Protamines are expressed in the spermatid nucleus and allow denser packaging of DNA compared with histones. Disruption of the coding sequence of one allele of either protamine 1 (Prm1) or Prm2 results in failure to produce offspring, although sperm with disrupted Prm1 or Prm2 alleles are produced. Here, we produced Prm1-deficient female chimeric mice carrying Prm1-deficient oocytes. These mice successfully produced Prm1(+/-) male mice. Healthy Prm1(+/-) offspring were then produced by transferring blastocysts obtained via in vitro fertilization using zona-free oocytes and sperm from Prm1(+/-) mice. This result suggests that sperm lacking Prm1 can generate offspring despite being abnormally shaped and having destabilised DNA, decondensed chromatin and a reduction in mitochondrial membrane potential. Nevertheless, these mice showed little derangement of expression profiles.
Viable offspring obtained from Prm1-deficient sperm in mice.
从缺乏 Prm1 的小鼠精子中获得可存活的后代
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作者:Takeda Naoki, Yoshinaga Kazuya, Furushima Kenryo, Takamune Kazufumi, Li Zhenghua, Abe Shin-Ichi, Aizawa Shin-Ichi, Yamamura Ken-Ichi
| 期刊: | Scientific Reports | 影响因子: | 3.900 |
| 时间: | 2016 | 起止号: | 2016 Jun 2; 6:27409 |
| doi: | 10.1038/srep27409 | 研究方向: | 发育与干细胞 |
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