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Molecular and Cellular Biology, June 2000, p. 4106-4114, Vol. 20, No. 11
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Analysis of Fractalkine Receptor CX3CR1 Function by Targeted Deletion and Green Fluorescent Protein Reporter Gene Insertion

Steffen Jung,1,* Julio Aliberti,2 Petra Graemmel,3 Mary Jean Sunshine,1 Georg W. Kreutzberg,3 Alan Sher,2 and Dan R. Littman1

Skirball Institute of Biomolecular Medicine and Howard Hughes Medical Institute New York University Medical Center, New York, New York1; Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland2; and Department of Neuromorphology, Max-Planck-Institute for Neurobiology, Martinsried, Germany3

Received 1 March 2000/Accepted 6 March 2000

The seven-transmembrane receptor CX3CR1 is a specific receptor for the novel CX3C chemokine fractalkine (FKN) (neurotactin). In vitro data suggest that membrane anchoring of FKN, and the existence of a shed, soluble FKN isoform allow for both adhesive and chemoattractive properties. Expression on activated endothelium and neurons defines FKN as a potential target for therapeutic intervention in inflammatory conditions, particularly central nervous system diseases. To investigate the physiological function of CX3CR1-FKN interactions, we generated a mouse strain in which the CX3CR1 gene was replaced by a green fluorescent protein (GFP) reporter gene. In addition to the creation of a mutant CX3CR1 locus, this approach enabled us to assign murine CX3CR1 expression to monocytes, subsets of NK and dendritic cells, and the brain microglia. Analysis of CX3CR1-deficient mice indicates that CX3CR1 is the only murine FKN receptor. Yet, defying anticipated FKN functions, absence of CX3CR1 interferes neither with monocyte extravasation in a peritonitis model nor with DC migration and differentiation in response to microbial antigens or contact sensitizers. Furthermore, a prominent response of CX3CR1-deficient microglia to peripheral nerve injury indicates unimpaired neuronal-glial cross talk in the absence of CX3CR1.

* Corresponding author. Mailing address: Molecular Pathogenesis Program, Skirball Institute of Biomolecular Medicine, New York University Medical Center, 540 First Ave., New York, NY 10016. Phone: (212) 263-6957. Fax: (212) 263-5711. E-mail: jung{at}saturn.med.nyu.edu.

Molecular and Cellular Biology, June 2000, p. 4106-4114, Vol. 20, No. 11
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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