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Science 29 September 1989:
Vol. 245. no. 4925, pp. 1496 - 1499
DOI: 10.1126/science.2551043
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Articles

Science, Vol 245, Issue 4925, 1496-1499
Copyright © 1989 by American Association for the Advancement of Science

articles

Transformation by v-sis occurs by an internal autoactivation mechanism

BE Bejcek, DY Li, and TF Deuel

Department of Medicine, Jewish Hospital, Washington University Medical Center, St. Louis, MO 63110.

Transformation by the v-sis oncogene appears to require an interaction of its protein product, p28v-sis, with the receptor for the platelet-derived growth factor (PDGF). However, this interaction may not occur at the cell surface as predicted by the autocrine hypothesis because phenotypic transformation was not reversed by incubation of SSV-NRK cells with antisera to PDGF and because morphological transformation did not occur when nontransformed NRK cells were cultured continuously with p28v-sis. A mutant of the wild-type v-sis gene was constructed that encodes a v-sis protein targeted for retention within the endoplasmic reticulum and Golgi. NRK cells expressing the mutant v-sis gene did not secrete any detectable v-sis protein but were as fully transformed as wild-type v-sis transfectants. The results support a mechanism of transformation by v-sis in which internal activation of the PDGF receptor occurs before expression of either p28v-sis or the PDGF receptor at the cell surface.


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