mdm2 deletion does not alter growth characteristics of p53-deficient embryo fibroblasts.
The mdm2 gene encodes a protein that is necessary for the negative regulation of p53 function in vivo. Deletion of the mdm2 gene in mice results in early embryonic death while concomitant mdm2 and p53 deletion results in viable offspring. The viability of these mice prompted us to ask if MDM2 had an important growth regulatory function independent of p53. We established mouse embryo fibroblasts null for both p53 and mdm2 and compared them with p53-null fibroblasts. The cells did not differ in their growth rates or their ability to bypass a G1 arrest. Both cell lines formed colonies efficiently when plated at low density and showed a similar degree of genetic instability. Thus, the analysis of several growth parameters indicated no difference between p53-null and p53/mdm2-null cell lines.
McMasters
K M
KM
Department of Surgical Oncology, University of Texas MD Anderson Cancer Center, Houston 77030, USA.
Montes de Oca Luna
R
R
Peña
J R
JR
Lozano
G
G
D000818:Animals; D002453:Cell Cycle; D002455:Cell Division / Q000235:genetics*; D004622:Embryo, Mammalian / Q000166:cytology* / Q000378:metabolism; D005838:Genotype; D051379:Mice; D008810:Mice, Inbred C57BL; D009154:Mutation; D009687:Nuclear Proteins; D011518:Proto-Oncogene Proteins / Q000235:genetics*; D051736:Proto-Oncogene Proteins c-mdm2; D017384:Sequence Deletion; D016159:Tumor Suppressor Protein p53 / Q000235:genetics*
D009687:Nuclear Proteins; D011518:Proto-Oncogene Proteins; D016159:Tumor Suppressor Protein p53; C497207:Mdm2 protein, mouse; D051736:Proto-Oncogene Proteins c-mdm2