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Association between spindle assembly checkpoint expression and maternal age in human oocytes
N Steuerwald1, J Cohen, R J Herrera
1Gamete and Embryo Research Laboratory, Institute for Reproductive Medicine and Science of Saint Barnabas, West Orange, NJ 07052, USA. nury.steuerwald@embryos.net
Molecular Human Reproduction
|January 3, 2001
Summary
Aging human oocytes show decreased spindle assembly checkpoint gene transcripts (MAD2, BUB1). This degradation may impair checkpoint function, contributing to age-related aneuploidy and genomic instability.
Area of Science:
- Cell Biology
- Genetics
- Reproductive Biology
Background:
- The spindle assembly checkpoint (SAC) is crucial for preventing aneuploidy by halting cell cycle progression upon detection of chromosome alignment defects.
- Genes like MAD2 and BUB1 encode proteins essential for SAC function, ensuring accurate chromosome segregation during cell division.
- Genomic instability and aneuploidy increase with maternal age, suggesting potential age-related defects in cell cycle regulation.
Purpose of the Study:
- To investigate the hypothesis that age-related changes in SAC gene transcript levels contribute to aneuploidy in human oocytes.
- To quantify the concentrations of MAD2 and BUB1 transcripts in human oocytes across different maturation stages.
Main Methods:
- Quantitative analysis of MAD2 and BUB1 transcript concentrations.
- Real-time rapid cycle fluorescent reverse transcription-polymerase chain reaction (RT-PCR) was employed for transcript quantification.
Main Results:
- Transcript levels of MAD2 and BUB1 were found to degrade as human oocytes age.
- Quantitative analysis indicated a decline in these key checkpoint gene messages in older oocytes.
Conclusions:
- The observed degradation of MAD2 and BUB1 transcripts in aging oocytes suggests a potential impairment of the spindle assembly checkpoint.
- This age-related decline in checkpoint function may be a contributing factor to the increased incidence of aneuploidy in gametes from older women.
- These findings highlight a potential molecular mechanism underlying age-related reproductive challenges.