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mTor is required for hypertrophy of Pten-deficient neuronal soma in vivo
Abstract
The mechanisms that regulate mammalian cell size during development and homeostatic maintenance are poorly understood. The tumor suppressor Pten is required for correct maintenance of mammalian neuronal soma size. Selective inactivation of Pten in postnatal granule neurons of the cerebellum and dentate gyrus in mouse causes cell-autonomous hypertrophy as well as more complex phenotypes, including progressive macrocephaly, seizures, and premature death. To determine the contribution of mTor signaling to Pten-mediated growth regulation in the mammalian nervous system, we treated Pten conditional knockout mice with CCI-779, a specific mTor inhibitor. mTor inhibition decreased the seizure frequency and death rate in Pten mutant mice, prevented the increase in Pten-deficient neuronal soma size in young mice, and reversed neuronal soma enlargement in adult mice. mTor inhibition did not decrease the size of wild-type adult neurons. Thus, mTor is required for neuronal hypertrophy downstream of Pten deficiency, but is not required for maintenance of normal neuronal soma size. mTOR inhibitors may be useful therapeutic agents for diseases in brain resulting from PTEN deficiency such as Lhermitte–Duclos disease or glioblastoma multiforme.
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“a null mutation of the *Pten* gene caused some of the same phenotypes described for the *Tsc1*cc–αCaMKII-Cre mice”
From Reversal of learning deficits in a Tsc2+/− mouse model of tuberous sclerosis (2008) · cites this paper as [21]
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“and mTOR antagonists also rescued these phenotypes[21]”
From Reversal of learning deficits in a Tsc2+/− mouse model of tuberous sclerosis (2008) · cites this paper as [21]
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Metadata
- Authors
- Kwon, C.-H., Zhu, X., Zhang, J., & Baker, S. J.
- Affiliations
- Department of Developmental Neurobiology, St. Jude Children's Research Hospital, 332 North Lauderdale, Memphis, TN 38105; and Department of Pathology, University of Tennessee, Memphis, TN 38105
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2003-10-08
- Volume
- 100
- Issue
- 22
- Pages
- 12923-12928
- ISSN
- 0027-8424
- 1091-6490
- Cited by
- 235
- References
- 5
- Language
- en
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