Article

Nature 428, 44-49 (4 March 2004) | ; Received 13 November 2003; Accepted 14 January 2004; Published online 15 February 2004

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

  1. Whitehead Institute for Biomedical Research and Department of Biology, Massachusetts Institute of Technology, 9 Cambridge Center, Cambridge, Massachusetts 02142, USA
  2. 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
  3. These authors contributed equally to this work
  4. 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

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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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