When Genome Integrity and Cell Cycle Decisions Collide: Roles of Polo Kinases in Cellular Adaptation to DNA Damage

Overview

Journal Syst Synth Biol

Publisher Springer

Specialty Biotechnology

Date 2014 Aug 20

PMID 25136381

Citations 16

Authors

Diego Serrano

Damien DAmours

Affiliations

Soon will be listed here.

Abstract

The drive to proliferate and the need to maintain genome integrity are two of the most powerful forces acting on biological systems. When these forces enter in conflict, such as in the case of cells experiencing DNA damage, feedback mechanisms are activated to ensure that cellular proliferation is stopped and no further damage is introduced while cells repair their chromosomal lesions. In this circumstance, the DNA damage response dominates over the biological drive to proliferate, and may even result in programmed cell death if the damage cannot be repaired efficiently. Interestingly, the drive to proliferate can under specific conditions overcome the DNA damage response and lead to a reactivation of the proliferative program in checkpoint-arrested cells. This phenomenon is known as adaptation to DNA damage and is observed in all eukaryotic species where the process has been studied, including normal and cancer cells in humans. Polo-like kinases (PLKs) are critical regulators of the adaptation response to DNA damage and they play key roles at the interface of cell cycle and checkpoint-related decisions in cells. Here, we review recent progress in defining the specific roles of PLKs in the adaptation process and how this conserved family of eukaryotic kinases can integrate the fundamental need to preserve genomic integrity with effective cellular proliferation.

Citing Articles

The Polo kinase Cdc5 is regulated at multiple levels in the adaptation response to telomere dysfunction.

Coutelier H, Ilioaia O, Le Peillet J, Hamon M, DAmours D, Teixeira M Genetics. 2022; 223(1).

PMID: 36342193 PMC: 9836022. DOI: 10.1093/genetics/iyac171.

DNA damage checkpoint execution and the rules of its disengagement.

Yam C, Lim H, Surana U Front Cell Dev Biol. 2022; 10:1020643.

PMID: 36274841 PMC: 9582513. DOI: 10.3389/fcell.2022.1020643.

Adaptation to DNA Damage, an Asymptotic Approach for a Cooperative Non-local System.

Leculier A, Roux P Acta Appl Math. 2022; 180(1):1.

PMID: 35756144 PMC: 9213332. DOI: 10.1007/s10440-022-00501-1.

Adaptation to DNA damage as a bet-hedging mechanism in a fluctuating environment.

Roux P, Salort D, Xu Z R Soc Open Sci. 2021; 8(8):210460.

PMID: 34457341 PMC: 8385375. DOI: 10.1098/rsos.210460.

A guiding torch at the poles: the multiple roles of spindle microtubule-organizing centers during cell division.

Rincon A, Monje-Casas F Cell Cycle. 2020; 19(12):1405-1421.

PMID: 32401610 PMC: 7480817. DOI: 10.1080/15384101.2020.1754586.

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