Targeted mutation in the neurotrophin-3 gene results in loss of muscle sensory neurons

Lino Tessarollo, Kristine S Vogel, Mary Ellen Palko, Susan W. Reid, Luis F. Parada

Research output: Contribution to journalArticle

181 Citations (Scopus)

Abstract

Neurotrophin 3 (NT-3) is one of four related polypeptide growth factors that share structural and functional homology to nerve growth factor (NGF). NT-3 and its receptor, called neurotrophic tyrosine kinase receptor type 3 (Ntrk3; also called TrkC), are expressed early and throughout embryogenesis. We have inactivated the NT-3 gene in embryonic stem (ES) cells by homologous recombination. The mutated allele has been transmitted through the mouse germ line, and heterozygote intercrosses have yielded homozygous mutant newborn pups. The NT-3-deficient mutants fail to thrive and exhibit severe neurological dysfunction. Analysis of mutant embryos uncovers loss of Ntrk3/TrkC-expressing sensory neurons and abnormalities at early stages of sensory neuronal development. NT-3-deficient mice will permit further study of the role of this neurotrophin in neural development.

Original languageEnglish (US)
Pages (from-to)11844-11848
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume91
Issue number25
DOIs
StatePublished - Dec 6 1994
Externally publishedYes

Fingerprint

Neurotrophin 3
Sensory Receptor Cells
trkC Receptor
Muscles
Mutation
Genes
Embryo Loss
Homologous Recombination
Nerve Growth Factors
Nerve Growth Factor
Embryonic Stem Cells
Heterozygote
Germ Cells
Embryonic Development
Intercellular Signaling Peptides and Proteins
Alleles
Peptides

ASJC Scopus subject areas

  • Genetics
  • General

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Targeted mutation in the neurotrophin-3 gene results in loss of muscle sensory neurons. / Tessarollo, Lino; Vogel, Kristine S; Palko, Mary Ellen; Reid, Susan W.; Parada, Luis F.

In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 91, No. 25, 06.12.1994, p. 11844-11848.

Research output: Contribution to journalArticle

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