Abstract:
:The transforming growth factor betas (TGFbetas) are context-dependent regulators of neurons in vitro, but their physiological functions in the brain are unclear. Haploinsufficiency of either Tgfbeta1 or Tgfbeta2 leads to age-related deterioration of neurons, but the development of the brain is normal in the full absence of either of these genes. However, some individuals with mis-sense mutations of TGFbeta receptors are mentally retarded, suggesting that the TGFbeta isoforms can compensate for each other during brain development. This possibility was tested by generating mice (NSE x PTR) with neuron-specific expression of a dominant-negative inhibitor of TGFbeta signaling. The NSE x PTR mice with a FVBxC57Bl/6 genetic background were viable and developed normally despite strong neuronal expression of the inhibitor of TGFbeta signaling. Their cerebella were of normal size and contained normal numbers of neurons. When the genetic background of the mice was changed to C57BL/6, the phenotype of the mice became neonatal lethal, with the neonates exhibiting various malformations. The malformations correlated with sites of non-neuronal expression of the transgenes and included facial dysmorphogenesis, incomplete closure of the ventral body wall and absence of intestinal motility. The C57BL/6 Tgfbm1-3 alleles, which modulate the phenotype of Tgfbeta1(-/-) mice, were not major determinants of the NSE x PTR phenotype. The data suggest that the development of the cerebellum is insensitive to the level of TGFbeta signaling, although this may be dependent on the genetic background.
journal_name
Cell Mol Neurobioljournal_title
Cellular and molecular neurobiologyauthors
Asano Y,Koishi K,Frugier T,McLennan ISdoi
10.1007/s10571-009-9354-xsubject
Has Abstractpub_date
2009-07-01 00:00:00pages
621-33issue
5eissn
0272-4340issn
1573-6830journal_volume
29pub_type
杂志文章abstract::Exposure to stress induces profound physiological and behavioral changes in the organisms and some of these changes may be important regarding stress-induced pathologies and animal models of psychiatric diseases. Consequences of stress are dependent on the duration of exposure to stressors (acute, chronic), but also o...
journal_title:Cellular and molecular neurobiology
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