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Cell-cycle and Age-Related Modulations in Mouse Chromosome Stiffness
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Abstract
The intricate structure of chromosomes is complex, and many aspects of chromosome configuration/organization remain to be fully understood. Measuring chromosome stiffness can provide valuable insights into their structure. However, the nature of chromosome stiffness, whether static or dynamic, remains elusive. In this study, we analyzed chromosome stiffness in MI and MII oocytes. We revealed that MI oocytes had a ten-fold increase in stiffness compared to mitotic chromosomes, whereas chromosome stiffness in MII oocytes was relatively low chromosome. We then investigated the contribution of meiosis-specific cohesin complexes to chromosome stiffness in MI and MII oocytes. Surprisingly, the Young’s modulus of chromosomes from the three meiosis-specific cohesin mutants did not exhibit significant differences compared to the wild type, indicating that these proteins may not play a substantial role in determining chromosome stiffness. Additionally, our findings revealed an age-related increase in chromosome stiffness in MI oocytes. Age correlates with elevated DNA damage levels, so we investigated the impact of etoposide-induced DNA damage on chromosome stiffness, discovering a reduction in stiffness in response to such damage in MI oocytes. Overall, our study underscores the dynamic nature of chromosome stiffness, subject to changes influenced by the cell cycle and age.
Title: Cell-cycle and Age-Related Modulations in Mouse Chromosome Stiffness
Description:
Abstract
The intricate structure of chromosomes is complex, and many aspects of chromosome configuration/organization remain to be fully understood.
Measuring chromosome stiffness can provide valuable insights into their structure.
However, the nature of chromosome stiffness, whether static or dynamic, remains elusive.
In this study, we analyzed chromosome stiffness in MI and MII oocytes.
We revealed that MI oocytes had a ten-fold increase in stiffness compared to mitotic chromosomes, whereas chromosome stiffness in MII oocytes was relatively low chromosome.
We then investigated the contribution of meiosis-specific cohesin complexes to chromosome stiffness in MI and MII oocytes.
Surprisingly, the Young’s modulus of chromosomes from the three meiosis-specific cohesin mutants did not exhibit significant differences compared to the wild type, indicating that these proteins may not play a substantial role in determining chromosome stiffness.
Additionally, our findings revealed an age-related increase in chromosome stiffness in MI oocytes.
Age correlates with elevated DNA damage levels, so we investigated the impact of etoposide-induced DNA damage on chromosome stiffness, discovering a reduction in stiffness in response to such damage in MI oocytes.
Overall, our study underscores the dynamic nature of chromosome stiffness, subject to changes influenced by the cell cycle and age.
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