Mechanistic study reveals that CAF-1 loss impairs histone H3.3 deposition at transcribed genomic loci in Arabidopsis, indicating a novel role for CAF-1 in histone variant maintenance.
Eukaryotic organisms organize their genetic material in chromatin rather than naked DNA. Efficient chromatin assembly is essential for all DNA-templated processes, including replication, transcription, and DNA repair. Our research focused on two major histone H3 deposition complexes: Chromatin Assembly Factor (CAF-1) and Histone Regulator A (HIRA). CAF-1 deposits canonical H3 on naked DNA immediately after replication during the S-phase in yeast and metazoans, and HIRA is thought to incorporate the H3.3 variant in a replication-independent manner. By combining biochemical, genetic, genomic, and proteomic data, we revealed that CAF-1 activity might be associated with the maintenance of the histone variant H3.3 in Arabidopsis chromatin. Moreover, this CAF-1's potential function in H3.3 homeostasis may be particularly significant in the transcribed regions of the genome.
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Yang et al. (2026) studied this question.
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