Rasmusson K E, Raymond J D, Simmons M J
Department of Genetics and Cell Biology, University of Minnesota, St. Paul 55108-1095.
Genetics. 1993 Mar;133(3):605-22. doi: 10.1093/genetics/133.3.605.
Individual P elements that were genetically isolated from wild-type strains were tested for their abilities to repress two aspects of hybrid dysgenesis: gonadal dysgenesis and mutability of a double-P element-insertion allele of the singed locus (snw). These elements were also characterized by Southern blotting, polymerase chain reaction amplification and DNA sequencing. Three of the elements were 1.1-kb KP elements, one was a 1.2-kb element called D50, and one was a 0.5-kb element called SP. These three types of elements could encode polypeptides of 207, 204, and 14 amino acids, respectively. Gonadal dysgenesis was repressed by two of the KP elements (denoted KP(1) and KP(6)) and by SP, but not by the third KP element (KP(D)), nor by D50. Repression of gonadal dysgenesis was mediated by a maternal effect, or by a combination of zygotic and maternal effects generated by the P elements themselves. The mutability of snw was repressed by the KP(1) and KP(6) elements, by D50 and by SP, but not by KP(D); however, the SP element repressed snw mutability only when the transposase came from complete P elements and the D50 element repressed it only when the transposase came from the modified P element known as delta 2-3. In all cases, repression of snw mutability appeared to be mediated by a zygotic effect of the isolated P element. Each of the isolated elements was also tested for its ability to suppress the phenotype of a P-insertion mutation of the vestigial locus (vg21-3). D50 was a moderate suppressor whereas SP and the three KP elements had little or no effect. These results indicate that each isolated P element had its own profile of repression and suppression abilities. It is suggested that these abilities may be mediated by P-encoded polypeptides or by antisense P RNAs initiated from external genomic promoters.
从野生型菌株中通过遗传分离得到的单个P因子，被检测其抑制杂种劣势两个方面的能力：性腺发育不全以及单基因座（snw）双P因子插入等位基因的突变性。这些因子还通过Southern印迹法、聚合酶链反应扩增和DNA测序进行了表征。其中三个因子是1.1kb的KP因子，一个是1.2kb的名为D50的因子，还有一个是0.5kb的名为SP的因子。这三种类型的因子分别可以编码207、204和14个氨基酸的多肽。两个KP因子（分别记为KP(1)和KP(6)）以及SP因子能抑制性腺发育不全，但第三个KP因子（KP(D)）和D50因子则不能。性腺发育不全的抑制是由母体效应介导的，或者是由P因子自身产生的合子效应和母体效应共同介导的。snw的突变性被KP(1)和KP(6)因子、D50因子以及SP因子所抑制，但不被KP(D)因子抑制；然而，SP因子只有在转座酶来自完整的P因子时才会抑制snw的突变性，而D50因子只有在转座酶来自被称为delta 2-3的修饰P因子时才会抑制它。在所有情况下，snw突变性的抑制似乎是由分离出的P因子的合子效应介导的。每个分离出的因子还被检测了其抑制残翅基因座（vg21-3）P插入突变表型的能力。D50是一个中等程度的抑制因子，而SP因子和三个KP因子几乎没有或没有影响。这些结果表明，每个分离出的P因子都有其自身的抑制和抑制能力特征。有人提出，这些能力可能是由P编码的多肽或从外部基因组启动子起始的反义P RNA介导的。
