Non-transcriptional control of DNA replication by c-Myc

David Dominguez-Sola, Carol Y. Ying, Carla Grandori, Luca Ruggiero, Brenden Chen, Muyang Li, Denise A. Galloway, Wei Gu, Jean Gautier () and Riccardo Dalla-Favera ()
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David Dominguez-Sola: Institute for Cancer Genetics, Columbia University Medical Center, New York, New York 10032, USA
Carol Y. Ying: Institute for Cancer Genetics, Columbia University Medical Center, New York, New York 10032, USA
Carla Grandori: Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA
Luca Ruggiero: Institute for Cancer Genetics, Columbia University Medical Center, New York, New York 10032, USA
Brenden Chen: Institute for Cancer Genetics, Columbia University Medical Center, New York, New York 10032, USA
Muyang Li: Institute for Cancer Genetics, Columbia University Medical Center, New York, New York 10032, USA
Denise A. Galloway: Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA
Wei Gu: Institute for Cancer Genetics, Columbia University Medical Center, New York, New York 10032, USA
Jean Gautier: Institute for Cancer Genetics, Columbia University Medical Center, New York, New York 10032, USA
Riccardo Dalla-Favera: Institute for Cancer Genetics, Columbia University Medical Center, New York, New York 10032, USA

Nature, 2007, vol. 448, issue 7152, 445-451

Abstract: Abstract The c-Myc proto-oncogene encodes a transcription factor that is essential for cell growth and proliferation and is broadly implicated in tumorigenesis. However, the biological functions required by c-Myc to induce oncogenesis remain elusive. Here we show that c-Myc has a direct role in the control of DNA replication. c-Myc interacts with the pre-replicative complex and localizes to early sites of DNA synthesis. Depletion of c-Myc from mammalian (human and mouse) cells as well as from Xenopus cell-free extracts, which are devoid of RNA transcription, demonstrates a non-transcriptional role for c-Myc in the initiation of DNA replication. Overexpression of c-Myc causes increased replication origin activity with subsequent DNA damage and checkpoint activation. These findings identify a critical function of c-Myc in DNA replication and suggest a novel mechanism for its normal and oncogenic functions.

Date: 2007
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DOI: 10.1038/nature05953

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