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APOBEC3G cytidine deaminase inhibits retrotransposition of endogenous retroviruses

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  • Cécile Esnault

    (Unité des Rétrovirus Endogènes et Éléments Retroïdes des Eucaryotes Supérieurs, UMR8122 CNRS, Institut Gustave Roussy
    Institut Pasteur, CNRS URA1930)

  • Odile Heidmann

    (Unité des Rétrovirus Endogènes et Éléments Retroïdes des Eucaryotes Supérieurs, UMR8122 CNRS, Institut Gustave Roussy)

  • Frédéric Delebecque

    (Institut Pasteur, CNRS URA1930)

  • Marie Dewannieux

    (Unité des Rétrovirus Endogènes et Éléments Retroïdes des Eucaryotes Supérieurs, UMR8122 CNRS, Institut Gustave Roussy)

  • David Ribet

    (Unité des Rétrovirus Endogènes et Éléments Retroïdes des Eucaryotes Supérieurs, UMR8122 CNRS, Institut Gustave Roussy)

  • Allan J. Hance

    (INSERM U552, Hôpital Bichat-Claude Bernard)

  • Thierry Heidmann

    (Unité des Rétrovirus Endogènes et Éléments Retroïdes des Eucaryotes Supérieurs, UMR8122 CNRS, Institut Gustave Roussy)

  • Olivier Schwartz

    (Institut Pasteur, CNRS URA1930)

Abstract

Endogenous retroviruses are multicopy retroelements accounting for nearly 10% of murine or human genomes1,2. These retroelements spread into our ancestral genome millions of years ago and have acted as a driving force for genome evolution2,3,4. Endogenous retroviruses may also be deleterious for their host, and have been implicated in cancers and autoimmune diseases5. Most retroelements have lost replication competence because of the accumulation of inactivating mutations, but several, including some murine intracisternal A-particle (IAP) and MusD sequences, are still mobile6,7. These elements encode a reverse transcriptase activity and move by retrotransposition, an intracellular copy-and-paste process involving an RNA intermediate. The host has developed mechanisms to silence their expression, mainly cosuppression and gene methylation4,8. Here we identify another level of antiviral control, mediated by APOBEC3G, a member of the cytidine deaminase family that was previously shown to block HIV replication9,10,11,12. We show that APOBEC3G markedly inhibits retrotransposition of IAP and MusD elements, and induces G-to-A hypermutations in their DNA copies. APOBEC3G, by editing viral genetic material, provides an ancestral wide cellular defence against endogenous and exogenous invaders.

Suggested Citation

  • Cécile Esnault & Odile Heidmann & Frédéric Delebecque & Marie Dewannieux & David Ribet & Allan J. Hance & Thierry Heidmann & Olivier Schwartz, 2005. "APOBEC3G cytidine deaminase inhibits retrotransposition of endogenous retroviruses," Nature, Nature, vol. 433(7024), pages 430-433, January.
    • Handle: RePEc:nat:nature:v:433:y:2005:i:7024:d:10.1038_nature03238
    DOI: 10.1038/nature03238
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    Cited by:

    1. Ahmad Luqman-Fatah & Yuzo Watanabe & Kazuko Uno & Fuyuki Ishikawa & John V. Moran & Tomoichiro Miyoshi, 2023. "The interferon stimulated gene-encoded protein HELZ2 inhibits human LINE-1 retrotransposition and LINE-1 RNA-mediated type I interferon induction," Nature Communications, Nature, vol. 14(1), pages 1-26, December.
    2. Diako Ebrahimi & Hamid Alinejad-Rokny & Miles P Davenport, 2014. "Insights into the Motif Preference of APOBEC3 Enzymes," PLOS ONE, Public Library of Science, vol. 9(1), pages 1-9, January.
    3. Patric Jern & Rebecca A Russell & Vinay K Pathak & John M Coffin, 2009. "Likely Role of APOBEC3G-Mediated G-to-A Mutations in HIV-1 Evolution and Drug Resistance," PLOS Pathogens, Public Library of Science, vol. 5(4), pages 1-9, April.

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