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Molecular and Cellular Biology, October 2006, p. 7145-7154, Vol. 26, No. 19
0270-7306/06/$08.00+0     doi:10.1128/MCB.00476-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Characterization of R-Ras3/M-Ras Null Mice Reveals a Potential Role in Trophic Factor Signaling{dagger}

Nelson Nuñez Rodriguez, Ivy N. L. Lee, Asoka Banno, Hui F. Qiao, Rui F. Qiao, Zhong Yao, Thuong Hoang, Alec C. Kimmelman,{ddagger} and Andrew M.-L. Chan*

Department of Oncological Sciences, The Mount Sinai School of Medicine, New York, New York 10029

Received 17 March 2006/ Returned for modification 28 April 2006/ Accepted 7 July 2006

R-Ras3/M-Ras is a member of the RAS superfamily of small-molecular-weight GTP-binding proteins. Previous studies have demonstrated high levels of expression in several regions of the central nervous system, and a constitutively active form of M-Ras promotes cytoskeletal reorganization, cellular transformation, survival, and differentiation. However, the physiological functions of M-Ras during embryogenesis and postnatal development have not been elucidated. By using a specific M-Ras antibody, we demonstrated a high level of M-Ras expression in astrocytes, in addition to neurons. Endogenous M-Ras was activated by several trophic factors in astrocytes, including epidermal growth factor (EGF), basic fibroblast growth factor, and hepatocyte growth factor. Interestingly, M-Ras activation by EGF was more sustained compared to prototypic Ras. A mouse strain deficient in M-Ras was generated to investigate its role in development. M-Ras null mice appeared phenotypically normal, and there was a lack of detectable morphological and neurological defects. In addition, primary astrocytes derived from Mras–/– mice did not appear to display substantial alterations in the activation of both the mitogen-activated protein kinase and phosphatidylinositol 3-kinase pathways in response to trophic factors.

* Corresponding author. Mailing address: Mount Sinai School of Medicine, 1425 Madison Ave., Box 1130, New York, NY 10029. Phone: (212) 659-5490. Fax: (212) 849-2446. E-mail: andrew.chan{at}mssm.edu.

{dagger} Supplemental material for this article may be found at http://mcb.asm.org/.

{ddagger} Present address: Harvard Radiation Oncology Program, Harvard Medical School, Boston, MA 02115.

Molecular and Cellular Biology, October 2006, p. 7145-7154, Vol. 26, No. 19
0270-7306/06/$08.00+0     doi:10.1128/MCB.00476-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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