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Titolo:
Dissection of NT3 functions in vivo by gene replacement strategy
Autore:
Coppola, V; Kucera, J; Palko, ME; Martinez-De Velasco, J; Lyons, WE; Fritzsch, B; Tessarollo, L;
Indirizzi:
NCI, Neural Dev Grp, Mouse Canc Genet Program, Frederick, MD 21701 USA NCI Frederick MD USA 21701 se Canc Genet Program, Frederick, MD 21701 USA Boston Univ, Sch Med, Dept Neurol, Boston, MA 02118 USA Boston Univ Boston MA USA 02118 ch Med, Dept Neurol, Boston, MA 02118 USA Creighton Univ, Dept Biomed Sci, Omaha, NE 68178 USA Creighton Univ OmahaNE USA 68178 v, Dept Biomed Sci, Omaha, NE 68178 USA
Titolo Testata:
DEVELOPMENT
fascicolo: 21, volume: 128, anno: 2001,
pagine: 4315 - 4327
SICI:
0950-1991(200111)128:21<4315:DONFIV>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
NERVE GROWTH-FACTOR; MUSCLE SENSORY NEURONS; DORSAL-ROOT-GANGLIA; NEUROTROPHIC FACTOR; SIGNAL-TRANSDUCTION; MESSENGER-RNA; INNER-EAR; IN-VIVO; TARGET INNERVATION; PRECURSOR CELLS;
Keywords:
NT3; BDNF; TrkA; TrkB; TrkC; DRG; cochlea; sensory neurons; mouse;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
61
Recensione:
Indirizzi per estratti:
Indirizzo: Tessarollo, L NCI, Neural Dev Grp, Mouse Canc Genet Program, Frederick, MD21701 USA NCI Frederick MD USA 21701 Program, Frederick, MD 21701 USA
Citazione:
V. Coppola et al., "Dissection of NT3 functions in vivo by gene replacement strategy", DEVELOPMENT, 128(21), 2001, pp. 4315-4327

Abstract

The development of the peripheral nervous system is governed in part by a family of neurotrophic factors that signal through Trk tyrosine kinase receptors. Neurotrophin 3 (NT3) ablation in mice causes a more severe neuronal phenotype than deletion of its receptor TrkC, suggesting that NT3 acts alsothrough other non-preferred Trk receptors. To study the role of low-affinity ligand receptor interactions in vivo, we have replaced the Nt3 gene withthe gene for brain-derived neurotrophic factor (BDNF), a TrkB ligand. As in NT3 and TrkC null mice, the proprioception system of these mutants failedto assemble. However, sensory fiber projections in the embryonic spinal cord suggest chemotropic effects of BDNF in vivo. In the dorsal root ganglia,the developmental dynamic of neuron numbers demonstrates that NT3 is required for activation of TrkB during neurogenesis and that TrkA is required during target tissue innervation. In the inner ear, the ectopic BDNF rescued the severe neuronal deficits caused by NT3 absence, indicating that TrkB and TrkC activate equivalent pathways to promote survival of cochlear neurons. However, specific increased innervation densities suggest unique functions for BDNF and NT3 beyond promoting neuronal survival. This mouse model hasallowed the dissection of specific spatiotemporal Trk receptor activation by NT3. Our analysis provides examples of how development can be orchestrated by complex high- and low-affinity interactions between ligand and receptor families.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/12/20 alle ore 14:17:43