Wang Y, Balter H, Levitan M, Margulies L
Department of Microbiology and Immunology, New York Medical College, Valhalla 10595.
Genet Res. 1993 Oct;62(2):111-23. doi: 10.1017/s0016672300031700.
Three Harwich P sublines with different P-element activity potential were used to investigate the influence of P-derived chromosomes on snw mutability and vg suppression and to relate the induction of these dysgenic traits to the number and structure of P elements. Destabilization of the snw allele, a measure of P transposase activity, was differentially influenced by the major autosomes. Chromosome 2 of the standard Harwich subline, Hw, induced only 60% of the level of mutability relative to chromosome 3, whereas chromosome 3 of the weakest Harwich subline, Hf, induced only 50% of the mutability relative to chromosome 2. In somatic suppression of the vg21-3 allele, chromosome 3 of the Hf subline produced a lower level of complete suppression as compared to chromosome 3 of the Hw or the Hs subline (the high hybrid-dysgenesis-inducing subline). The level of these dysgenic traits and GD sterility, was not correlated with the number of P elements per individual (67-68) or per chromosome arm which was very similar among the sublines. The number of complete P elements per genome, based on Southern blot analysis of the X and major autosomes, ranged from 15 to 19. Destabilization of the snw allele and vg suppression by chromosome 3 was correlated with a greater number of complete P elements. Two novel unexpected observations emerged from these studies: both snw mutability and vg suppression data demonstrated high P-element activity in hybrids derived from non-dysgenic crosses irrespective of Harwich subline, indicating a lack of P-cytotype regulation. Mutability in non-dysgenic males ranged from 40 to 60% of the level found in dysgenic males. The high snw mutability and low GD sterility in non-dysgenic hybrids suggests that these traits may arise by a different mechanism.
使用具有不同P因子活性潜力的三个哈维奇P亚系来研究P衍生染色体对snw突变率和vg抑制的影响,并将这些杂种不育性状的诱导与P因子的数量和结构相关联。snw等位基因的不稳定是P转座酶活性的一种度量,它受到主要常染色体的不同影响。标准哈维奇亚系Hw的2号染色体相对于3号染色体仅诱导出60%的突变水平,而最弱的哈维奇亚系Hf的3号染色体相对于2号染色体仅诱导出50%的突变率。在vg21 - 3等位基因的体细胞抑制中,与Hw或Hs亚系(高杂种不育诱导亚系)的3号染色体相比,Hf亚系的3号染色体产生的完全抑制水平较低。这些杂种不育性状和GD不育的水平与每个个体(67 - 68个)或每个染色体臂的P因子数量无关,这些数量在亚系之间非常相似。基于对X染色体和主要常染色体的Southern印迹分析,每个基因组完整P因子的数量范围为15至19个。3号染色体对snw等位基因的不稳定和vg抑制与更多的完整P因子相关。这些研究出现了两个新的意外发现:无论哈维奇亚系如何,snw突变率和vg抑制数据都表明来自非杂种不育杂交的杂种中P因子活性很高,这表明缺乏P细胞质类型调控。非杂种不育雄性的突变率为杂种不育雄性中发现水平的40%至60%。非杂种不育杂种中高snw突变率和低GD不育表明这些性状可能通过不同的机制产生。