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酪氨酸磷酸酶cdc25可选择性抑制非洲爪蟾卵母细胞型tRNAtyrC基因的转录。

The tyrosine phosphatase cdc25 selectively inhibits transcription of the Xenopus oocyte-type tRNAtyrC gene.

作者信息

Reynolds W F

机构信息

La Jolla Cancer Research Foundation, CA 92037.

出版信息

Nucleic Acids Res. 1993 Sep 11;21(18):4372-7. doi: 10.1093/nar/21.18.4372.

Abstract

The Xenopus tyrosine tRNAtyrC (TyrC) genes are developmentally regulated. These multicopy genes are expressed in early oocytes and inactivated as oocytes reach maturity. As shown here, this developmental regulation can be reproduced in vitro in extracts of early and late stage oocytes: the TyrC gene is transcribed in early oocyte extracts but is virtually inactive in mature oocyte extracts. The inability to transcribe the TyrC gene is not due to the lack of functional pol III transcriptional components, since the somatic-type TyrD gene is fully active in mature oocyte extracts. Instead, the loss of TyrC transcription appears to be due to a change in the template specificity of transcription factor TFIIIC: addition of TFIIIC from immature extracts restores TyrC transcription in mature extracts. In mixtures of immature and mature extracts, the transcriptional activity of the TyrC gene is reduced. The presence of sodium vanadate, an inhibitor of tyrosine phosphatases, increases the level of TyrC transcription in the extract mixtures. Also, cdc25 phosphatase treatment of immature extracts causes a decrease in TyrC transcription which is reversed by addition of exogenous TFIIIC. These findings indicate that changes in phosphorylation state alters the template specificity of TFIIIC leading to the selective inactivation of oocyte type TyrC genes.

摘要

非洲爪蟾酪氨酸tRNAtyrC(TyrC)基因受到发育调控。这些多拷贝基因在早期卵母细胞中表达,并在卵母细胞成熟时失活。如本文所示,这种发育调控可以在早期和晚期卵母细胞提取物中体外重现:TyrC基因在早期卵母细胞提取物中被转录,但在成熟卵母细胞提取物中几乎无活性。TyrC基因无法转录并非由于缺乏功能性的RNA聚合酶III转录成分,因为体细胞型TyrD基因在成熟卵母细胞提取物中完全有活性。相反,TyrC转录的丧失似乎是由于转录因子TFIIIC模板特异性的改变:从未成熟提取物中添加TFIIIC可恢复成熟提取物中TyrC的转录。在未成熟和成熟提取物的混合物中,TyrC基因的转录活性降低。酪氨酸磷酸酶抑制剂钒酸钠的存在会增加提取物混合物中TyrC的转录水平。此外,对未成熟提取物进行cdc25磷酸酶处理会导致TyrC转录减少,而添加外源TFIIIC可使其逆转。这些发现表明,磷酸化状态的变化会改变TFIIIC的模板特异性,导致卵母细胞型TyrC基因选择性失活。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7518/310075/ba8f6a8d0043/nar00067-0228-a.jpg

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