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性致死基因通过一种非剪接机制控制果蝇的剂量补偿效应。

Sex lethal controls dosage compensation in Drosophila by a non-splicing mechanism.

作者信息

Kelley R L, Wang J, Bell L, Kuroda M I

机构信息

Department of Cell Biology, Baylor College of Medicine, Houston, Texas 77030, USA.

出版信息

Nature. 1997 May 8;387(6629):195-9. doi: 10.1038/387195a0.

DOI:10.1038/387195a0
PMID:9144292
Abstract

Dosage compensation in Drosophila requires the male-specific lethal (msl) proteins (MSL) to make gene expression from the single male X chromosome equivalent to that from both female X chromosomes. Expression of ms12 is repressed post-transcriptionally by Sex lethal (SXL), a female-specific RNA-binding protein that regulates alternative splicing in the sex-determination hierarchy. Although msl2 RNA is alternatively spliced in males and females, this does not alter its coding potential and splicing is not required for male-specific expression of MSL2 protein. Instead, our results suggest that the association of SXL protein with multiple sites in the 5' and 3' untranslated regions of the mx12 transcript represses its translation in females. Thus, this well characterized alternative splicing factor regulates at least one target transcript by a distinct mechanism.

摘要

果蝇中的剂量补偿需要雄性特异性致死(msl)蛋白(MSL),以使单条雄性X染色体上的基因表达等同于两条雌性X染色体上的基因表达。msl2的表达在转录后受到性别致死(SXL)的抑制,SXL是一种雌性特异性RNA结合蛋白,在性别决定层次中调节可变剪接。尽管msl2 RNA在雄性和雌性中都进行可变剪接,但这并不改变其编码潜能,并且MSL2蛋白的雄性特异性表达不需要剪接。相反,我们的结果表明,SXL蛋白与msl2转录本5'和3'非翻译区的多个位点结合,抑制了其在雌性中的翻译。因此,这种特征明确的可变剪接因子通过一种独特的机制调节至少一个靶转录本。

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Sex lethal controls dosage compensation in Drosophila by a non-splicing mechanism.性致死基因通过一种非剪接机制控制果蝇的剂量补偿效应。
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2
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