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Retrotransposon derepression leads to activation of the unfolded protein response and apoptosis in pro-B cells.
Development 143, 1788-1799 (2016)
The H3K9me3-specific histone methyltransferase Setdb1 impacts on transcriptional regulation by repressing both developmental genes and retrotransposons. How impaired retrotransposon silencing may lead to developmental phenotypes is currently unclear. Here we show that loss of Setdb1 in pro-B cells completely abrogates B cell development. In pro-B cells, Setdb1 is dispensable for silencing of lineage-inappropriate developmental genes. Instead, we detect strong derepression of endogenous Murine Leukemia Virus (MLV) copies. This activation coincides with an unusual change in chromatin structure with only partial loss of H3K9me3 and unchanged DNA methylation, but strongly increased H3K4me3. Production of MLV proteins leads to activation of the unfolded protein response pathway and apoptosis. Thus, our data demonstrate that B cell development critically depends on the proper repression of retrotransposon sequences through Setdb1.
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Times Cited
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6.059
1.480
12
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Heterochromatin ; Mouse ; Retrotransposon ; Setdb1 ; Unfolded Protein Response; Embryonic Stem-cells; Eset Histone Methyltransferase; Fc-gamma-riib; Progenitor Cells; Differentiation; Networks; Genes; Mice; Retroviruses; Transcripts
Language
english
Publication Year
2016
HGF-reported in Year
2016
ISSN (print) / ISBN
0950-1991
e-ISSN
1477-9129
Quellenangaben
Volume: 143,
Issue: 10,
Pages: 1788-1799
Publisher
Company of Biologists
Publishing Place
Cambridge
Reviewing status
Peer reviewed
Institute(s)
Institute of Molecular Immunology (IMI)
POF-Topic(s)
30504 - Mechanisms of Genetic and Environmental Influences on Health and Disease
Research field(s)
Immune Response and Infection
PSP Element(s)
G-501793-001
WOS ID
WOS:000389588300018
Scopus ID
84968779632
PubMed ID
27013243
Erfassungsdatum
2016-04-18