Analysis of the Om(1D) locus in Drosophila ananassae.

Analysis of the Om(1D) locus in Drosophila ananassae.
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果蝇 Om(1D) 基因座分析。

DOI:
10.1093/genetics/123.3.495
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发表时间:
1989
期刊:
影响因子:
3.3
通讯作者:
Langley,CH
Langley,CH
中科院分区:
生物学2区
文献类型:
--
作者:
Tanda,S;Shrimpton,AE;Hinton,CW;Langley,CH

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从CA; px原种是由tom反转录转座子插入引起的Om突变体的祖先,通过tom标签和染色体步移克隆了包括Om(1D)位点的50 kb基因组DNA。Southern印迹分析的6个OM(1D)突变体暴露一个或两个汤姆元素插入在5个非随机位点内的限制性内切酶图谱的18 kb的远端段,这些突变体之间的表型一致性不受影响的位置,数量或方向的变化,其插入。自发回复突变体或更极端的衍生物的Om(1D)等位基因与损失或收益的汤姆插入非线性相关。8个辐射诱导的Om(1D)突变体衍生物中有7个在包括Om(1D)位点的多线13 A区段具有一个染色体重排断裂点。两个Om(1D)衍生物,一个自发回复突变体和一个诱导的极端等位基因,与重叠缺陷相关,这些缺陷定义了一个可能包含靠近tom插入位点的Om(1D)编码序列的区域。偶然的结果证实了先前指出的Om(1D)基因座与果蝇Bar基因座的同源性。
From the ca;px stock, which is the progenitor of Om mutants caused by insertions of the tom retrotransposon, 50 kb of genomic DNA including the Om(1D) locus was cloned by tom tagging and chromosome walking. Southern blot analyses of six Om(1D) mutants exposed one or two tom elements inserted at five nonrandom sites within an 18-kb distal segment of the restriction map; the phenotypic uniformity between these mutants was not affected by variations in the position, number or orientation of their inserts. Spontaneous revertants or more extreme derivatives of Om(1D) alleles were nonlinearly associated with losses or gains of tom inserts. Seven of eight radiation induced derivatives of Om(1D) mutants had one breakpoint of a chromosome rearrangement in polytene section 13A which includes the Om(1D) locus. Two Om(1D) derivatives, a spontaneous revertant and an induced extreme allele, were associated with overlapping deficiencies which define a region that is likely to contain the Om(1D) coding seguences proximal to the tom insertion sites. Incidental results confirm the previously indicated homology of the Om(1D) locus with the Bar locus of Drosophila melanogaster.
果蝇 ANANASSAE 中的 OM 突变与转座元件的插入有关。
DOI: --
发表时间: 1986
期刊: Genetics
影响因子: 3.3
作者:
A. Shrimpton;E. Montgomery;C. Langley
通讯作者: C. Langley
DOI: --
发表时间: 1984
期刊: Genetics
影响因子: 3.3
作者:
C. W. Hinton
通讯作者: C. W. Hinton