Abstract
Transcription of the murine thymidine kinase gene, which is coregulated with the G1/S phase transition, is activated by changing the binding of protein complexes Yi1 and Yi2 to three upstream DNA motifs. Yi1 is replaced by Yi2 shortly before S phase. Yi1 contains a protein of 110 kDa that binds to the DNA motif sites and may be an underphosphorylated murine retinoblastoma protein, shown by its molecular mass, timing of its activity, and antibody recognition. An H1 kinase related to cdc2 cofractionates with both complexes. We propose that this kinase phosphorylates the murine retinoblastoma protein, releasing transcriptional inhibitions by Yi1 and permitting cell cycle progression. These results provide a cycle-related molecular target for such complexes. They are based on investigations of cycle control in uninfected cells. The Yi complexes are similar but not identical to complexes that include a cellular protein, E2F, that was originally found to bind to adenovirus DNA.
MeSH Terms
Animals
CDC2 Protein Kinase/isolation & purification,metabolism
Cell Line
Cell Nucleus/physiology
DNA-Binding Proteins/isolation & purification,metabolism
G1 Phase/physiology
Gene Expression Regulation, Enzymologic
Humans
Immunoblotting
Macromolecular Substances
Mice
Oligodeoxyribonucleotides
Retinoblastoma Protein/isolation & purification,metabolism
S Phase/physiology
Thymidine Kinase/genetics
Transcription, Genetic
Chemicals
DNA-Binding Proteins
Macromolecular Substances
Oligodeoxyribonucleotides
Retinoblastoma Protein
Thymidine Kinase
CDC2 Protein Kinase
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Dou Q P
Division of Cell Growth and Regulation, Dana-Farber Cancer Institute, Boston, MA 02115.
Markell P J
Pardee A B
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