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Cell Growth & Differentiation Vol. 13, 215-225, May 2002
© 2002 American Association for Cancer Research

Specificity of E2F1, E2F2, and E2F3 in Mediating Phenotypes Induced by Loss of Rb1

Harold I. Saavedra, Lizhao Wu, Alain de Bruin, Cynthia Timmers, Thomas J. Rosol, Michael Weinstein, Michael L. Robinson and Gustavo Leone2

Human Cancer Genetics Program, Department of Molecular Virology, Immunology and Medical Genetics and Departments of Molecular Genetics [H. I. S., L. W., A. d. B., C. T., M. W., G. L.], Veterinary Biosciences [A. d. B., T. J. R.], and Pediatrics [M. L. R.], and Division of Molecular and Human Genetics, Children’s Research Institute [M. L. R.], The Ohio State University, Columbus, Ohio 43210

The Rb/E2F pathway plays a critical role in the control of cellular proliferation. Here, we report that E2F1, E2F2, and E2F3 make major individual contributions toward the in vivo phenotypic consequences of Rb deficiency. In the developing lens of Rb-/- embryos, loss of E2F1, E2F2, or E2F3 reduces the unscheduled proliferation of fiber cells, with the loss of E2F3 having the most pronounced effect. In Rb-deficient retinas, all three E2Fs contribute equally to the ectopic proliferation of postmitotic neuronal cells. In contrast, E2F1 is unique in mediating apoptosis in both Rb-/- lenses and retinas. In the central nervous system, loss of E2F1 or E2F3 can almost completely eliminate the ectopic DNA replication and apoptosis observed in Rb-/- embryos, and loss of E2F2 partially reduces the unscheduled DNA replication and has no effect on apoptosis. These results provide clear evidence for functional specificity among E2Fs in the control of Rb-dependent proliferation and apoptosis in a tissue-specific manner.




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Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cell Growth & Differentiation
Copyright © 2002 by the American Association of Cancer Research.