Nuclear phosphoinositide specific phospholipase C (PI-PLC)-ß1: a central intermediary in nuclear lipid-dependent signal transduction
A.M. Martelli1,2, R. Fiume1, I. Faenza1, G. Tabellini3, C. Evangelisti1, R. Bortul4, M.Y. Follo1, F. Falà1 and L. Cocco1
1Department of Human Anatomical Sciences and Muscoloskeletal System Physiopathology, Section of Human Anatomy, Cell Signalling Laboratory, University of Bologna, Bologna, Italy, 2Institute for Organ Transplantation and Immunocytology of the Italian National Research Council, Section of Bologna, c/o IOR, Bologna, Italy, 3Department of Biomedical Sciences and Biotechnology, Section of Cytology and Histology, University of Brescia, Brescia, Italy and 4Department Human Morphology, University of Trieste, Trieste, Italy
Offprint requests to: Dr. Alberto M. Martelli, Dipartimento di Scienze Anatomiche Umane e Fisiopatologia dell’Apparato Locomotore, Università di Bologna, via Irnerio 48, 40126 Bologna, Italy. e-mail: amartell@biocfarm.unibo.it
Summary. Several studies have demonstrated the existence of an autonomous intranuclear phospho-inositide cycle that involves the activation of nuclear PI-PLC and the generation of diacylglycerol (DG) within the nucleus. Although several distinct isozymes of PI-PLC have been detected in the nucleus, the isoform that has been most consistently highlighted as being nuclear is PI-PLC-ß1. Nuclear PI-PLC-ß1 has been linked with either cell proliferation or differentiation. Remarkably, the activation mechanism of nuclear PI-PLC-ß1 has been shown to be different from its plasma membrane counterpart, being dependent on phosphorylation effected by p44/42 mitogen activated protein (MAP) kinase. In this review, we report the most up-dated findings about nuclear PI-PLC-ß1, such as the localization in nuclear speckles, the activity changes during the cell cycle phases, and the possible involvement in the progression of myelodisplastic syndrome to acute myeloid leukemia. Histol Histopathol 20, 1251-1260 (2005)
Key words: Nucleus, Phosphoinositides, Proliferation, Differentiation, Myelodisplastic syndromes
DOI: 10.14670/HH-20.1251