Fpr1 Knockout

Constitutive Knockout

Fpr1 Constitutive Knockout Mouse Model
The NIAID Exchange Program has closed and live production of this model has ceased. This webpage is retained for historical reference, but this model is not available from Taconic.

C57BL/6NTac Background

  • Model #
  • Genotype
  • Nomenclature
  • 4169-F
    C57BL/6NTac-Fpr1tm1Gao N6
  • 4169-M
    C57BL/6NTac-Fpr1tm1Gao N6
N-formylpeptides derive from bacterial and mitochondrial proteins, and bind to specific receptors on mammalian phagocytes. Since binding induces chemotaxis and activation of phagocytesin vitro, it has been postulated that N-formylpeptide receptor signaling in vivo may be important in antibacterial host defense, although direct proof has been lacking. Mice genetically deficient in formyl peptide receptor (FPR-/-) have no obvious developmental defects and do not develop spontaneous infection when derived in specific pathogen-free conditions. This suggests that, under these conditions, FPR is dispensable. However, when challenged with Listeria monocytogenes, FPR-/- mice have accelerated mortality and increased bacterial burden in liver and spleen early after infection, which suggests a role for FPR in host defense, specifically through regulation of innate immunity.


Drs. Ji-Liang Gao and Philip Murphy in the Laboratory of Molecular Immunology, NIAID, made the FPR-/- mouse by targeted gene disruption in 1999. The Fpr1 gene was mutated by replacing a 150 bp DNA fragment in the Fpr1 open reading frame with a neomycin resistance gene. The disrupted Fpr1 gene was introduced to 129/Sv ES cells to create chimeric mice, and then the chimeric founders were backcrossed to C57BL/6NAi mice for 10 generations in the NIAID barrier facility at Taconic. At this point, it was discovered that the C57BL/6NAi line had become contaminated with the IFNγ knockout gene. Line 4169 was then backcrossed to C57BL/6NTac (Taconic B6) for 5 generations in order to eliminate the contaminating gene and put the strain onto the Taconic C57BL/6 subline background.





Initial Publication:

Gao J-L, Lee E, and Murphy PM. (1999) Impaired anti-bacterial host defense in mice lacking the N-formylpeptide receptor. J. Exp. Med., 189: 657-662.


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