Shiels A, Griffin C S
Department of Haematology, St Mary's Hospital Medical School, Imperial College of Science Technology and Medicine, London, UK.
Curr Eye Res. 1993 Oct;12(10):913-21. doi: 10.3109/02713689309020398.
Immunocytochemistry fails to detect expression of the lens major intrinsic protein (MIP) in 16-day embryos of the congenitally cataractous mouse, CAT, which inherits a dominant mutation assigned to the distal end of mouse chromosome 10. In situ hybridisation, however, detects MIP mRNA in CAT embryo lens fibre cells at a level approximating 60% of that detected in embryonic lens fibres of the non-cataractous MF1 mouse. Northern blot hybridisation reveals that the most abundant MIP mRNA transcript in the adult CAT lens is truncated when compared to that in the adult MF1 lens. The results are consistent with a cataractogenic mutation in the mouse gene for MIP (Mip) which has also been mapped to the distal end of mouse chromosome 10.
免疫细胞化学未能在先天性白内障小鼠CAT的16天胚胎中检测到晶状体主要内在蛋白(MIP)的表达,该小鼠继承了一个位于小鼠10号染色体远端的显性突变。然而,原位杂交检测到CAT胚胎晶状体纤维细胞中的MIP mRNA水平约为非白内障MF1小鼠胚胎晶状体纤维中检测到水平的60%。Northern印迹杂交显示,与成年MF1晶状体相比,成年CAT晶状体中最丰富的MIP mRNA转录本被截断。这些结果与小鼠MIP基因(Mip)中的致白内障突变一致,该基因也被定位到小鼠10号染色体的远端。