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Essential Role for Nuclear Phospholipase C ß₁ in Insulin-like Growth Factor I-induced Mitogenesis¹

Institute of Human Anatomy, University of Bologna, Via Irnerio 48, I-40126 Bologna, Italy [L. M., A. M. B., S. R., L. C.]; CNR Cytomorphology Institute and Laboratory of Cell Biology and Electron Microscopy, Istituti Ortopedici Rizzoli, 40136 Bologna, Italy [A. B., I. F.]; Department of Molecular Medicine, School of Medicine, University of Auckland, New Zealand [R. S. G.]; and Laboratory of Cell Signaling, National Heart, Lung, and Blood Institute, NIH, Bethesda, Maryland 20892 [S-G. R.]

The nucleus has been shown to be a site for the inositol lipid cycle that can be affected by treatment of quiescent cells with growth factors such as insulin-like growth factor I (IGF-I). Indeed, the exposure of Swiss 3T3 cells to IGF-I results in a rapid and transient increase in nuclear phospholipase C (PLC) ß₁ activity. In addition, several other reports have shown the involvement of PLC ß₁ in nuclear signaling in different cell types. Although the demonstration of phosphatidylinositol 4-phosphate and phosphatidylinositol 4,5-bisphosphate hydrolysis by nuclear PLC ß₁ established the existence of nuclear PLC signaling, the significance of this autonomous pathway in the nucleus has yet to be thoroughly clarified. By inducing both the inhibition of PLC ß₁ expression by antisense RNA and its overexpression, we show that this nuclear PLC is essential for the onset of DNA synthesis following IGF-I stimulation of quiescent Swiss 3T3 cells.

¹ This work was supported by the Italian Association for Cancer Research (AIRC).

² To whom requests for reprints should be addressed. Phone: 39 51 244467; Fax: 39 51 251735.

Received 1/24/97. Accepted 4/22/97.

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