Simmons Michael J, Haley Kevin J, Grimes Craig D, Raymond John D, Fong Joseph C L
Department of Genetics, Cell Biology and Development, University of Minnesota, Saint Paul, Minnesota 55108-1095, USA.
Genetics. 2002 May;161(1):205-15. doi: 10.1093/genetics/161.1.205.
Fusions between the Drosophila hsp70 promoter and three different incomplete P elements, KP, SP, and BP1, were inserted into the Drosophila genome by means of hobo transformation vectors and the resulting transgenic stocks were tested for repression of P-element transposase activity. Only the H(hsp/KP) transgenes repressed transposase activity, and the degree of repression was comparable to that of a naturally occurring KP element. The KP transgenes repressed transposase activity both with and without heat-shock treatments. Both the KP element and H(hsp/KP) transgenes repressed the transposase activity encoded by the modified P element in the P(ry(+), Delta2-3)99B transgene more effectively than that encoded by the complete P element in the H(hsp/CP)2 transgene even though the P(ry(+), Delta2-3)99B transgene was the stronger transposase source. Repression of both transposase sources appeared to be due to a zygotic effect of the KP element or transgene. There was no evidence for repression by a strictly maternal effect; nor was there any evidence for enhancement of KP repression by the joint maternal transmission of H(hsp/KP) and H(hsp/CP) transgenes. These results are consistent with the idea that KP-mediated repression of P-element activity involves a KP-repressor polypeptide that is not maternally transmitted and that KP-mediated repression is not strengthened by the 66-kD repressor produced by complete P elements through alternate splicing of their RNA.
通过hobo转化载体将果蝇hsp70启动子与三种不同的不完整P元件（KP、SP和BP1）融合，插入果蝇基因组中，并对产生的转基因品系进行测试，以检测其对P元件转座酶活性的抑制作用。只有H（hsp/KP）转基因能抑制转座酶活性，且抑制程度与天然存在的KP元件相当。无论有无热休克处理，KP转基因均能抑制转座酶活性。尽管P（ry（+），Delta2-3）99B转基因是更强的转座酶来源，但KP元件和H（hsp/KP）转基因对P（ry（+），Delta2-3）99B转基因中修饰的P元件所编码的转座酶活性的抑制作用，比H（hsp/CP）2转基因中完整P元件所编码的转座酶活性的抑制作用更有效。两种转座酶来源的抑制作用似乎都归因于KP元件或转基因的合子效应。没有证据表明存在严格的母体效应抑制；也没有证据表明H（hsp/KP）和H（hsp/CP）转基因的母体联合传递会增强KP的抑制作用。这些结果与以下观点一致：KP介导的P元件活性抑制涉及一种不通过母体传递的KP抑制多肽，并且完整P元件通过其RNA的可变剪接产生的66-kD抑制因子不会增强KP介导的抑制作用。
