Enhanced susceptibility of mouse embryos heterozygous for oligosyndactyly (Os/+) to mitomycin C-induced skeletal abnormalities.
Enhanced susceptibility of mouse embryos heterozygous for oligosyndactyly (Os/+) to mitomycin C-induced skeletal abnormalities.
复制标题
寡并指杂合子小鼠胚胎 (Os/ ) 对丝裂霉素 C 诱导的骨骼异常的易感性增强。
DOI：
10.1002/tera.1420350213
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发表时间：
1987
期刊：
影响因子：
--
通讯作者：
Epstein,CJ
中科院分区：
文献类型：
--
作者：
Moreno,PA;Epstein,CJ
The mouse mutation, oligosyndactyly (Os), results in syndactyly, muscle anomalies, and deficiency of nephrons in heterozygous animals and early embryonic lethality in homozygotes. Since the homozygous lethality results from mitotic arrest with intact spindles at the time of implantation, we have hypothesized that the heterozygous manifestations may result from impairment of cell proliferation in regions with high proliferative rates. To test this hypothesis,Os/+ and +/+ mouse embryos at 6.5 days of gestation were exposed to mitomycin C (MMC), an agent that causes a high degree of embryonic cell death which is “compensated” for by a period of rapid cell proliferation. 17.9% of MMC‐treated +/+ fetuses had fused vertebrae, a significant increase over untreated fetuses, and this frequency was further increased to 33.6% in MMC‐treatedOs/+ fetuses. Saline treatedOs/+ and +/+ fetuses showed the same low rate (0.3%) of vertebral fusion. These results indicate thatOs/+ embryos have an increased sensitivity to the vertebral fusioninducing effect of MMC at 6.5 days of gestation, a finding compatible with the hypothesis that rapid cell proliferation may be impaired inOs/+ embryos and fetuses.
