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Journal Article

Histone variant H2A.Z regulates zygotic genome activation

MPS-Authors

Ibarra-Morales,  Dafne
Department of Chromatin Regulation, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Rauer,  Michael
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Rabbani,  Leily
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Zenk,  Fides
Department of Chromatin Regulation, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Schulte-Sasse,  Mariana
Department of Chromatin Regulation, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Cardamone,  Francesco
Department of Chromatin Regulation, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Gomez-Auli,  Alejandro
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Iovino,  Nicola
Department of Chromatin Regulation, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Ibarra-Morales et al. 2021.pdf
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Citation

Ibarra-Morales, D., Rauer, M., Quarato, P., Rabbani, L., Zenk, F., Schulte-Sasse, M., et al. (2021). Histone variant H2A.Z regulates zygotic genome activation. Nature Communications, 12: 7002 (2021). doi:10.1038/s41467-021-27125-7.


Cite as: http://hdl.handle.net/21.11116/0000-0009-8F59-3
Abstract
During embryogenesis, the genome shifts from transcriptionally quiescent to extensively active in a process known as Zygotic Genome Activation (ZGA). In Drosophila, the pioneer factor Zelda is known to be essential for the progression of development; still, it regulates the activation of only a small subset of genes at ZGA. However, thousands of genes do not require Zelda, suggesting that other mechanisms exist. By conducting GRO-seq, HiC and ChIP-seq in Drosophila embryos, we demonstrate that up to 65% of zygotically activated genes are enriched for the histone variant H2A.Z. H2A.Z enrichment precedes ZGA and RNA Polymerase II loading onto chromatin. In vivo knockdown of maternally contributed Domino, a histone chaperone and ATPase, reduces H2A.Z deposition at transcription start sites, causes global downregulation of housekeeping genes at ZGA, and compromises the establishment of the 3D chromatin structure. We infer that H2A.Z is essential for the de novo establishment of transcriptional programs during ZGA via chromatin reorganization.