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APOBEC3B Nuclear Localization Requires Two Distinct N-Terminal Domain Surfaces

Daniel J Salamango1, Jennifer L McCann1, Özlem Demir2

  • 1Department of Biochemistry, Molecular Biology and Biophysics, University of Minnesota, Minneapolis, MN 55455, USA; Masonic Cancer Center, University of Minnesota, Minneapolis, MN 55455, USA; Institute for Molecular Virology, University of Minnesota, Minneapolis, MN 55455, USA.

Journal of Molecular Biology
|May 23, 2018
PubMed

Insights

The APOBEC3B (A3B) enzyme, linked to cancer, has two new nuclear import surfaces. Disrupting these surfaces blocks A3B

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Enzymology

Background:

  • APOBEC3 (A3) enzymes are cytosine deaminases involved in antiviral immunity.
  • APOBEC3B (A3B) is implicated in cancer mutagenesis, with upregulated mRNA and correlation to poor outcomes.
  • Previous studies identified one region in A3B's N-terminal domain (NTD) for nuclear localization.

Purpose of the Study:

  • To identify novel determinants of APOBEC3B (A3B) nuclear localization.
  • To investigate the role of distinct surface-exposed regions in A3B's NTD.
  • To explore therapeutic potential of A3B nuclear import mechanisms.

Main Methods:

  • Mutagenesis studies to disrupt specific residues in A3B's NTD.
  • Analysis of A3B nuclear localization using microscopy.
  • Grafting of A3B import determinants into related APOBEC3 family members.

Main Results:

  • Two distinct surface-exposed NTD regions (import surface 1 and import surface 2) are critical for A3B nuclear localization.
  • Disruption of residues in the first 30 amino acids or loop 5/α-helix 3 completely abolishes nuclear import.
  • These identified import determinants can confer nuclear localization to other A3 family members.

Conclusions:

  • Both identified NTD regions are essential for non-canonical A3B nuclear localization.
  • These unique nuclear import surfaces represent potential novel therapeutic targets in cancer.
  • Understanding A3B's localization mechanisms provides insights into its role in tumor evolution.
Keywords:
APOBEC3Bcancer genomic DNA deaminasenuclear importretrovirus restriction factorsubcellular localization

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