| First Author | Takeda N | Year | 2016 |
| Journal | Sci Rep | Volume | 6 |
| Pages | 27409 | PubMed ID | 27250771 |
| Mgi Jnum | J:272291 | Mgi Id | MGI:6216745 |
| Doi | 10.1038/srep27409 | Citation | Takeda N, et al. (2016) Viable offspring obtained from Prm1-deficient sperm in mice. Sci Rep 6:27409 |
| abstractText | 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. |
