Ezh2 Represses Transcription of Innate Lymphoid Genes in B Lymphocyte Progenitors and Maintains the B-2 Cell Fate
(2020) In Journal of immunology 204(7). p.1760-1769- Abstract
Lymphocyte lineage specification and commitment requires the activation of lineage-specific genes and repression of alternative lineage genes, respectively. The mechanisms governing alternative lineage gene repression and commitment in lymphocytes are largely unknown. In this study, we demonstrate that Ezh2, which represses gene expression through methylation of histone 3 lysine 27, was essential for repression of numerous genes, including genes encoding innate lymphocyte transcription factors, specifically in murine B lymphocyte progenitors, but these cells maintained their B lymphocyte identity. However, adult Ezh2-deficient B lymphocytes expressed Lin28b, which encodes an RNA-binding protein associated with fetal hematopoietic gene... (More)
Lymphocyte lineage specification and commitment requires the activation of lineage-specific genes and repression of alternative lineage genes, respectively. The mechanisms governing alternative lineage gene repression and commitment in lymphocytes are largely unknown. In this study, we demonstrate that Ezh2, which represses gene expression through methylation of histone 3 lysine 27, was essential for repression of numerous genes, including genes encoding innate lymphocyte transcription factors, specifically in murine B lymphocyte progenitors, but these cells maintained their B lymphocyte identity. However, adult Ezh2-deficient B lymphocytes expressed Lin28b, which encodes an RNA-binding protein associated with fetal hematopoietic gene expression programs, and these cells acquired a fetal B-1 lymphocyte phenotype in vitro and in vivo. Therefore, Ezh2 coordinates the repression of multiple gene programs in B lymphocytes and maintains the adult B-2 cell fate.
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- author
- Jacobsen, Jennifer A. ; Bartom, Elizabeth T. ; Sigvardsson, Mikael LU and Kee, Barbara L.
- organization
- publishing date
- 2020
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Journal of immunology
- volume
- 204
- issue
- 7
- pages
- 10 pages
- publisher
- American Association of Immunologists
- external identifiers
-
- pmid:32094206
- scopus:85082342644
- ISSN
- 1550-6606
- DOI
- 10.4049/jimmunol.1901188
- language
- English
- LU publication?
- yes
- id
- 2ba87a4a-3a0a-4ed8-8cb6-266201c997bc
- date added to LUP
- 2020-04-03 09:15:23
- date last changed
- 2022-04-18 21:40:28
@article{2ba87a4a-3a0a-4ed8-8cb6-266201c997bc,
abstract = {{<p>Lymphocyte lineage specification and commitment requires the activation of lineage-specific genes and repression of alternative lineage genes, respectively. The mechanisms governing alternative lineage gene repression and commitment in lymphocytes are largely unknown. In this study, we demonstrate that Ezh2, which represses gene expression through methylation of histone 3 lysine 27, was essential for repression of numerous genes, including genes encoding innate lymphocyte transcription factors, specifically in murine B lymphocyte progenitors, but these cells maintained their B lymphocyte identity. However, adult Ezh2-deficient B lymphocytes expressed Lin28b, which encodes an RNA-binding protein associated with fetal hematopoietic gene expression programs, and these cells acquired a fetal B-1 lymphocyte phenotype in vitro and in vivo. Therefore, Ezh2 coordinates the repression of multiple gene programs in B lymphocytes and maintains the adult B-2 cell fate.</p>}},
author = {{Jacobsen, Jennifer A. and Bartom, Elizabeth T. and Sigvardsson, Mikael and Kee, Barbara L.}},
issn = {{1550-6606}},
language = {{eng}},
number = {{7}},
pages = {{1760--1769}},
publisher = {{American Association of Immunologists}},
series = {{Journal of immunology}},
title = {{Ezh2 Represses Transcription of Innate Lymphoid Genes in B Lymphocyte Progenitors and Maintains the B-2 Cell Fate}},
url = {{http://dx.doi.org/10.4049/jimmunol.1901188}},
doi = {{10.4049/jimmunol.1901188}},
volume = {{204}},
year = {{2020}},
}