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Molecular and Cellular Biology, March 2004, p. 2083-2090, Vol. 24, No. 5
0270-7306/04/$08.00+0     DOI: 10.1128/MCB.24.5.2083-2090.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Id2 Is Dispensable for Myc-Induced Epidermal Neoplasia

Daniel J. Murphy,1 Lamorna Brown Swigart,1 Mark A. Israel,2 and Gerard I. Evan1*

Cancer Research Institute, University of California at San Francisco, San Francisco, California 94143-0875,1 Norris Cotton Cancer Center, Lebanon, New Hampshire 037562

Received 17 October 2003/ Accepted 9 December 2003

We have previously described a transgenic mouse model of epidermal neoplasia wherein expression of a switchable form of c-Myc, MycERTAM, is targeted to the postmitotic suprabasal keratinocytes of murine epidermis via the involucrin promoter. Sustained activation of c-MycERTAM results in a progressive neoplastic phenotype characterized by aberrant ectopic proliferation and delayed differentiation of suprabasal keratinocytes, culminating in papillomatosis. Transcription of the Id2 gene is regulated by Myc family proteins. Moreover, Id2 is implicated as a pivotal determinant of cell fate in multiple lineages and has a demonstrated role in mediating Myc-dependent cell proliferation in vitro through its interaction with retinoblastoma protein. Using Id2 nullizygous mice, we assessed in vivo the requirement for Id2 in mediating Myc-induced papilloma formation in skin. We show that absence of Id2 has no discernible impact on any measurable attribute of Myc function or on the timing or extent of eventual tumor formation. Thus, our data argue against any essential role for Id2 in mediating Myc action in vivo.

* Corresponding author. Mailing address: 2340 Sutter St., Rm. S-236, San Francisco, CA 94115. Phone: (415) 514-1570. Fax: (415) 502-6779. E-mail: gevan{at}cc.ucsf.edu.

Molecular and Cellular Biology, March 2004, p. 2083-2090, Vol. 24, No. 5
0022-538X/04/$08.00+0     DOI: 10.1128/MCB.24.5.2083-2090.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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