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Cell cycle dependent regulation of cdc2 mRNA in mouse fibroblasts: Requirement of protein synthesis and of continued mitogenic stimulation
Author(s) -
BuquetFagot Christine,
Fagot Dominique,
Mester Jan
Publication year - 1993
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041550126
Subject(s) - cycloheximide , cyclin dependent kinase 1 , messenger rna , protein biosynthesis , microbiology and biotechnology , cell cycle , biology , gene expression , phorbol , cell culture , chemistry , gene , biochemistry , signal transduction , protein kinase c , genetics
Abstract In the chemically transformed mouse fibroblasts (BP‐A31) placed in a serum‐free medium, the cdc2 mRNA content decreases in parallel with the cessation of [ 3 H]thymidine incorporation. Extinction of the cdc2 gene expression is also observed in BP‐A31 cells overexpressing the human c‐myc oncogene. At quies‐cence, the cdc2 gene expression can be reinduced with serum or with other mitogens such as insulin or 12‐O‐tetradecanoyl phorbol 13‐acetate (TPA). The kinetics of induction is characterized by a lag period which differs according to the mitogen used and reflects the length of the G1 phase (4–6 h with insulin or serum, 9–12 h with TPA). The cdc2 mRNA accumulation is prevented when protein synthesis is blocked with cycloheximide, also if the drug is added at a time when the synthesis of cdc2 mRNA is already under way. Similarly, removal of the mitogen leads to a cessation of the cdc2 mRNA accumulation. These results suggest that the increased expression of the cdc2 gene is mediated by (a) short‐lived, growth factor‐regulated protein(s). © 1993 Wiley‐Liss, Inc.