Somatic effects of P element activity in Drosophila melanogaster: pupal lethality.
Somatic effects of P element activity in Drosophila melanogaster: pupal lethality.
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P 元素活性对果蝇的体细胞影响：蛹致死率。
DOI：
10.1093/genetics/117.4.745
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发表时间：
1987
期刊：
影响因子：
3.3
通讯作者：
Robertson,HM
中科院分区：
文献类型：
--
作者：
Engels,WR;Benz,WK;Preston,CR;Graham,PL;Phillis,RW;Robertson,HM
非自主性元件通常仅在提供转座酶源时并且仅在种系中切除和转座。种系特异性取决于转座酶基因的内含子之一，该内含子在体细胞中不被剪接。为了研究体细胞 P 活性的影响，使用缺乏该内含子的修饰 P 元素 (Δ2-3) 作为转座酶的来源。来自伯明翰菌株的非自主P元素，当通过Δ2-3在体细胞中动员时，被发现会导致致命性，尽管这两种成分本身都不致命。三个主要的伯明翰染色体在产生致命效应时几乎独立地发挥作用。这种致死率表现出对温度的强烈依赖性。尽管温度敏感性仅限于幼虫阶段，但实际死亡发生在蛹阶段。幸存者可以通过降低温度或减少伯明翰基因组的比例来恢复，但他们常常表现出多种发育异常和寿命缩短，让人想起辐射损伤造成的细胞死亡的影响。尽管遗传损伤发生在分裂的成虫盘细胞中，但直到后来才观察到表型表现（死亡和异常）。幸存者还表现出性腺发育不良（GD）不育，这是 P-M 杂种发育不全的众所周知的特征。为了解释这些发现，我们认为蛹致死性和GD不育都是由幼虫细胞中大量染色体断裂引起的，这是由于作为转座酶底物的基因组P元件的切除和转座造成的。
NonautonomousPelements normally excise and transpose only when a source of transposase is supplied, and only in the germline. The germline specificity depends on one of the introns of the transposase gene which is not spliced in somatic cells. To study the effects of somatic P activity, a modifiedPelement (Δ2-3) lacking this intron was used as a source of transposase. NonautonomousPelements from a strain called Birmingham, when mobilized in somatic cells by Δ2-3, were found to cause lethality, although neither component was lethal by itself. The three major Birmingham chromosomes acted approximately independently in producing the lethal effect. This lethality showed a strong dependence on temperature. Although temperature sensitivity was limited to larval stages, the actual deaths occurred at the pupal stage. Survivors, which could be recovered by decreasing the temperature or by reducing the proportion of the Birmingham genome present, often showed multiple developmental anomalies and reduced longevity reminiscent of the effects of cell death from radiation damage. Although the genetic damage occurred in dividing imaginal disc cells, the phenotypic manifestations—death and abnormalities—are not observed until later. The survivors also showed gonadal dysgenic (GD) sterility, a well-known characteristic of P-M hybrid dysgenesis. To explain these findings, we suggest that pupal lethality and GD sterility are both caused by massive chromosome breakage in larval cells, resulting from excision and transposition of genomicPelements acting as substrate for the transposase.