Bingham P M, Kidwell M G, Rubin G M
Cell. 1982 Jul;29(3):995-1004. doi: 10.1016/0092-8674(82)90463-9.
We have shown previously that four of five white mutant alleles arising in P-M dysgenic hybrids result from the insertion of strongly homologous DNA sequence elements. We have named these P elements. We report that P elements are present in 30-50 copies per haploid genome in all P strains examined and apparently are missing entirely from all M strains examined, with one exception. Furthermore, members of the P family apparently transpose frequently in P-M dysgenic hybrids; chromosomes descendant from P-M dysgenic hybrids frequently show newly acquired P elements. Finally, the strain-specific breakpoint hotspots for the rearrangement of the pi 2 P X chromosome occurring in P-M dysgenic hybrids are apparently sites of residence of P elements. These observations strongly support the P factor hypothesis for the mechanistic basis of P-M hybrid dysgenesis.
我们之前已经表明，在P-M杂种不育的杂种中出现的五个白色突变等位基因中有四个是由高度同源的DNA序列元件插入导致的。我们将这些元件命名为P元件。我们报告称，在所有检测的P品系中，每个单倍体基因组中存在30 - 50个P元件拷贝，而在所有检测的M品系中，除了一个例外，P元件显然完全缺失。此外，P家族的成员在P-M杂种不育的杂种中显然频繁转座；来自P-M杂种不育杂种的染色体经常显示出新获得的P元件。最后，在P-M杂种不育杂种中发生的pi 2 P X染色体重排的品系特异性断裂热点显然是P元件的驻留位点。这些观察结果有力地支持了关于P-M杂种不育机制基础的P因子假说。
