Histone variants H3.3 and H2A.Z are incorporated into the β-globin locus during transcription activation via different mechanisms.

08:00 EDT 4th June 2018 | BioPortfolio

Summary of "Histone variants H3.3 and H2A.Z are incorporated into the β-globin locus during transcription activation via different mechanisms."

Histone variants H3.3 and H2A.Z are often enriched in enhancers and transcriptionally active genes. However, the incorporation dynamics of these variants and the mechanisms of their incorporation are unclear. Here, we examined the distribution of H3.3 and H2A.Z in the human β-globin locus and analyzed their incorporation dynamics during transcription activation. Locus control region hypersensitive sites (LCR HSs), acting as enhancers, and active globin genes were enriched by H3.3 and H2A.Z in erythroid K562 cells, but inactive globin genes were not. Both variants were dynamically incorporated into the β-globin locus after transcription induction in MEL/ch11 cells, and prior to gene transcription the LCR HSs became enriched with the variants. In the activated β-globin gene, H3.3 was highly incorporated during transcription, whereas H2A.Z incorporation appeared to precede it. To further explore the relationship between gene transcription and variant incorporation, we deleted the LCR HS3 enhancer or the β-globin proximal promoter from the β-globin locus using the CRISPR-Cas9 genome editing system. H2A.Z was incorporated into the β-globin gene in the locus lacking promoter, even though the β-globin gene transcription was abolished by these deletions. However, H3.3 incorporation was reduced in the untranscribed β-globin gene. These results suggest that H3.3 and H2A.Z are systematically incorporated into the LCR enhancer and β-globin gene as part of transcription activation, but that their incorporation is carried out via different mechanisms.


Journal Details

This article was published in the following journal.

Name: Biochimica et biophysica acta
ISSN: 0006-3002


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Medical and Biotech [MESH] Definitions

A regulatory region first identified in the human beta-globin locus but subsequently found in other loci. The region is believed to regulate GENETIC TRANSCRIPTION by opening and remodeling CHROMATIN structure. It may also have enhancer activity.

A class II histone deacetylase that removes acetyl groups from N-terminal LYSINES of HISTONE H2A; HISTONE H2B; HISTONE H3; and HISTONE H4. It plays a critical role in EPIGENETIC REPRESSION and regulation of GENETIC TRANSCRIPTION, as well as CELL MOTILITY through deacetylation of TUBULIN. It also targets misfolded proteins for clearance by AUTOPHAGY when MOLECULAR CHAPERONE-mediated folding is overwhelmed.

Members of the beta-globin family. In humans, they are encoded in a gene cluster on CHROMOSOME 11. They include epsilon-globin, gamma-globin, delta-globin and beta-globin. There is also a pseudogene of beta (theta-beta) in the gene cluster. Adult HEMOGLOBIN is comprised of two ALPHA-GLOBIN chains and two beta-globin chains.

Members of the beta-globin family. In humans, two non-allelic types of gamma-globin - A gamma and G gamma are encoded in the beta-globin gene cluster on CHROMOSOME 11. Two gamma-globin chains combine with two ZETA-GLOBIN chains to form the embryonic hemoglobin Portland. Fetal HEMOGLOBIN F is formed from two gamma-globin chains combined with two ALPHA-GLOBIN chains.

A member of the alpha-globin family. In humans, zeta-globin is encoded in the alpha-globin gene cluster located on CHROMOSOME 16. Two zeta-globin chains combine with two EPSILON GLOBIN chains to form the embryonic HEMOGLOBIN Gower 1.

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