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首页> 外文期刊>Molecular and Cellular Biology >Genetic enhancement of RNA-processing defects by a dominant mutation in B52, the Drosophila gene for an SR protein splicing factor.
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Genetic enhancement of RNA-processing defects by a dominant mutation in B52, the Drosophila gene for an SR protein splicing factor.

机译：通过B52的显性突变（SR蛋白剪接因子的果蝇基因）对RNA处理缺陷进行遗传增强。

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摘要

SR proteins are essential for pre-mRNA splicing in vitro, act early in the splicing pathway, and can influence alternative splice site choice. Here we describe the isolation of both dominant and loss-of-function alleles of B52, the gene for a Drosophila SR protein. The allele B52ED was identified as a dominant second-site enhancer of white-apricot (wa), a retrotransposon insertion in the second intron of the eye pigmentation gene white with a complex RNA-processing defect. B52ED also exaggerates the mutant phenotype of a distinct white allele carrying a 5' splice site mutation (wDR18), and alters the pattern of sex-specific splicing at doublesex under sensitized conditions, so that the male-specific splice is favored. In addition to being a dominant enhancer of these RNA-processing defects, B52ED is a recessive lethal allele that fails to complement other lethal alleles of B52. Comparison of B52ED with the B52+ allele from which it was derived revealed a single change in a conserved amino acid in the beta 4 strand of the first RNA-binding domain of B52, which suggests that altered RNA binding is responsible for the dominant phenotype. Reversion of the B52ED dominant allele with X rays led to the isolation of a B52 null allele. Together, these results indicate a critical role for the SR protein B52 in pre-mRNA splicing in vivo.
机译：SR蛋白对于mRNA之前的体外剪接至关重要，在剪接途径的早期起作用，并且可以影响其他剪接位点的选择。在这里，我们描述了果蝇SR蛋白B52基因的主要和功能丧失的等位基因的分离。等位基因B52ED被确定为白杏（wa）的主要第二位增强子，是在具有复杂的RNA处理缺陷的眼睛色素沉着基因白色的第二内含子中的反转录转座子插入。 B52ED还夸大了带有5'剪接位点突变（wDR18）的独特白色等位基因的突变表型，并在致敏条件下改变了双性恋时性别特异性剪接的模式，因此有利于男性特异性剪接。除了是这些RNA加工缺陷的主要增强剂外，B52ED是一种隐性致死等位基因，无法与B52的其他致死等位基因互补。将B52ED与源自其的B52 +等位基因进行比较，发现B52的第一个RNA结合结构域的beta 4链中保守氨基酸有一个单一变化，这表明改变的RNA结合是显性表型的原因。用X射线还原B52ED优势等位基因导致隔离B52无效等位基因。总之，这些结果表明SR蛋白B52在体内预mRNA剪接中具有关键作用。

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