Complementation of Myc-dependent cell proliferation by cDNA expression library screening.
The targeted knockout of the c-myc gene from rat fibroblasts leads to a stable defect in cell proliferation. We used complex cDNA libraries expressed from retroviral vectors and an efficient sorting procedure to rapidly select for cDNAs that can restore the growth rate of c-myc deficient cells. All of the biologically active cDNAs contained either c-myc or N-myc, suggesting that no other cellular genes can effectively bypass the requirement for c-myc in fibroblast proliferation. This approach provides a powerful screening method for cell cycle changes in genetically defined systems.
Nikiforov
M A
MA
Department of Molecular Biology, Princeton University, New Jersey 08544-1014, USA.
Kotenko
I
I
Petrenko
O
O
Beavis
A
A
Valenick
L
L
Lemischka
I
I
Cole
M D
MD
D000818:Animals; D002455:Cell Division / Q000235:genetics*; D018076:DNA, Complementary / Q000235:genetics*; D005347:Fibroblasts / Q000166:cytology; D015723:Gene Library; D018390:Gene Targeting; D018816:Genes, cdc; D016259:Genes, myc; D005816:Genetic Complementation Test; D006801:Humans; D051379:Mice; D016133:Polymerase Chain Reaction; D016271:Proto-Oncogene Proteins c-myc / Q000502:physiology*; D051381:Rats; D012641:Selection, Genetic
D018076:DNA, Complementary; D016271:Proto-Oncogene Proteins c-myc