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Inhibited mechanism during the post-transcription in nuclei of El mouse brain.

El小鼠脑细胞核转录后的抑制机制。

基本信息

批准号：
62570493
负责人：
YAMAGAMI Sakae
金额：
$ 1.09万
依托单位：
Osaka City University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1987
资助国家：
日本
起止时间：
1987 至 1988
项目状态：
已结题

项目摘要

The poly(A)^+ polymerase activity was estimated with respect to brain nuclei of various areas such as cerebral cortex, white matter, diencephalon, mesencephalon, hippocampus and cerebellum from seizure-susceptible El mice. Hippocampus showed a higher activity of this enzyme as compared with other brain regions. This enzyme activity was decreased to 65% of interictal level by the seizures, but restored to a normal value at 30 min after the seizures. These results suggest that poly(A)^+ polymerase of hippocampus is responsible for seizure-susceptibitity. Poly(A)^+ polymerase of whole brain was divided into two forms, which are located in nuclear cell sap designating as Form I, and bind chromatin as Form II. The former activity was 5 times higher than the latter one, which was lower in El(+) as compared with ddY mice. Form II enzyme was involved in initiating the polyadenylation of mRNA synthesized on the chromatin. The addition of poly(A)^+ segment to hnRNA is insufficient in El mouse brain, and mRNAs did not enough synthesize during interictal period. Immediately after the seizures, the activity of Form II decreased to 75% of interictal value. While Form I enzyme which lengths the chain of poly(A)^+ tracts did not alter significantly during and/or after the seizures. Further experiments are needed to elucidate the relationship between seizure-susceptibility and alteration of subunits of poly(A)^+ polymerase. The regulatory mechanism of posttranscription in El mouse brain will be obvious.

评估了癫痫易感E1小鼠的各个区域的脑核，例如大脑皮层、白质、间脑、中脑、海马和小脑的poly(A) + 聚合酶活性。与其他大脑区域相比，海马显示出这种酶的更高活性。癫痫发作时该酶活性降低至发作间期水平的 65%，但在癫痫发作后 30 分钟恢复到正常值。这些结果表明海马的poly(A)^+聚合酶与癫痫易感性有关。全脑Poly(A)^+聚合酶分为两种形式，位于核细胞液中的为I型，与染色质结合的为II型。前者的活性比后者高5倍，而El(+)小鼠的活性低于ddY小鼠。 II 型酶参与启动染色质上合成的 mRNA 的聚腺苷酸化。 El小鼠大脑中向hnRNA添加的poly(A)^+片段不足，并且在发作间期mRNA合成不足。癫痫发作后，II 型活性立即降至发作间期值的 75%。而延长 Poly(A)^+ 束链的 I 型酶在癫痫发作期间和/或之后没有显着改变。需要进一步的实验来阐明癫痫易感性和poly(A)^+聚合酶亚基改变之间的关系。 El小鼠大脑中转录后的调控机制将是显而易见的。