Electrophoretic analysis of liver neuraminidase-1 variation in mice and additional evidence concerning the location of NEU-1.
Electrophoretic analysis of liver neuraminidase-1 variation in mice and additional evidence concerning the location of NEU-1.
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小鼠肝脏神经氨酸酶 1 变异的电泳分析以及有关 NEU-1 位置的其他证据。
DOI：
10.1111/j.1744-313x.1986.tb01080.x
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发表时间：
1986
期刊：
影响因子：
--
通讯作者：
David,CS
中科院分区：
文献类型：
--
作者：
Samollow,PB;VandeBerg,JL;Ford,AL;Douglas,TC;David,CS
神经氨酸酶-1（NEU-1）是两种神经氨酸酶同工酶之一，可在小鼠肝脏提取物中通过电泳检测到。通过对SM/J和MA/MyJ自交系的回交分析，以及对B10.SM、B10.SM（22 R）和B10.RVB 3个同源系的NEU-1表型分析，研究了NEU-1变异的遗传规律和控制该变异的基因的连锁关系。数据表明NEU-1受Neu-1控制，Neu-1是一种先前通过其对全组织匀浆中总肝脏神经氨酸酶活性的影响而鉴定的基因。同源菌株的分析显示，所有三种菌株的低活性（SM/J-型：Neu-1α/Neu-1α）NEU-1表型相同。这表明Neu ‐ I位于SM/J‐衍生的H ‐ 2区域的片段中，这是所有三种菌株所共有的：H‐ 2 E α至H ‐2D。此外，我们研究了NEU-1与肝酸性磷酸酶（AP;描述了一种新的分型方法）的表型变异之间的关系，以及与H-2相关的其他几种酶编码基因之间的连锁顺序。在所有可以确信地对AP进行评分的动物中，NEU-1和AP表型一致，这为两种表型均受Neu-1控制的假设提供了支持。6个H-2连锁标记位点的扩增率出乎意料地低，但足以验证Upg-1作为端粒侧翼标记相对于Glo-1、H-2（C4）、Neu-1（Apl）、Ce-2和Pgk-2的位置。
Neuraminidase‐1 (NEU‐1) is one of two neuraminidase isozymes which can be detected electrophoretically in mouse liver extracts. The inheritance of variation in NEU‐1 and the linkage relationships of the gene controlling this variation were studied through a backcross analysis involving the SM/J and MA/MyJ inbred strains, and by examination of NEU‐1 phenotypes in three congenic strains: Bl0.SM, Bl0.SM(22R) and B10.RVB. The data indicate that NEU‐1 is controlled byNeu‐1, a gene previously identified by its effect on total liver neuraminidase activity in whole tissue homogenates. Analysis of the congenic strains revealed identical low activity (SM/J‐type:Neu‐1α/Neu‐1α) NEU‐1 phenotypes in all three strains. This indicates thatNeu‐Ilies in the segment of the SM/J‐derivedH‐2region that is common to all three strains:H‐2EαtoH‐2D. In addition, we examined the relationship between NEU‐1 and phenotypic variation in liver acid phosphatase (AP; for which a new typing method is described) and linkage order among several other enzyme‐coding genes linked toH‐2. In all animals that could be scored confidently for AP, the NEU‐1 and AP phenotypes were concordant, adding support to the hypothesis that both phenotypes are controlled byNeu‐1. Recombination rates among six H‐2‐Linked marker loci were unexpectedly low, but were sufficient to verify the position ofUpg‐1as the telomeric flanking marker relative toGlo‐I, H‐2 (C4), Neu‐1 (Apl), Ce‐2andPgk‐2.