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果蝇中P因子诱导的重组:杂种因子插入

P-element-induced recombination in Drosophila melanogaster: hybrid element insertion.

作者信息

Gray Y H, Tanaka M M, Sved J A

机构信息

School of Biological Sciences, University of Sydney, New South Wales, Australia.

出版信息

Genetics. 1996 Dec;144(4):1601-10. doi: 10.1093/genetics/144.4.1601.

Abstract

It has previously been shown that the combination of two deleted P elements in trans, one containing the left functional end and the second element the right functional end, can lead to high levels of male recombination. This finding strongly suggests that P-element ends from different chromosomes can become associated, followed by "pseudo-excision". We show that two different processes are involved in resolving the pseudo-excision event: (1) the excised P-element ends continue to function as a single unit (Hybrid Element) and insert at a nearby site in the chromosome or into the element itself [Hybrid Element Insertion (HEI)] and (2) free ends that do not contain P elements repair and rejoin [(Hybrid Excision and Repair (HER)]. Both types of resolution can lead to recombination, and this paper concentrates on the HEI class. One type of HEI event predicts the exact reverse complementary duplication of an 8-bp target site, and we have confirmed the existence of such a structure in six independently derived recombinant chromosomes. There is also a high tendency for insertion events to occur within a few bases of the original 8-bp target site, including six apparent cases of insertion into the exact site.

摘要

先前的研究表明,两个反式缺失的P元件(一个包含左侧功能端,另一个包含右侧功能端)组合在一起,可导致高水平的雄性重组。这一发现有力地表明,来自不同染色体的P元件末端可以发生关联,随后发生“假切除”。我们发现,解决假切除事件涉及两个不同的过程:(1)切除的P元件末端继续作为一个单一单元发挥作用(杂交元件),并插入到染色体上附近的位点或元件自身中[杂交元件插入(HEI)],以及(2)不含P元件的游离末端进行修复和重新连接[杂交切除与修复(HER)]。这两种类型的解决方式都可导致重组,本文重点关注HEI类型。一种类型的HEI事件预测了一个8bp靶位点的精确反向互补重复,我们已经在六个独立衍生的重组染色体中证实了这种结构的存在。插入事件也高度倾向于发生在原始8bp靶位点的几个碱基范围内,包括六个明显插入到精确位点的情况。

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引用本文的文献

本文引用的文献

1
Flanking duplications and deletions associated with P-induced male recombination in Drosophila.
Genetics. 1996 Dec;144(4):1623-38. doi: 10.1093/genetics/144.4.1623.

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