THE RELATIONSHIP BETWEEN RADIATION-INDUCED AND TRANSPOSON-INDUCED GENETIC-DAMAGE DURING DROSOPHILA SPERMATOGENESIS
THE RELATIONSHIP BETWEEN RADIATION-INDUCED AND TRANSPOSON-INDUCED GENETIC-DAMAGE DURING DROSOPHILA SPERMATOGENESIS
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DOI：
10.1016/0027-5107(87)90309-5
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发表时间：
1987-08-01
期刊：
影响因子：
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通讯作者：
WALLACE, SS
中科院分区：
文献类型：
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作者：
MARGULIES, L;BRISCOE, DI;WALLACE, SS
在杂种不育的P-M系统中，以F_1雄性杂种的生殖系为材料，测定了转座子迁移率和X射线对X连锁隐性致死和显性致死的联合效应。X-连锁致死突变率是在来源于M. P交叉。将辐照过的发育不良雄性动物中诱导的突变与未辐照过的雄性动物的突变以及来自Mx. M交叉。对三个四天的精子窝进行了X连锁致死和显性致死的测试。X连锁致死突变率在1、2、3窝中分别为6.38%、6.36%和4.55%，说明年龄较大的雄虫X连锁致死突变率降低。在同一窝中，受辐射的非劣化对照雄性的突变率分别为3.66%、4.46%和6.38%。在同3窝中，非遗传性辐射雄鼠的平均死亡率分别为10.33、11.16和7.97。这些结果表明，当X射线和P元素迁移率作为诱变源相结合时，在分别代表主要成熟精子和精子细胞的前两窝精子中观察到对遗传损伤的严格加性效应。第三窝，主要代表精母细胞表现出小于加性效应，可能是由于germinal选择。相比之下，显性致死的诱导表现出明显的协同效应，在最后两个窝的精子测试，当X射线和转座子的流动性相结合。血液1中主要代表成熟精子的显性致死率的X射线成分为阴性，表明在P元素迁移率存在的情况下X射线照射诱导的致死率低于预期。X射线诱导的显性致死率分量表示为在将从非发育不良和发育不良雄性的每窝精子获得的结果调整为其各自的未辐照对照后胚胎致死率的百分比。正常雄虫的第1、2、3窝卵的这一比例分别为32.3%、30.5%和64.7%，而不良雄虫的这一比例分别为14.1%、56.1%和71.4%。X射线对第1、2、3窝精子的鉴别效应分别为-18.2%、+25.6%和6.7%。这些结果表明，协同效应可能是由于X射线和P元素诱导的遗传损伤，即染色体断裂的共同组成部分，这些病变的相互作用导致了大于加性数目的未恢复的染色体断裂和不可行的染色体重排。
The combined effect of transposon mobility and X-rays on X-linked recessive lethals and dominant lethals was measured in the germ line of F1 male hybrids in the P-M system of hybrid dysgenesis. X-Linked lethal mutations rate was measured in the chromosome derived from the P-strain father of the M .times. P cross. Mutations induced in irradiated dysgenic males were compared to those of unirradiated males, as well as to irradiated nondysgenic males derived from M .times. M crosses. Three four-day broods of sperm were tested for both X-linked lethals and dominant lethals. X-Linked lethal mutation rate in dysgenic control males was 6.38%, 6.36% and 4.55% in broods 1, 2 and 3 respectively, thus showing a decrease in older males. The mutation rate in the same broods of irradiated, nondysgenic control males was 3.66%, 4.46% and 6.38%, respectively. The rate obtained in dysgenic irradiated males was 10.33, 11.16 and 7.97 in the same 3 broods. These results demonstrate that when X-rays and P element mobility were combined as a source of mutagenesis, a strictly additive effect on genetic damage was observed in the first two broods of sperm which represent primarily mature sperm and spermatids respectively. The third brood, representing mostly spermatocytes showed a less than additive effect, probably due to germinal selection. In contrast, the induction of dominant lethals showed a clearly synergistic effect in the last two broods of sperm tested, when X-rays and transposon mobility were combined. The X-ray component of dominant lethality in blood 1, representing mostly mature spermatozoa, was negative, indicating a lower than expected lethality induced by X-irradiation in the presence of P element mobility. The X-ray-induced component of dominant lethality, was expressed as the per cent of embryo lethality after adjusting the results obtained with each brood of sperm from nondysgenic and dysgenic males to their respective unirradiated controls. These values were 32.3%, 30.5% and 64.7% for brood 1, 2 and 3 respectively from nondysgenic males, and 14.1%, 56.1% and 71.4% for the same broods from dysgenic males. Thus the differential effect of X-rays in sperm broods 1, 2 and 3 was -18.2, +25.6 and +6.7% respectively. These results suggest that the synergistic effect may be due to the common component of X-ray and P element-induced genetic damage, namely chromosome breaks, and that the interaction of these lesions resulted in a greater than additive number of unrestituted chromosome breaks and nonviable chromosomal rearrangements.