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Molecular phylogeny of Fv1

C F Qi1, F Bonhomme, A Buckler-White

  • 1Laboratory of Immunopathology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 7, Room 304, MSC 0760, Bethesda, Maryland 20892-0760, USA.

Insights

The Fv1 gene in mice, crucial for resisting murine leukemia viruses (MuLV), likely originated from endogenous retroviruses. Its unique evolutionary path suggests horizontal gene transfer and positive selection.

Area of Science:

  • Virology
  • Genetics
  • Evolutionary Biology

Background:

  • The Fv1 gene in mice provides resistance against murine leukemia viruses (MuLV) through its different alleles.
  • The Fv1 gene sequence shows similarity to human endogenous retrovirus (HERV-L) gag sequences and is closely related to mouse endogenous retroviruses (MuERV-L), suggesting an endogenous origin.

Purpose of the Study:

  • To investigate the evolutionary origins and phylogenetic relationships of the Fv1 gene.
  • To explore the evolutionary pressures acting on the Fv1 gene by comparing its sequence data with other genes.

Main Methods:

  • Polymerase chain reaction (PCR) primers were designed to amplify the coding region of both Fv1 alleles (n and b).
  • Sequences were amplified from various species within the genus Mus and sequenced.
  • Phylogenetic analysis was performed using the obtained Fv1 sequences and compared with trees from other genes.

Main Results:

  • Homologous Fv1 genes were found in Mus species that evolved after divergence from Rattus, but absent in Rattus.
  • A phylogenetic tree based on Fv1 sequences differed significantly from trees based on other genes.
  • Non-synonymous changes occurred twice as frequently as synonymous changes in Fv1, deviating from typical structural gene behavior.

Conclusions:

  • The Fv1 gene likely originated from endogenous retroviral sequences.
  • Evidence suggests the Fv1 gene may have undergone horizontal gene transfer.
  • The observed mutation patterns indicate positive Darwinian selection may have acted on the Fv1 gene.

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