Abnormal Expression of the Myelin‐Associated Glycoprotein in the Central Nervous System of Dysmyelinating Mutant Mice
Abnormal Expression of the Myelin‐Associated Glycoprotein in the Central Nervous System of Dysmyelinating Mutant Mice
复制标题
髓鞘异常突变小鼠中枢神经系统髓磷脂相关糖蛋白的异常表达
DOI：
10.1111/j.1471-4159.1985.tb05525.x
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发表时间：
1985
影响因子：
4.7
通讯作者：
P. E. Braun
中科院分区：
文献类型：
--
作者：
D. Frail;P. E. Braun
摘要：从3只神经系统突变小鼠（qk/qk、jp/Y和shi/shi）及其表面正常的幼崽中分离出2个不同年龄的脑细胞质总RNA。该RNA在兔网织细胞裂解液系统中进行了体外翻译。髓鞘相关糖蛋白（MAG）相关多肽通过免疫沉淀从突变动物、正常产仔或对照动物的mRNA中提取等量的总翻译产物。比较了突变体和正常动物的发育调节合成MAG多肽的情况。来自qk/qk脑的mRNA合成了过多的p67MAG（5 - 7倍），这可能是对p72MAG合成减少的补偿。jp/Y脑的mRNA合成量均低于正常水平的10%。与正常脑mRNA相比，15日龄狮/狮脑mRNA合成的MAG数量略有减少，但成年狮/狮脑mRNA合成的MAG数量正常。所研究的任何突变体合成的MAG多肽的大小均未发现明显差异。这些数据表明，qk/qk突变体的遗传缺陷直接或间接地影响了MAG多肽合成的协调发展的心理调节，导致MAG多肽过量，而这通常在老年动物中发现。jp/Y突变似乎影响一般髓磷脂蛋白的合成。最后，shi/shi突变体可能延迟了MAG的合成。这些数据是根据最近关于髓磷脂蛋白合成及其在髓磷脂组装中的作用的观察来讨论的。
Abstract: Total cytoplasmic brain RNA was isolated at two different ages from three neurological mutant mice (qk/qk, jp/Y, and shi/shi) and their apparently normal littermates. This RNA was translated in vitro in a rabbit reticulocyte lysate system. Myelin‐associated glycoprotein (MAG)‐related polypeptides were immunoprecipitated from equal amounts of total translation products derived from mRNA of mutant animals, normal litter mates, or control animals. The developmentally regulated synthesis of MAG polypeptides was compared among the mutants and normal animals. mRNA from qk/qk brains synthesized an overabundance of p67MAG (five‐ to sevenfold) which may be compensation for a decreased synthesis of p72MAG. mRNA from jp/Y brains synthesized less than 10% of normal amounts of both MAG polypep tides. The quantity of MAG synthesized by 15‐day shi/shi brain mRNA was slightly decreased compared with normal brain mRNA but the quantity of MAG synthe sized by adult shi/shi brain mRNA was normal. No apparent differences were detected in the sizes of the MAG polypeptides synthesized by any of the mutants studied. The data suggest that the genetic defect in qk/qk mutants directly or indirectly affects the coordinated develop mental regulation of MAG polypeptide synthesis leading to an overabundance of the MAG polypeptide that is normally found in older animals. The jp/Y mutation appears to affect general myelin protein synthesis. Finally, shi/shi mutants may have a delayed synthesis of MAG. The data are discussed in the light of recent observations concerning the synthesis of myelin proteins and their proposed role in myelin assembly.