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KAP1 controls endogenous retroviruses in embryonic stem cells.

Helen M Rowe¹, Johan Jakobsson, Daniel Mesnard

¹School of Life Sciences, Ecole Polytechnique Fédérale de Lausanne, 1015 Lausanne, Switzerland.

|January 16, 2010

Summary

KRAB-associated protein 1 (KAP1) controls endogenous retroviruses (ERVs) in early development. KAP1 deletion in mouse embryonic stem cells and embryos causes significant ERV upregulation, highlighting its role in genome integrity.

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Area of Science:

Genetics
Epigenetics
Developmental Biology

Background:

Mammalian genomes contain over 40% retroelements, including endogenous retroviruses (ERVs).
ERVs are transcriptionally silenced during early embryogenesis via DNA and histone methylation to maintain genome integrity.
The precise mechanisms and initiators of ERV silencing remain largely unknown.

Purpose of the Study:

To investigate the role of KRAB-associated protein 1 (KAP1) in the transcriptional control of endogenous retroelements during early embryonic development.
To determine if KAP1-mediated repression contributes to the silencing of ERVs in mouse embryonic stem cells and early embryos.

Main Methods:

KAP1 deletion in mouse embryonic stem (ES) cells and early embryos.
Analysis of endogenous retrovirus (ERV) expression using quantitative methods.
Chromatin immunoprecipitation to assess histone modifications (H3K9me3) and KAP1 enrichment.
Reporter assays to evaluate the repressive function of ERV sequences.

Main Results:

KAP1 deletion led to significant upregulation of various ERVs, particularly intracisternal A-type particles (IAPs), in mouse ES cells and early embryos.
KAP1 acts synergistically with DNA methylation to silence IAP elements.
KAP1 is enriched at the 5' untranslated region (5'UTR) of IAP genomes, and its deletion results in loss of H3K9me3.
IAP 5'UTR sequences confer KAP1-dependent repression on heterologous promoters.

Conclusions:

KAP1 is a key regulator of endogenous retroelement silencing during early mammalian development.
KAP1-mediated repression, in conjunction with DNA methylation, is crucial for controlling ERV activity and maintaining genome stability.