Nuclear Lipids

Transcriptional Regulation by the Nuclear Phosphoinositide Cycle

Science's STKE  03 Oct 2000:
Vol. 2000, Issue 52, pp. tw7
DOI: 10.1126/stke.2000.52.tw7

The role of the nuclear phosphoinositide cycle remains an unanswered question. Bunney et al. perform careful biochemical analysis of the phosphoinositide species formed from nuclei isolated from plants and show that the phosphatidylinositol 4-kinase (PI4K) activity is extracted with detergents and the phosphatidylinositol 3-kinase (PI3K) activity remains in detergent-resistant or inaccessible structures. Furthermore, an antibody against soybean PI3K recognizes a nuclear epitope that colocalizes with sites of active transcription identified by incorporation of bromo-uracil triphosphate. A second group, Faenza et al., studied the effect of overexpression of two differentially distributed isoforms of phospholipase C-β1 [PLC-β1a (nuclear and cytoplasmic) and PLC-β1b (nuclear)] on progression through the cell cycle in mammalian cells. Overexpression of either of these two isoforms resulted in increased expression of cyclin D3 and cyclin-dependent kinase 4, promoted phosphorylation of retinoblastoma protein (Rb), and increased the DNA-binding activity of E2F even under conditions in which the wild-type cells do not exhibit these characteristics. Each of these effects was eliminated when the nuclear targeting signal of PLC-β1b was inactivated. Together these two papers point to a role for the nuclear phosphoinositide cycle in the regulation of transcription.

Bunney, T.D., Watkins, P.A.C., Beven, A.F., Shaw, P.J., Hernandez, L.E., Lomonossof, G.P., Shanks, M., Peart, J., and Drøbak, B.K. (2000) Association of phosphatidylinositol 3-kinase with nuclear transcription sites in higher plants. Plant Cell 12: 1679-1687. [Abstract] [Full Text]

Faenza, I., Matteucci, A., Manzoli, L., Billi, A.M., Aluigu, M., Peruzzi, D., Vitale, M., Castorina, S., Suh, P.G., and Cocco, L. (2000) A role for nuclear phospholipase Cβ1in cell cycle control. J. Biol. Chem. 275: 30520-30524. [Abstract] [Full Text]