Abstract
The G1 D-type cyclins, in conjunction with cyclin-dependent kinases Cdk4 andCdk6, play key roles in the execution of mitogen-induced cellular proliferation. TRIPBr1,a member of the TRIP-Br family of transcriptional regulators, has been implicated inthe regulation of Cdk4/cyclin D activity. To further elucidate the functional role(s) of theTRIP-Br proteins in mitogenic signaling, we have developed the synthetic DNA enzymesE-Br1 and E-Br2 to specifically knock down the serum-inducible expression of TRIP-Br1and TRIP-Br2, respectively, in WI-38 human fibroblasts in culture, as well as generatedTRIP-Br2 null primary embryonic fibroblasts from a novel TRIP-Br2 knockout mousemodel. Both strategies consistently reveal that ablation of TRIP-Br1 or TRIP-Br2expression disrupts mitogenic signaling in a manner that suppresses serum-induced cyclinE expression, S phase entry and cellular proliferation. We conclude that both TRIP-Br1and TRIP-Br2 are required for proper transduction of mitogenic signals and execution ofserum-inducible cell cycle progression.
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