Genomic organization of prolactin and growth hormone coding sequences in dwarf and normal mice.
The genomic organization of DNA encoding growth hormone (GH) and prolactin (PRL) genes has been investigated in two types of homozygous dwarf mice and their normal counterparts. We have previously shown that dwarf mice of either strain fail to initiate pituitary synthesis of GH or PRL during perinatal development. Analysis by Southern transfer of restriction enzyme-digested DNA and hybridization to 32P-labeled cloned probes derived from bovine GH and rat PRL mRNAs revealed no evidence for deletions or rearrangements in or around the structural genes for GH or PRL in either dwarf genotype. In situ hybridization of the probes to pituitary and liver tissue slices failed to detect specifically hybridizing RNA species in dwarf pituitaries. These findings suggest that the pleiotropic effects of the dwarf mutations, which lead to abnormalities in transcription of the genes or in the processing of transcripts, may be due to blocks in the development of functional somatotrophs and mammotrophs.
D000818:Animals; D001483:Base Sequence; D004247:DNA; D004392:Dwarfism / Q000235:genetics*; D013006:Growth Hormone / Q000235:genetics*; D008099:Liver / Q000032:analysis; D051379:Mice; D009693:Nucleic Acid Hybridization; D010902:Pituitary Gland / Q000032:analysis; D011388:Prolactin / Q000235:genetics*; D012333:RNA, Messenger
D012333:RNA, Messenger; D011388:Prolactin; D013006:Growth Hormone; D004247:DNA