A coordinated interplay: Proteins with multiple functions in DNA replication, DNA repair, cell cycle/ checkpoint control, and transcription

2000 ◽  
pp. 261-298 ◽  
Author(s):  
Manuel Stucki ◽  
Igor Stagljar ◽  
Zophonias O. Jonsson ◽  
Ulrich Hübscher
Keyword(s):  
Cell Cycle ◽  
Dna Repair ◽  
Dna Replication ◽  
Cell Cycle Checkpoint ◽  
Checkpoint Control ◽  
Multiple Functions ◽  
Cycle Checkpoint

scholarly journals DNA repair and cell cycle checkpoint defects in a mouse model of ‘BRCAness’ are partially rescued by 53BP1 deletion

Cell Cycle ◽  
2018 ◽  
Vol 17 (7) ◽  
pp. 881-891 ◽  
Author(s):  
Sarah M. Misenko ◽  
Dharm S. Patel ◽  
Joonyoung Her ◽  
Samuel F. Bunting
Keyword(s):  
Cell Cycle ◽  
Dna Repair ◽  
Mouse Model ◽  
Cell Cycle Checkpoint ◽  
Cycle Checkpoint

DNA damage checkpoint kinases in cancer

2020 ◽  
Vol 22 ◽  
Author(s):  
Hannah L. Smith ◽  
Harriet Southgate ◽  
Deborah A. Tweddle ◽  
Nicola J. Curtin
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Environmental Dna ◽  
Cell Cycle Checkpoint ◽  
Checkpoint Control ◽  
Integrated Network ◽  
Checkpoint Kinases ◽  
G1 Checkpoint ◽  
Cycle Checkpoint ◽  
High Level

Abstract DNA damage response (DDR) pathway prevents high level endogenous and environmental DNA damage being replicated and passed on to the next generation of cells via an orchestrated and integrated network of cell cycle checkpoint signalling and DNA repair pathways. Depending on the type of damage, and where in the cell cycle it occurs different pathways are involved, with the ATM-CHK2-p53 pathway controlling the G1 checkpoint or ATR-CHK1-Wee1 pathway controlling the S and G2/M checkpoints. Loss of G1 checkpoint control is common in cancer through TP53, ATM mutations, Rb loss or cyclin E overexpression, providing a stronger rationale for targeting the S/G2 checkpoints. This review will focus on the ATM-CHK2-p53-p21 pathway and the ATR-CHK1-WEE1 pathway and ongoing efforts to target these pathways for patient benefit.

scholarly journals Plasma membrane/cell wall perturbation activates a novel cell cycle checkpoint during G1 inSaccharomyces cerevisiae

2016 ◽  
Vol 113 (25) ◽  
pp. 6910-6915 ◽  
Author(s):  
Keiko Kono ◽  
Amr Al-Zain ◽  
Lea Schroeder ◽  
Makoto Nakanishi ◽  
Amy E. Ikui
Keyword(s):  
Cell Cycle ◽  
Wound Healing ◽  
Cell Wall ◽  
Plasma Membrane ◽  
Dna Replication ◽  
Membrane Damage ◽  
Cell Cycle Checkpoint ◽  
Plasma Membrane Damage ◽  
Cycle Checkpoint ◽  
Membrane Cell

Cellular wound healing or the repair of plasma membrane/cell wall damage (plasma membrane damage) occurs frequently in nature. Although various cellular perturbations, such as DNA damage, spindle misalignment, and impaired daughter cell formation, are monitored by cell cycle checkpoint mechanisms in budding yeast, whether plasma membrane damage is monitored by any of these checkpoints remains to be addressed. Here, we define the mechanism by which cells sense membrane damage and inhibit DNA replication. We found that the inhibition of DNA replication upon plasma membrane damage requires GSK3/Mck1-dependent degradation of Cdc6, a component of the prereplicative complex. Furthermore, the CDK inhibitor Sic1 is stabilized in response to plasma membrane damage, leading to cell integrity maintenance in parallel with the Mck1-Cdc6 pathway. Cells defective in both Cdc6 degradation and Sic1 stabilization failed to grow in the presence of plasma membrane damage. Taking these data together, we propose that plasma membrane damage triggers G1 arrest via Cdc6 degradation and Sic1 stabilization to promote the cellular wound healing process.

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