van Leeuwen F W, Evans D A, Meloen R, Sonnemans M A
Graduate School of Neurosciences Amsterdam, Netherlands Institute for Brain Research.
Brain Res. 1994 Jan 28;635(1-2):328-30. doi: 10.1016/0006-8993(94)91456-7.
In the homozygous Brattleboro rat (di/di) a single base deletion in the vasopressin (VP) gene causes diabetes insipidus, resulting in the synthesis of a VP precursor with a different C-terminus. We reported previously that a small number of post-mitotic VP neurons in di/di rats undergo a switch to a heterozygous phenotype, suggesting the existence of VP mRNAs with a restored reading frame coding for a normal VP precursor. In the present study we report that the increase in the number of these revertant cells declines after 79 weeks of age. Furthermore, we provide evidence that the neurophysin (NP) moiety in solitary neurons is different from normal NP. Comparing the immunoreactivities of two different NP antibodies we deduced that the restoration of the reading frame may take place downstream of the deletion between amino acids 75 and 93 of the VP-NP.
在纯合的布拉德福德大鼠（di/di）中，血管加压素（VP）基因中的单个碱基缺失导致尿崩症，从而合成具有不同C末端的VP前体。我们之前报道过，di/di大鼠中少数有丝分裂后的VP神经元会转变为杂合表型，这表明存在具有恢复读码框的VP mRNA，其编码正常的VP前体。在本研究中，我们报告这些回复细胞数量的增加在79周龄后下降。此外，我们提供证据表明，孤立神经元中的神经垂体素（NP）部分与正常NP不同。通过比较两种不同NP抗体的免疫反应性，我们推断读码框的恢复可能发生在VP-NP氨基酸75至93之间缺失的下游。
