BINDING OF THE DROSOPHILA SEX-LETHAL GENE-PRODUCT TO THE ALTERNATIVE SPLICE SITE OF TRANSFORMER PRIMARY TRANSCRIPT

BINDING OF THE DROSOPHILA SEX-LETHAL GENE-PRODUCT TO THE ALTERNATIVE SPLICE SITE OF TRANSFORMER PRIMARY TRANSCRIPT
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DOI:
10.1038/344461a0
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发表时间:
1990-03-29
期刊:
影响因子:
64.8
通讯作者:
SHIMURA, Y
SHIMURA, Y
中科院分区:
综合性期刊1区
文献类型:
--
作者:
INOUE, K;HOSHIJIMA, K;SHIMURA, Y

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黑腹果蝇的体细胞性别分化是由1-5oF基因层级完成的,其中性致死基因(SXL)6,7是直接下游调控基因Transformer(TrA)转录产物的雌性特异性剪接所必需的。四元转录本的第一个外显子被剪接到两个受体位点之一。与上游位点的剪接产生信使RNA,该信使RNA既不具有性别特异性,也不具有功能性,但与下游受体位点剪接后产生的信使RNA产生功能性的雌性特有的mRNA。在这里,我们讨论Sx1基因产物如何决定初级转录本的选择性剪接的问题。一种建议是,雌性果蝇与上游受体的非性别特异性剪接被性别特异性因子8阻止,但雌性特异性因子的身份和阻断的机制都没有具体说明。我们现在已经进行了Sx1互补DNA和四基因在果蝇Kc细胞中表达的共转染实验。此外,我们发现女性Sx1编码的蛋白在非性别特异的受体位置或附近与转录本特异结合,这意味着女性Sx1基因产物是调节选择性剪接的反式作用因子。
SOMATIC sexual differentiation inDrosophila melanogasteris accomplished by a hierarchy of genes1–5of which one,Sex-lethal (Sxl)6,7, is required for the functional female-specific splicing of the transcripts of the immediately downstream regulatory gene,transformer (tra). The first exon of thetraprimary transcript is spliced to one of two acceptor sites. Splicing to the upstream site yields a messenger RNA which is neither sex-specific nor func-tional, but that produced after splicing to the downstream acceptor site yields a functional female-specific mRNA. Here we address the question of how theSxlgene product determines the alternative splicing oftraprimary transcripts. One suggestion is that non-sex-specific splicing to the upstream acceptor is blocked in female flies by sex-specific factors8, but neither the identity of the female-specific factors nor the mechanism of the blockage has been specified. We have now performed co-transfection experiments in whichSxlcomplementary DNA and thetragene are expressed inDrosophilaKc cells. Moreover, we find that femaleSxl-encoded protein binds specifically to thetratranscript at or near the non-sex-specific acceptor site, implying that the femaleSxlgene product is thetrans-acting factor that regulates the alternative splicing.