---
_id: '9497'
abstract:
- lang: eng
  text: The regulation of eukaryotic chromatin relies on interactions between many
    epigenetic factors, including histone modifications, DNA methylation, and the
    incorporation of histone variants. H2A.Z, one of the most conserved but enigmatic
    histone variants that is enriched at the transcriptional start sites of genes,
    has been implicated in a variety of chromosomal processes. Recently, we reported
    a genome-wide anticorrelation between H2A.Z and DNA methylation, an epigenetic
    hallmark of heterochromatin that has also been found in the bodies of active genes
    in plants and animals. Here, we investigate the basis of this anticorrelation
    using a novel h2a.z loss-of-function line in Arabidopsis thaliana. Through genome-wide
    bisulfite sequencing, we demonstrate that loss of H2A.Z in Arabidopsis has only
    a minor effect on the level or profile of DNA methylation in genes, and we propose
    that the global anticorrelation between DNA methylation and H2A.Z is primarily
    caused by the exclusion of H2A.Z from methylated DNA. RNA sequencing and genomic
    mapping of H2A.Z show that H2A.Z enrichment across gene bodies, rather than at
    the TSS, is correlated with lower transcription levels and higher measures of
    gene responsiveness. Loss of H2A.Z causes misregulation of many genes that are
    disproportionately associated with response to environmental and developmental
    stimuli. We propose that H2A.Z deposition in gene bodies promotes variability
    in levels and patterns of gene expression, and that a major function of genic
    DNA methylation is to exclude H2A.Z from constitutively expressed genes.
article_number: e1002988
article_processing_charge: No
article_type: original
author:
- first_name: Devin
  full_name: Coleman-Derr, Devin
  last_name: Coleman-Derr
- first_name: Daniel
  full_name: Zilberman, Daniel
  id: 6973db13-dd5f-11ea-814e-b3e5455e9ed1
  last_name: Zilberman
  orcid: 0000-0002-0123-8649
citation:
  ama: Coleman-Derr D, Zilberman D. Deposition of histone variant H2A.Z within gene
    bodies regulates responsive genes. <i>PLoS Genetics</i>. 2012;8(10). doi:<a href="https://doi.org/10.1371/journal.pgen.1002988">10.1371/journal.pgen.1002988</a>
  apa: Coleman-Derr, D., &#38; Zilberman, D. (2012). Deposition of histone variant
    H2A.Z within gene bodies regulates responsive genes. <i>PLoS Genetics</i>. Public
    Library of Science. <a href="https://doi.org/10.1371/journal.pgen.1002988">https://doi.org/10.1371/journal.pgen.1002988</a>
  chicago: Coleman-Derr, Devin, and Daniel Zilberman. “Deposition of Histone Variant
    H2A.Z within Gene Bodies Regulates Responsive Genes.” <i>PLoS Genetics</i>. Public
    Library of Science, 2012. <a href="https://doi.org/10.1371/journal.pgen.1002988">https://doi.org/10.1371/journal.pgen.1002988</a>.
  ieee: D. Coleman-Derr and D. Zilberman, “Deposition of histone variant H2A.Z within
    gene bodies regulates responsive genes,” <i>PLoS Genetics</i>, vol. 8, no. 10.
    Public Library of Science, 2012.
  ista: Coleman-Derr D, Zilberman D. 2012. Deposition of histone variant H2A.Z within
    gene bodies regulates responsive genes. PLoS Genetics. 8(10), e1002988.
  mla: Coleman-Derr, Devin, and Daniel Zilberman. “Deposition of Histone Variant H2A.Z
    within Gene Bodies Regulates Responsive Genes.” <i>PLoS Genetics</i>, vol. 8,
    no. 10, e1002988, Public Library of Science, 2012, doi:<a href="https://doi.org/10.1371/journal.pgen.1002988">10.1371/journal.pgen.1002988</a>.
  short: D. Coleman-Derr, D. Zilberman, PLoS Genetics 8 (2012).
date_created: 2021-06-07T10:55:27Z
date_published: 2012-10-11T00:00:00Z
date_updated: 2021-12-14T08:29:57Z
day: '11'
department:
- _id: DaZi
doi: 10.1371/journal.pgen.1002988
extern: '1'
external_id:
  pmid:
  - '23071449'
intvolume: '         8'
issue: '10'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://doi.org/10.1371/journal.pgen.1002988
month: '10'
oa: 1
oa_version: Published Version
pmid: 1
publication: PLoS Genetics
publication_identifier:
  eissn:
  - 1553-7404
  issn:
  - 1553-7390
publication_status: published
publisher: Public Library of Science
quality_controlled: '1'
scopus_import: '1'
status: public
title: Deposition of histone variant H2A.Z within gene bodies regulates responsive
  genes
type: journal_article
user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9
volume: 8
year: '2012'
...
---
_id: '9499'
abstract:
- lang: eng
  text: EMBRYONIC FLOWER1 (EMF1) is a plant-specific gene crucial to Arabidopsis vegetative
    development. Loss of function mutants in the EMF1 gene mimic the phenotype caused
    by mutations in Polycomb Group protein (PcG) genes, which encode epigenetic repressors
    that regulate many aspects of eukaryotic development. In Arabidopsis, Polycomb
    Repressor Complex 2 (PRC2), made of PcG proteins, catalyzes trimethylation of
    lysine 27 on histone H3 (H3K27me3) and PRC1-like proteins catalyze H2AK119 ubiquitination.
    Despite functional similarity to PcG proteins, EMF1 lacks sequence homology with
    known PcG proteins; thus, its role in the PcG mechanism is unclear. To study the
    EMF1 functions and its mechanism of action, we performed genome-wide mapping of
    EMF1 binding and H3K27me3 modification sites in Arabidopsis seedlings. The EMF1
    binding pattern is similar to that of H3K27me3 modification on the chromosomal
    and genic level. ChIPOTLe peak finding and clustering analyses both show that
    the highly trimethylated genes also have high enrichment levels of EMF1 binding,
    termed EMF1_K27 genes. EMF1 interacts with regulatory genes, which are silenced
    to allow vegetative growth, and with genes specifying cell fates during growth
    and differentiation. H3K27me3 marks not only these genes but also some genes that
    are involved in endosperm development and maternal effects. Transcriptome analysis,
    coupled with the H3K27me3 pattern, of EMF1_K27 genes in emf1 and PRC2 mutants
    showed that EMF1 represses gene activities via diverse mechanisms and plays a
    novel role in the PcG mechanism.
article_number: e1002512
article_processing_charge: No
article_type: original
author:
- first_name: Sang Yeol
  full_name: Kim, Sang Yeol
  last_name: Kim
- first_name: Jungeun
  full_name: Lee, Jungeun
  last_name: Lee
- first_name: Leor
  full_name: Eshed-Williams, Leor
  last_name: Eshed-Williams
- first_name: Daniel
  full_name: Zilberman, Daniel
  id: 6973db13-dd5f-11ea-814e-b3e5455e9ed1
  last_name: Zilberman
  orcid: 0000-0002-0123-8649
- first_name: Z. Renee
  full_name: Sung, Z. Renee
  last_name: Sung
citation:
  ama: Kim SY, Lee J, Eshed-Williams L, Zilberman D, Sung ZR. EMF1 and PRC2 cooperate
    to repress key regulators of Arabidopsis development. <i>PLoS Genetics</i>. 2012;8(3).
    doi:<a href="https://doi.org/10.1371/journal.pgen.1002512">10.1371/journal.pgen.1002512</a>
  apa: Kim, S. Y., Lee, J., Eshed-Williams, L., Zilberman, D., &#38; Sung, Z. R. (2012).
    EMF1 and PRC2 cooperate to repress key regulators of Arabidopsis development.
    <i>PLoS Genetics</i>. Public Library of Science. <a href="https://doi.org/10.1371/journal.pgen.1002512">https://doi.org/10.1371/journal.pgen.1002512</a>
  chicago: Kim, Sang Yeol, Jungeun Lee, Leor Eshed-Williams, Daniel Zilberman, and
    Z. Renee Sung. “EMF1 and PRC2 Cooperate to Repress Key Regulators of Arabidopsis
    Development.” <i>PLoS Genetics</i>. Public Library of Science, 2012. <a href="https://doi.org/10.1371/journal.pgen.1002512">https://doi.org/10.1371/journal.pgen.1002512</a>.
  ieee: S. Y. Kim, J. Lee, L. Eshed-Williams, D. Zilberman, and Z. R. Sung, “EMF1
    and PRC2 cooperate to repress key regulators of Arabidopsis development,” <i>PLoS
    Genetics</i>, vol. 8, no. 3. Public Library of Science, 2012.
  ista: Kim SY, Lee J, Eshed-Williams L, Zilberman D, Sung ZR. 2012. EMF1 and PRC2
    cooperate to repress key regulators of Arabidopsis development. PLoS Genetics.
    8(3), e1002512.
  mla: Kim, Sang Yeol, et al. “EMF1 and PRC2 Cooperate to Repress Key Regulators of
    Arabidopsis Development.” <i>PLoS Genetics</i>, vol. 8, no. 3, e1002512, Public
    Library of Science, 2012, doi:<a href="https://doi.org/10.1371/journal.pgen.1002512">10.1371/journal.pgen.1002512</a>.
  short: S.Y. Kim, J. Lee, L. Eshed-Williams, D. Zilberman, Z.R. Sung, PLoS Genetics
    8 (2012).
date_created: 2021-06-07T11:07:56Z
date_published: 2012-03-22T00:00:00Z
date_updated: 2021-12-14T08:31:14Z
day: '22'
department:
- _id: DaZi
doi: 10.1371/journal.pgen.1002512
extern: '1'
external_id:
  pmid:
  - '22457632'
intvolume: '         8'
issue: '3'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://doi.org/10.1371/journal.pgen.1002512
month: '03'
oa: 1
oa_version: Published Version
pmid: 1
publication: PLoS Genetics
publication_identifier:
  eissn:
  - 1553-7404
  issn:
  - 1553-7390
publication_status: published
publisher: Public Library of Science
quality_controlled: '1'
scopus_import: '1'
status: public
title: EMF1 and PRC2 cooperate to repress key regulators of Arabidopsis development
type: journal_article
user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9
volume: 8
year: '2012'
...