ArticleGenome biology2025
H3K4me3 binding ALFIN-LIKE proteins recruit SWR1 for gene-body deposition of H2A.Z.
Article in Genome biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Antagonistic histone H2A variants and autonomous heterochromatin formation shape epigenomic patterns in Arabidopsis.Nature communications · 2026Article
- Review
- Traversing the effects of ploidy changes in different Eragrostis curvula genotypes through high-throughput RNA sequencing.The plant genome · 2026Article
- Histone variant H2A.X represses deposition of active H3K4me3 marks and restricts H2A.W incorporation.Nucleic acids research · 2026Article
- H3K4me2 orchestrates H2A.Z and Polycomb repressive marks in Arabidopsis.Nature communications · 2025Article
- Arabidopsis INHIBITOR OF GROWTH 2 promotes flowering by regulating NuA4-dependent H4 acetylation levels at FT and SOC1.Plant physiology · 2025Article
- CRISPR targeting of H3K4me3 activates gene expression and unlocks centromere-proximal crossover recombination in Arabidopsis.Nature communications · 2025Article
- H3K4me3 binding ALFIN-LIKE proteins recruit SWR1 for gene-body deposition of H2A.Z.Genome biology · 2025Article
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8 authors.
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Abstract
backgroundThe H2A.Z histone variant is highly enriched over gene bodies, playing an essential role in several genome-templated processes, including transcriptional regulation and epigenetic patterning across eukaryotes. Deposition of H2A.Z is mediated by the SWR1 remodeling complex. How SWR1 is directed to gene bodies is largely unknown.
resultsHere, we show that ALFIN-LIKE (AL) proteins are responsible for H2A.Z gene body patterning in Arabidopsis. AL proteins encode H3K4me3-binding PHD domains, and by ChIP-seq, we confirm preferential binding of AL5 to H3K4me3 over H3K4me1/2 in planta. We observe a global reduction in H2A.Z in al septuple mutants (al7m), especially over H3K4me3-enriched genic regions. While MBD9 recruits SWR1 to nucleosome-free regions, ALs act non-redundantly with MBD9 for deposition of H2A.Z. Notably, al7m mutants show severe developmental abnormalities and upregulation of H2A.Z gene body-enriched responsive genes.
conclusionsTherefore, we propose a model whereby AL proteins direct gene body enrichment of H2A.Z by recruiting SWR1 to H3K4me3-containing responsive genes.
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