Related Experiment Videos
Inadequate function of sterile tw5/tw32 spermatozoa overcome by intracytoplasmic sperm injection
S Kuretake1, M Maleszewski, A Tokumasu
1Department of Anatomy and Reproductive Biology, University of Hawaii School of Medicine, Honolulu 96822, USA.
Abstract:
Mice carrying two t complementary haplotypes (tw5/tw32) are totally sterile. Their spermatozoa have poor motility and fertilize neither zona-intact nor zona-free oocytes, even though they are structurally indistinguishable from control (wild-type) spermatozoa. However, when injected directly into oocytes, these infertile spermatozoa are able to participate in normal development. This suggests that infertility of tw5/tw32 male (spermatozoa) is more likely to be due to poor sperm-oocyte interaction than to genetic incompetence of sperm nuclei.
Insights
Male mice with tw5/tw32 haplotypes are sterile due to poor sperm-oocyte interaction, not genetic defects. Their infertile spermatozoa can still support normal development when directly injected into oocytes.
Area of Science:
- Reproductive Biology
- Genetics
- Developmental Biology
Background:
- Male sterility in mice can arise from various genetic factors affecting sperm function.
- The t haplotypes are known to cause complex effects on male fertility.
Purpose of the Study:
- To investigate the cause of infertility in mice with the tw5/tw32 t haplotypes.
- To determine if the infertility is due to sperm nuclear genetic incompetence or impaired sperm-oocyte interaction.
Main Methods:
- Comparative analysis of spermatozoa from sterile (tw5/tw32) and fertile (wild-type) mice.
- In vitro fertilization assays with zona-intact and zona-free oocytes.
- Intracytoplasmic sperm injection (ICSI) into oocytes.
Main Results:
- Spermatozoa from tw5/tw32 mice exhibited poor motility and failed to fertilize oocytes in standard assays.
- Structurally, tw5/tw32 spermatozoa were indistinguishable from wild-type spermatozoa.
- Direct injection of tw5/tw32 spermatozoa into oocytes resulted in normal embryonic development.
Conclusions:
- The infertility of tw5/tw32 male mice is primarily attributed to a defect in sperm-oocyte interaction.
- Genetic competence of the sperm nucleus is likely intact, suggesting a functional or surface-level issue affecting fertilization.