The exon encoding the extracellular domain was replaced with sequence encoding the transmembrane domain of the human NTRK1 receptor followed by lacZ and neo genes. The deletion was designed to generate a chimeric protein in which the fibronectin type III-like domains were absent from the extracellular region, leaving only 116 carboxy terminal residues intact, and in which the entire cytoplasmic region was replaced by lacZ. LacZ activity was detected during embryonic stages and undetected during postnatal development.