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Id2 Required for Myc Signals

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Science's STKE  10 Oct 2000:
Vol. 2000, Issue 53, pp. tw6
DOI: 10.1126/stke.2000.53.tw6

The helix-loop-helix protein family member Id2 has been implicated in regulation of cell proliferation, differentiation, and apoptosis. Id2 is thought to act by interacting with basic helix-loop-helix transcription factors and inhibiting their interaction with DNA. Lasorella et al. provide new insight into how cell proliferation is influenced by Id2. They show that Id2 is required for oncoproteins of the Myc family to cause cell proliferation. Neuroblastoma cells often contain extra copies of the N-myc gene, and Lasorella et al. show that the Id2 gene is a direct target of N-Myc. The excess Id2 produced in neuroblastoma cells appears to sequester the active form of tumor supressor retinoblastoma protein (Rb). Disruption of the Rb pathway is characteristic of cancer cells, and overexpression of Myc or Id2 provides a potential mechanism by which this can occur without alterations in the Rb pathway itself. When normal amounts of Id2 are present in cells, Id2 appears to act as a target of Rb. Animals that lack Rb die during embryogenesis, but Lasorella et al. report that Id2-deficient mice develop further before dying at birth. Rb, in this case, may inhibit the action of Id2 on its normal targets. Thus loss of Id2 can rescue phenotypic effects of the loss of Rb.

Lasorella, A., Noseda, M. Beyna, M., and Iavarone, A. (2000) Id2 is a retinoblastoma protein target and mediates signalling by Myc oncoproteins. Nature 407: 592-598. [Online Journal]

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