Viable offspring obtained from Prm1-deficient sperm in mice
Naoki Takeda1, Kazuya Yoshinaga2, Kenryo Furushima3
1Division of Developmental Genetics, Institute of Resource Development and Analysis, Kumamoto University, 2-2-1 Honjo, Kumamoto 860-0811, Japan.
Scientific Reports
|June 3, 2016
Summary
Sperm lacking protamine 1 (Prm1) can still produce offspring, even with abnormal DNA packaging and structure. This finding challenges previous assumptions about Prm1
Area of Science:
- Reproductive Biology
- Genetics
- Spermatogenesis
Background:
- Protamines are crucial for dense DNA packaging in sperm, with protamine 1 (Prm1) and protamine 2 (Prm2) being essential.
- Disrupting Prm1 or Prm2 alleles typically leads to infertility, despite sperm production.
Purpose of the Study:
- To investigate the reproductive potential of sperm lacking protamine 1 (Prm1).
- To determine if Prm1-deficient sperm can contribute to viable offspring generation.
Main Methods:
- Generation of Prm1-deficient female chimeric mice carrying Prm1-deficient oocytes.
- Production of Prm1(+/-) male mice from these chimeras.
- In vitro fertilization using zona-free oocytes and sperm from Prm1(+/-) mice.
- Transfer of resulting blastocysts to produce healthy Prm1(+/-) offspring.
Main Results:
- Prm1-deficient female mice successfully produced Prm1(+/-) male offspring.
- Healthy Prm1(+/-) offspring were generated via IVF using Prm1-deficient sperm and oocytes.
- Prm1-deficient sperm exhibited abnormal morphology, DNA instability, decondensed chromatin, and reduced mitochondrial membrane potential.
- Despite these defects, Prm1-deficient sperm enabled successful fertilization and development.
Conclusions:
- Sperm lacking protamine 1 (Prm1) can generate viable offspring.
- The study challenges the necessity of Prm1 for male fertility and successful fertilization.
- Offspring derived from Prm1-deficient sperm showed minimal derangement in expression profiles, suggesting compensatory mechanisms.
