The homozygote Brattleboro rat exhibits a hereditary diabetes insipidus due to a deficiency of vasopressin, the antidiuretic hormone. It has previously been shown that in this animal a single nucleotide deletion in the provasopressin gene leads to a mutant precursor with a C-terminal amino acid sequence different from that of the wild-type. However the N-terminal region including the hormone moiety, the processing signal as well as the first two-thirds of the neurophysin is entirely preserved and absence of maturation has to be explained by an additional cause. We show here that the neurohypophysis of the homozygote Brattleboro rat, in contrast to the adenohypophysis, displays a significant decrease in the Lys-Arg processing endopeptidase activity when compared to the heterozygote or the wild-type Wistar. It is suggested that hypothalamic vasopressinergic neurons of the homozygote Brattleboro rat display a deficiency in the processing enzyme in contrast to the oxytocinergic neurons in which processing of prooxytocin is normal.
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December 01 1992
Processing endopeptidase deficiency in neurohypohysial secretory granules of the diabetes insipidus (Brattleboro) rat
R. Acher
R. Acher
1Laboratory of Biological Chemistry, University of Paris VI 96, Boulevard Raspail, 75006 Paris, (France)
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Publisher: Portland Press Ltd
Received:
June 22 1992
Revision Requested:
September 04 1992
Online ISSN: 1573-4935
Print ISSN: 0144-8463
© 1992 Plenum Publishing Corporation
1992
Biosci Rep (1992) 12 (6): 445–451.
Article history
Received:
June 22 1992
Revision Requested:
September 04 1992
Citation
J. Chauyet, Y. Rouille, A. Spang, A. M. Cardine, R. Acher; Processing endopeptidase deficiency in neurohypohysial secretory granules of the diabetes insipidus (Brattleboro) rat. Biosci Rep 1 December 1992; 12 (6): 445–451. doi: https://doi.org/10.1007/BF01122032
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