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Molecular and Cellular Biology, September 1998, p. 5435-5444, Vol. 18, No. 9
0270-7306/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Id2 Promotes Apoptosis by a Novel Mechanism Independent of Dimerization to Basic Helix-Loop-Helix Factors

Monica Florio,1 Maria-Clemencia Hernandez,1 Hui Yang,2 Hui-Kuo Shu,1,dagger John L. Cleveland,2,3 and Mark A. Israel1,*

Preuss Laboratory for Molecular Neuro-Oncology, Brain Tumor Research Center, Department of Neurological Surgery, University of California, San Francisco, California 94143-05201; Department of Biochemistry, St. Jude Children's Research Hospital, Memphis, Tennessee 381052; and Department of Biochemistry, University of Tennessee, Memphis, Tennessee 381633

Received 17 February 1998/Returned for modification 23 March 1998/Accepted 18 June 1998

Members of the helix-loop-helix (HLH) family of Id proteins have demonstrated roles in the regulation of differentiation and cell proliferation. Id proteins inhibit differentiation by HLH-mediated heterodimerization with basic HLH transcription factors. This blocks their sequence-specific binding to DNA and activation of target genes that are often expressed in a tissue-specific manner. Id proteins can also act as positive regulators of cell proliferation. The different mechanisms proposed for Id-mediated promotion of entry into S phase also involve HLH-mediated interactions affecting regulators of the G1/S transition. We have found that Id2 augments apoptosis in both interleukin-3 (IL-3)-dependent 32D.3 myeloid progenitors and U2OS osteosarcoma cells. We could not detect a similar activity for Id3. In contrast to the effects of Id2 on differentiation and cell proliferation, Id2-mediated apoptosis is independent of HLH-mediated dimerization. The ability of Id2 to promote cell death resides in its N-terminal region and is associated with the enhanced expression of a known component of the programmed cell death pathway, the proapoptotic gene BAX.

* Corresponding author. Mailing address: Brain Tumor Research Center, Department of Neurosurgery, University of California San Francisco, HSE 722, 513 Parnassus Ave., San Francisco, CA 94143-0520. Phone: (415) 476-6662. Fax: (415) 476-0388. E-mail: israel{at}cgl.ucsf.edu.

dagger Present address: Department of Radiation Oncology, University of California, San Francisco, CA 94143-0226.

Molecular and Cellular Biology, September 1998, p. 5435-5444, Vol. 18, No. 9
0270-7306/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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