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首页> 外文期刊>Journal of Virology >Impairment of reovirus mRNA methylation in extracts of interferon-treated Ehrilich ascites tumor cells: further characteristics of the phenomenon.
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Impairment of reovirus mRNA methylation in extracts of interferon-treated Ehrilich ascites tumor cells: further characteristics of the phenomenon.

机译：在干扰素治疗的Ehririco腹水肿瘤细胞提取物中止血剂mRNA甲基化的损伤：现象的进一步特征。

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We reported earlier that the methylation of unmethylated reovirus mRNA (reo mRNAU) by the cellular methylating enzymes is impaired in extracts of uninfected, interferon-treated Ehrilich ascites tumor cells (S30INT). We find now that after the methylation of reo mRNAU has stopped in S30INT, the RNA can be reisolated and further methylated in an extract of control cells (S30C). Thus the impairment of methylation in S30INT cannot be due to cleavage or irreversible inactivation of reo mRNAU. Freshly added reo mRNAU can be methylated in S30INT in which the methylation of previously added reo mRNAU has stopped. This indicates that the impairment is due to the depletion of S-adenosylme thionine (the methyl donor), the accumulation of S-adenosylhomocysteine (an inhibitor of methylation), or the irreversible inactivation of reo mRNAU. Freshly added reo mRNAU can be methylated in S30INT in which the methylation of previously added reo mRNAU has stopped. This indicates that the impairment is not due to the depletion of S-adenosylmethionine (the methyl donor), the accumulation of S-adenoxylhomocysteine (an inhibitor of methylation), or the irreversible inactivation of the methylating enzymes. It may be due, however, to the unavailability of reo mRNAU for methylation. The extent of the impairment of reo mRNAU methylation in S30INT decreases with an increasing concentration of reo mRNAU but is not affected by added poly (U), ribosomal RNA, or encephalomyocarditis virus RNA (an mRNA that is probably not capped or methylated at its 5' end). The methylation of reo mRNAU is also impaired in an extract from cells that have not been treated with interferon but with the interferon inducer poly(I) - poly(C). The inhibitor is apparently a macromolecule that is inactivated during incubation. It decreases the methylation at the 7 position of the 5' terminal guanylate residue. In vitro, the rate of reo mRNA synthesis by reovirus cores in the presence of S30INT is the same as in the presence of S30C. However, the methylation of the de novo synthesized reo mRNA by the core-associated methylating enzyme(s) in vitro is inhibited by S30INT but not by S30C. The relevance of these phenomena to the inhibition of reovirus replication in interferon-treated cells remains to be established.
机译：我们之前的报道称，未甲基化的reoVirus mRNA（Reo mrnau）的甲基化在未感染的干扰素处理的ehrilich腹水细胞（S30）中的提取物中受到损害。现在我们发现，在S30中的REO MRNAU的甲基化后，可以在对照细胞的提取物中重新坐出并进一步甲基化RNA（S30℃）。因此，S30中甲基化的损害不能是由于REO MRNAU的裂解或不可逆转的灭活。新增的REO MRNAU可以在S30中甲基化，其中先前添加的REO MRNAU的甲基化已停止。这表明损伤是由于S-腺苷胞嘧啶（甲基供体）的耗尽，S-腺苷肌细胞（甲基化抑制剂）的积累，或REO mRNAU的不可逆灭活。新增的REO MRNAU可以在S30中甲基化，其中先前添加的REO MRNAU的甲基化已停止。这表明损伤不是由于S-腺苷甲硫氨酸（甲基供体）的耗尽，S-腺苷的积累（甲基化抑制剂），或甲基化酶的不可逆灭活。然而，它可能是由于REO MRNAU的不可用甲基化。 S30inint的REO mRNau甲基化的减值程度随着REO mRNAU的浓度而降低，但不受添加的聚（U），核糖体RNA或脑膜眼炎病毒RNA的影响（可能未在其5中封装或甲基化的mRNA的mRNA ' 结尾）。 REO mRNAU的甲基化也在尚未用干扰素处理的细胞中的提取物中损害，但是与干扰素诱导剂聚（i） - 聚（C）进行治疗。抑制剂显然是在孵育期间灭活的大分子。它降低了5'末端瓜瓜酸盐残基的7位的甲基化。在体外，在S30int存在下，reoVirus芯的REO mRNA合成的速率与S30℃的存在相同。然而，通过S30或不通过S30℃抑制通过体外核心相关的甲基化酶的DE Novo合成的REO mRNA的甲基化。这些现象在干扰素治疗细胞中抑制抑制释放病毒复制的相关性仍有待建立。

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