Schenkein I, Levy M, Bueker ED, Wilson JD.Isoelectric focusing of androgen receptors from wild-type and Tfm mouse kidneys. The androgen receptor of the testicular-feminized (Tfm) mutant mouse is smaller than the wild-type receptor. Young CY, Johnson MP, Prescott JL, Tindall DJ.TfM mutation and masculinization versus feminization of the mouse central nervous system. Characterization of a hormone receptor defect in the androgen-insensitivity mutant. Androgen receptors in mouse kidney: a study of male, female and androgen-insensitive (tfm-y) mice. Cytosol androgen receptor from kidney of normal and testicular feminized (Tfm) mice. Testosterone: a major determinant of extragenital sexual dimorphism. Testosterone-"regulon" in the mouse kidney. X-linked gene for testicular feminization in the mouse. Links to PubMed are also available for Selected References. Get a printable copy (PDF file) of the complete article (1.3M), or click on a page image below to browse page by page. Full textįull text is available as a scanned copy of the original print version. The finding of the unsuspected termination codon and the evidence of internally initiated carboxyl-terminal polypeptides reconcile previous conclusions and account for all known phenotypic properties of the mutation. No other change could be identified by sequencing the complete coding region of Tfm cDNA. Transcriptional impairments of the Tfm gene were ruled out by a quantitative analysis of enzymatically amplified nuclear RNA precursors. Separately initiated carboxyl-terminal polypeptides are synthesized in vitro, starting probably at the in-frame AUG codon 1507-1509, which lies in a favorable context for translation initiation, and at the non-AUG codon 1144-1146. Sequence analysis of the relevant DNA segment disclosed that deletion of a single nucleotide in the hexacytidine stretch at position 1107-1112 alters the reading frame of the messenger and introduces 41 missense amino acids before a premature termination codon at position 1235-1237. However, cell-free translation of RNAs transcribed in vitro from enzymatically amplified overlapping segments of exon 1 revealed a truncated receptor protein and helped to localize the site of premature termination. No structural abnormality could be identified in the coding region of the messenger by a series of RNase-protection assays. The finding of the unsuspected termination codon and the evidence of internally initiated carboxyl-terminal poly-peptides reconcile previous conclusions and account for all known phenotypic properties of the mutation.Testosterone-resistant male mice hemizygous for the X-chromosome-linked mutant gene Tfm express detectable but severely reduced levels of androgen receptor mRNA, amounting to about 10% of the level found in normal male littermates. Testosterone-resistant male mice hemizygous for the X-chromosome-linked mutant gene Tfm express detectable but severely reduced levels of androgen receptor mRNA, amounting to about 10% of the level found in normal male littermates.
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