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Growth factor‐induced cell division is paralleled by translocation of G iα to the nucleus
Author(s) -
Crouch Michael F.
Publication year - 1991
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.5.2.1900794
Subject(s) - mitosis , microbiology and biotechnology , cell division , nucleus , biology , chromosomal translocation , receptor , cell nucleus , signal transduction , cell , endocrinology , medicine , biochemistry , gene
Induction of mitosis by certain growth factors is inhibited by pertussis toxin, indicating that the GTP‐binding protein, G i , is involved in receptor signal transduction to initiate cell division. However, the substrates of receptor‐activated G i that are involved in mitosis have not been determined. The present study has examined whether G i may directly modulate cell division by receptor‐induced subcellular translocation of the α subunit of G i (G iα ). Insulin and EGF, particularly when added together or in combination with phorbol dibutyrate (PdBu), induced a rapid (1–4 h) redistribution of G iα from the plasma membrane to perinuclear sites in the cell. After 2 days of stimulation, G iα had translocated into the nucleus of dividing cells and bound specifically to the separating chromatin of dividing nuclei. Unstimulated cells did not display translocation of G iα . This demonstrates a direct involvement of G iα in cell division, which provides an apparently uninterrupted link from growth factor receptor to nucleus.—Crouch, M. F. Growth factor‐induced cell division is paralleled by translocation of G iα to the nucleus. FASEB J. 5: 200–206; 1991.