MOLECULAR-CLONING, TISSUE DISTRIBUTION, AND EXPRESSION OF THE PROLACTIN RECEPTOR DURING VARIOUS REPRODUCTIVE STATES IN MELEAGRIS-GALLOPAVO

The primary sequence of the prolactin receptor (PRL-R) in turkeys was deduced from a cDNA clone isolated from a kidney cDNA library and from a polymerase chain reaction (PCR) product. The open reading frame of the turkey PRL-R (tPRL-R) predicted an 831-amino acid protein composed of a leader peptide, an extracellular domain, a single transmembrane domain, and an intracellular domain. The extracellular domain containe d two homologous repeat units with 63% amino acid sequence identity to each other. Each repeat unit contained all of the conserved cysteine pairs and a WSXWS motif found in mammalian PRL-Rs. A tPRL-R transcript with a molecular size of about 3000 nucleotides was identified by Nor thern blot analysis. The tPRL-R transcripts were detected in all 26 ti ssues examined using reverse transcriptase PCR (RT-PCR). The pituitary gland, hypothalamus, crop sac, duodenum, and gizzard were found to ex press the highest levels of tPRL-R among the 26 tissues. The expressio n levels of tPRL-R in 17 tissues were compared using semi-quantitative RT-PCR in nonphotostimulated, laying, out-of-lay, incubating, and mat ernal hens, and male birds. In most tissues examined there was no obvi ous relationship between blood levels of PRL, reproductive states, and estimated concentrations of the receptor mRNA. In the pituitary gland and hypothalamus, plasma levels of PRL and levels of tPRL-R transcrip t were inversely correlated. In the hypothalamus, increasing blood lev els of PRL were associated with decreasing levels of the receptor tran script (p less than or equal to 0.05), whereas the opposite was observ ed in the pituitary gland (p less than or equal to 0.05). These findin gs support the hypothesis that PRL itself may participate in the neuro endocrine control of incubation behavior through actions on both the h ypothalamus via a short-loop feedback mechanism and the pituitary glan d via autocrine and/or paracrine effects.