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J. Cell Biol.,
Volume 141, Number 2, April 20, 1998 503-514
* Department of Biology, Center for Cancer Research, Proliferation in mammalian cells is controlled primarily in the G1-phase of the cell cycle
through the action of the G1 cyclin-dependent kinases,
CDK4 and CDK2. To explore the mechanism of cellular response to extrinsic factors, specific loss of function
mutations were generated in two negative regulators of
G1 progression, p21 and pRB. Individually, these mutations were shown to have significant effects in G1 regulation, and when combined, Rb and p21 mutations caused more profound defects in G1. Moreover, cells
deficient for pRB and p21 were uniquely capable of anchorage-independent growth. In contrast, combined
absence of pRB and p21 function was not sufficient to
overcome contact inhibition of growth nor for tumor
formation in nude mice. Finally, animals with the genotype Rb+/ Howard Hughes Medical Institute, Massachusetts Institute of
Technology, Cambridge, Massachusetts 02139; and § Department of Pathology, Tufts University, Boston, Massachusetts 02111
;p21/ succumbed to tumors more rapidly
than Rb+/ mice, suggesting that in certain contexts
mutations in these two cell cycle regulators can cooperate in tumor development.
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