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Article
Nature 428, 44-49 (4 March 2004) | ; Received 13 November 2003; Accepted 14 January 2004; Published online 15 February 2004
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Mice cloned from olfactory sensory neurons
Kevin Eggan1,3,4, Kristin Baldwin2,3, Michael Tackett1, Joseph Osborne2,4, Joseph Gogos2, Andrew Chess1, Richard Axel2 & Rudolf Jaenisch1
- Whitehead Institute for Biomedical Research and Department of Biology, Massachusetts Institute of Technology, 9 Cambridge Center, Cambridge, Massachusetts 02142, USA
- Department of Biochemistry and Molecular Biophysics, Howard Hughes Medical Institute, College of Physicians and Surgeons, Columbia University, 701 West 168th Street, New York, New York 10032, USA
- These authors contributed equally to this work
- Present addresses: Department of Physiology and Cellular Biophysics, College of Physicians and Surgeons, Columbia University, 630 West 168th Street, New York, New York 10032, USA (J.O.); Department of Molecular and Cellular Biology, Harvard University, 7 Divinity Avenue, Cambridge, Massachusetts 02138, USA (K.E.)
Correspondence to: Andrew Chess1Rudolf Jaenisch1 Email: jaenisch@wi.mit.edu
Email: achess@wi.mit.edu
Abstract
Cloning by nuclear transplantation has been successfully carried out in various mammals, including mice. Until now mice have not been cloned from post-mitotic cells such as neurons. Here, we have generated fertile mouse clones derived by transferring the nuclei of post-mitotic, olfactory sensory neurons into oocytes. These results indicate that the genome of a post-mitotic, terminally differentiated neuron can re-enter the cell cycle and be reprogrammed to a state of totipotency after nuclear transfer. Moreover, the pattern of odorant receptor gene expression and the organization of odorant receptor genes in cloned mice was indistinguishable from wild-type animals, indicating that irreversible changes to the DNA of olfactory neurons do not accompany receptor gene choice.
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