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Department of Morphology, University of Trieste, Via Manzoni, 16, 34138 Trieste [A. M. M.], Institute of Anatomy, University of Bologna, Via Irnerio, 48, 40126 Bologna [A. M. B., L. C.], Institute of Anatomy, University of Ferrara, Via Fossato di Mortara, 66, 44100 Ferrara [L. M. N.], Institute of Anatomy, University of Chieti, Via dei Vestini, 66013 Chieti [L. M.], Institute of Cytomorphology, CNR [L. M. N.], and Laboratory for Electron Microscopy and Cell Biology IOR, Via di Barbiano 1/10, 40136 Bologna [A. O.], Italy, and Department of Molecular and Cellular Physiology, AFRC Institute of Animal Physiology and Genetics Research, Babraham, Cambridge CB2 4AT, United Kingdom [S. G.]
Previous investigations have demonstrated the existence of an autonomous intranuclear inositide cycle endowed with conventional lipid kinases and phospholipase C (PLC) which is the isoform ß in Swiss 3T3 cells, PC12 pheochromocytoma cells, human osteosarcoma SaOS-2 cells, and rat liver. The presence of PLC has been investigated in nuclei of Friend erythroleukemia cells. Both ß and
isoforms are present in these nuclei. When Friend cells undergo terminal erythroid differentiation in the presence of dimethyl sulfoxide the PLCß isoform is down-regulated as shown by immunochemical and immunocytochemical analysis, by determination of enzymatic activity directly and in the presence of neutralizing monoclonal antibodies and also by Northern blot for PLC ß message. By contrast, the amount of PLC
and its activity are unaffected by erythroid differentiation. Thus, the presence of a nuclear PLCß, the activity and expression of which are modulated during differentiation of erythroleukemia cells, implicates a role for nuclear phosphoinositide signaling in the processes of cell determination and indicates the nuclear PLCß as a key enzyme of the cycle in relation to the erythroid differentiative commitment of murine erythroleukemia cells.
1 This work was supported by Italian CNR Grants PF IG and PF ACRO and by the AFRC International Scientific Interchange Scheme.
2 To whom requests for reprints should be addressed.
Received 1/21/94. Accepted 4/ 5/94.
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