compaction at H3K4-hypomethylated genomic loci
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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Guan, B.-B., Yan, Z., Du, P., Sia, Y., Yuan, D.-Y., Luo, Y.-X., Li, J.-X., Su, X.-M., Su, Y.-N., Guo, J., Liu, Z.-Z., Liu, X.-Y., Li, L., Chen, S., Chen, Z., He, X.-J.. 2026-09-16. J-domain proteins stimulate PKL-mediated chromatin compaction at H3K4-hypomethylated genomic loci. https://doi.org/10.64898/2026.09.14.751395
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