Centriole Elimination: A Mechanism for Resetting Entropy in the Cell

Authors

  • Jaba Tkemaladze Author

DOI:

https://doi.org/10.5281/zenodo.15053431

Keywords:

Centrioles, Elimination, Entropy, Totipotency, Differentiation, Aging

Abstract

Centrioles are highly conserved organelles within the eukaryotic domain of life, playing an indispensable role in microtubule organization, cellular differentiation, and the formation of cilia and flagella. However, in the processes of oogenesis and spermatogenesis in certain organisms, centrioles undergo elimination, thereby preventing the transmission of either young or aged centrioles to the zygote, depending on the specific system of asymmetric division. The removal of centrioles in gametes can be interpreted as a mechanism of resetting cellular entropy and restoring totipotency, which is crucial for embryonic development. In somatic cells, centriole elimination is also observed during terminal differentiation, suggesting a potential connection to replicative aging. Research indicates that the programmed removal of centrioles is linked to degradation mechanisms involving microtubule breakdown and the ubiquitin-proteasome system. Centrioles are unique in the cellular architecture as they lack self-repair mechanisms, leading to the continuous accumulation of entropy, thereby contributing to cellular and organismal aging. Consequently, eliminating centrioles where they are no longer needed can be seen as a countermeasure against aging. Furthermore, centriole elimination plays a pivotal role in preventing centrosome-related pathologies, abnormal cell division, and possibly even oncogenesis. Investigating the mechanisms of centriole elimination opens promising avenues in biomedicine, including strategies for tissue rejuvenation and aging control.

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Published

2025-02-15

Issue

Section

Theoretical Frameworks

How to Cite

Tkemaladze, J. (2025). Centriole Elimination: A Mechanism for Resetting Entropy in the Cell. Longevity Horizon, 1(2). DOI : https://doi.org/10.5281/zenodo.15053431

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