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黑腹果蝇中的遗传不稳定性:通过基因转换进行P因子诱变。

Genetic instability in Drosophila melanogaster: P-element mutagenesis by gene conversion.

作者信息

Geyer P K, Richardson K L, Corces V G, Green M M

机构信息

Department of Biology, Johns Hopkins University, Baltimore, MD 21218.

出版信息

Proc Natl Acad Sci U S A. 1988 Sep;85(17):6455-9. doi: 10.1073/pnas.85.17.6455.

Abstract

We report the molecular characterization of several P element-induced mutations and their revertants at the yellow (y) locus of Drosophila melanogaster. One of the mutants analyzed, y76d28, results from the insertion of a P element into the 5'-transcribed, untranslated portion of the y gene. Sequence analysis of several revertants of y76d28 shows that P excision occurs imprecisely. These events result in insertion of additional ATG codons in the y locus mRNA but are without phenotypic effect. In addition, we describe the molecular structure of P-associated mutations induced in a near wild-type revertant of y76d28 that carries an internally deleted 0.4-kilobase P element in the 5' noncoding region. Sequence analysis of two of these mutants demonstrates that they arose as a result of the integration of a larger P element at the exact location as in the parental stock without the 8-base-pair additional duplication associated with P insertions. The phenotype of these y alleles is dependent on the size and orientation of the integrated P element. We infer that P-element replacement in these mutants has occurred by a recombination/gene conversion mechanism.

摘要

我们报告了果蝇黑腹果蝇黄色(y)位点上几个P因子诱导的突变及其回复突变体的分子特征。分析的其中一个突变体y76d28,是由于一个P因子插入到y基因5'转录的非翻译区所致。对y76d28的几个回复突变体的序列分析表明,P因子的切除是不准确的。这些事件导致y位点mRNA中额外的ATG密码子插入,但没有表型效应。此外,我们描述了在y76d28的一个近野生型回复突变体中诱导的与P相关的突变的分子结构,该回复突变体在5'非编码区携带一个内部缺失0.4千碱基的P因子。对其中两个突变体的序列分析表明,它们是由于一个更大的P因子在与亲本品系相同的精确位置整合而产生的,没有与P插入相关的8碱基对额外重复。这些y等位基因的表型取决于整合的P因子的大小和方向。我们推断这些突变体中的P因子替换是通过重组/基因转换机制发生的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b35e/281991/590981f91fe9/pnas00296-0238-a.jpg

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