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Peer-reviewedCC BY-NC 4.0Nucleic Acids Research

CFDP1 is required for histone variant H2A.Z deposition by the human SRCAP chromatin remodeling complex

  • Naoe Moro1
  • Dandan Yang2
  • Vincent L Butty2
  • Stuart S Levine2
  • Craig L Peterson1
  • Laurie A Boyer2,3
  • Shinya Watanabe1
  1. 1Program in Molecular Medicine, University of Massachusetts Chan Medical School , Worcester, MA 01605 ,
  2. 2Department of Biology, Massachusetts Institute of Technology , Cambridge, MA 02139 ,
  3. 3Department of Biological Engineering, Massachusetts Institute of Technology , Cambridge, MA 02139 ,
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Abstract

Craniofacial Developmental Protein 1 (CFDP1) is a member of the evolutionarily conserved family of Bucentaur (BCNT) proteins and is required for cell survival and differentiation during tooth development. Its yeast homolog is involved in histone variant H2A.Z deposition by the yeast SWR1C remodeler. Direct connections between CFDP1, H2A.Z deposition, and the mammalian SWR1 homolog, Snf2-Related CREBBP Activator Protein (SRCAP), are poorly understood. Here, we perform detailed biochemical reconstitution and characterization of the human SRCAP complex (SRCAP-C). We find that CFDP1 weakly interacts with SRCAP-C in a salt concentration-dependent manner and is essential for H2A.Z dimer exchange by SRCAP-C. We show that CFDP1 stimulates the basal ATPase activity of reconstituted SRCAP-C, suggesting a requirement for CFDP1 in regulating intrinsic catalytic ATPase activity. Additionally, CFDP1 deficiency in human induced pluripotent stem cells (hiPSCs) leads to a genome-wide reduction of H2A.Z, H3K27me3, and H3K4me3 deposition, accompanied by the upregulation of developmental genes normally marked by these modifications. Taken together, our results provide mechanistic insights into how CFDP1 regulates histone variant H2A.Z deposition by SRCAP-C. Given mutations in the SRCAP gene cause Floating-Harbor syndrome, a rare, dominant developmental disorder, our study provides an additional link between craniofacial development and SRCAP-mediated H2A.Z deposition.

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Cite

BibTeXRIS
BibTeX
@article{moro2026cfdp1,
  title = {{CFDP1 is required for histone variant H2A.Z deposition by the human SRCAP chromatin remodeling complex}},
  author = {Naoe Moro and Dandan Yang and Vincent L Butty and Stuart S Levine and Craig L Peterson and Laurie A Boyer and Shinya Watanabe},
  journal = {Nucleic Acids Research},
  year = {2026},
  month = nov,
  doi = {10.1093/nar/gkag1099},
  url = {https://academic.oup.com/nar/article/doi/10.1093/nar/gkag1099/9011585},
  note = {CC BY-NC 4.0},
}
RIS
TY  - JOUR
TI  - CFDP1 is required for histone variant H2A.Z deposition by the human SRCAP chromatin remodeling complex
AU  - Naoe Moro
AU  - Dandan Yang
AU  - Vincent L Butty
AU  - Stuart S Levine
AU  - Craig L Peterson
AU  - Laurie A Boyer
AU  - Shinya Watanabe
PY  - 2026
DA  - 2026/11/04
JO  - Nucleic Acids Research
DO  - 10.1093/nar/gkag1099
UR  - https://academic.oup.com/nar/article/doi/10.1093/nar/gkag1099/9011585
AB  - Craniofacial Developmental Protein 1 (CFDP1) is a member of the evolutionarily conserved family of Bucentaur (BCNT) proteins and is required for cell survival and differentiation during tooth development. Its yeast homolog is involved in histone variant H2A.Z deposition by the yeast SWR1C remodeler. Direct connections between CFDP1, H2A.Z deposition, and the mammalian SWR1 homolog, Snf2-Related CREBBP Activator Protein (SRCAP), are poorly understood. Here, we perform detailed biochemical reconstitution and characterization of the human SRCAP complex (SRCAP-C). We find that CFDP1 weakly interacts with SRCAP-C in a salt concentration-dependent manner and is essential for H2A.Z dimer exchange by SRCAP-C. We show that CFDP1 stimulates the basal ATPase activity of reconstituted SRCAP-C, suggesting a requirement for CFDP1 in regulating intrinsic catalytic ATPase activity. Additionally, CFDP1 deficiency in human induced pluripotent stem cells (hiPSCs) leads to a genome-wide reduction of H2A.Z, H3K27me3, and H3K4me3 deposition, accompanied by the upregulation of developmental genes normally marked by these modifications. Taken together, our results provide mechanistic insights into how CFDP1 regulates histone variant H2A.Z deposition by SRCAP-C. Given mutations in the SRCAP gene cause Floating-Harbor syndrome, a rare, dominant developmental disorder, our study provides an additional link between craniofacial development and SRCAP-mediated H2A.Z deposition.
SN  - 0305-1048
SN  - 1362-4962
ER  -