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Cell cycle and Age-Related Modulations of Mouse Chromosome Stiffness

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Abstract Chromosome structure is complex, and many aspects of chromosome organization are still not understood. Measuring the stiffness of chromosomes offers valuable insight into their structural properties. In this study, we analyzed the stiffness of chromosomes from metaphase I (MI) and metaphase II (MII) oocytes. Our results revealed a ten-fold increase in stiffness (Young’s modulus) of MI chromosomes compared to somatic chromosomes. Furthermore, the stiffness of MII chromosomes was found to be lower than that of MI chromosomes. We examined the role of meiosis-specific cohesin complexes in regulating chromosome stiffness. Surprisingly, the stiffness of chromosomes from three meiosis-specific cohesin mutants did not significantly differ from that of wild-type chromosomes, indicating that these cohesins may not be primary determinants of chromosome stiffness. Additionally, our findings revealed an age-related increase of chromosome stiffness for MI oocytes. Since aging is associated with elevated levels of DNA damage, we investigated the impact of etoposide-induced DNA damage on chromosome stiffness and found that it led to a reduction in stiffness in MI oocytes. Overall, our study underscores the dynamic and cyclical nature of chromosome stiffness, modulated by both the cell cycle, and by age-related factors.
Title: Cell cycle and Age-Related Modulations of Mouse Chromosome Stiffness
Description:
Abstract Chromosome structure is complex, and many aspects of chromosome organization are still not understood.
Measuring the stiffness of chromosomes offers valuable insight into their structural properties.
In this study, we analyzed the stiffness of chromosomes from metaphase I (MI) and metaphase II (MII) oocytes.
Our results revealed a ten-fold increase in stiffness (Young’s modulus) of MI chromosomes compared to somatic chromosomes.
Furthermore, the stiffness of MII chromosomes was found to be lower than that of MI chromosomes.
We examined the role of meiosis-specific cohesin complexes in regulating chromosome stiffness.
Surprisingly, the stiffness of chromosomes from three meiosis-specific cohesin mutants did not significantly differ from that of wild-type chromosomes, indicating that these cohesins may not be primary determinants of chromosome stiffness.
Additionally, our findings revealed an age-related increase of chromosome stiffness for MI oocytes.
Since aging is associated with elevated levels of DNA damage, we investigated the impact of etoposide-induced DNA damage on chromosome stiffness and found that it led to a reduction in stiffness in MI oocytes.
Overall, our study underscores the dynamic and cyclical nature of chromosome stiffness, modulated by both the cell cycle, and by age-related factors.

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