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Intrinsic restriction activity by apolipoprotein B mRNA editing enzyme APOBEC1 against the mobility of autonomous

Terumasa Ikeda1, Khaled Hussein Abd El Galil, Kenzo Tokunaga

  • 1Department of Retrovirology and Self-Defense, Faculty of Life Sciences, Kumamoto University, Kumamoto 860-8556, Japan.

Nucleic Acids Research
|March 15, 2011
PubMed

Insights

Mammalian APOBEC1 proteins restrict retrotransposons like LINE-1 and LTRs. APOBEC1 uses deamination-independent mechanisms against LINE-1 and deamination-dependent mechanisms against LTRs.

Area of Science:

  • Molecular Biology
  • Genetics
  • Virology

Background:

  • Mammalian cytidine deaminases, APOBEC3 (A3) family, are known to restrict endogenous retroelements and exogenous retroviruses like HIV-1.
  • Apolipoprotein B (apo B)-editing catalytic subunit 1 (APOBEC1; A1), involved in lipid transport and mRNA editing, has shown activity against exogenous retroviruses, but its role against endogenous retroelements was unclear.

Purpose of the Study:

  • To investigate the activity of mammalian APOBEC1 (A1) proteins against endogenous retroelements, specifically LINE-1 and LTR retrotransposons.
  • To elucidate the mechanisms by which A1 proteins regulate retrotransposon mobility.

Main Methods:

  • Cell culture-based retrotransposition assays were employed.
  • The activity of A1 proteins from various mammalian species against LINE-1 and LTR retrotransposons (IAP, MusD) was assessed.
  • Mechanisms of anti-L1 activity, including deamination-dependence and subcellular localization, were investigated.

Main Results:

  • APOBEC1 (A1) family proteins from multiple mammalian species were found to reduce the mobility and infectivity of LINE-1 and LTR retrotransposons.
  • The anti-LINE-1 activity of A1 was primarily deamination-independent and unaffected by protein localization.
  • Inhibition of LTR-retrotransposons by A1 required deaminase activity.

Conclusions:

  • Mammalian APOBEC1 (A1) proteins possess activity against endogenous retroelements, including LINE-1 and LTR retrotransposons.
  • The AID/APOBEC family, including A1, utilizes diverse mechanisms to control autonomous retrotransposon mobility across mammalian species.

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