Abstract
The maintenance of genome integrity is important for normal cellular functions, organism development and the prevention of diseases, such as cancer. Cellular pathways respond immediately to DNA breaks leading to the initiation of a multi-facetted DNA damage response, which leads to DNA repair and cell cycle arrest. Cell cycle checkpoints provide the cell time to complete replication and repair the DNA damage before it can continue to the next cell cycle phase. The G2/M checkpoint plays an especially important role in ensuring the propagation of error-free copies of the genome to each daughter cell. Here, we review recent progress in our understanding of DNA repair and checkpoint pathways in late S and G2 phases. This review will first describe the current understanding of normal cell cycle progression through G2 phase to mitosis. It will also discuss the DNA damage response including cell cycle checkpoint control and DNA double-strand break repair. Finally, we discuss the emerging concept that DNA repair pathways play a major role in the G2/M checkpoint pathway thereby blocking cell division as long as DNA lesions are present.
Highlights
It is essential for the survival and function of living cells to safeguard genomic integrity and to ensure the proper transmission of genetic information encoded by DNA
We discuss the emerging concept that DNA repair pathways play a major role in the G2/M checkpoint pathway thereby blocking cell division as long as DNA
We focus on how the DNA Double Strand Break (DSB) activates the checkpoint and initiation of repair
Summary
It is essential for the survival and function of living cells to safeguard genomic integrity and to ensure the proper transmission of genetic information encoded by DNA. DNA replication, the proper partitioning of chromosomes to daughter cells during cell division and the ability to identify and correct DNA lesions that arise spontaneously or are induced by exogenous agents The accumulation of these mutations and the resulting genetic instability can promote aging, genetic diseases and oncogenesis. Different pathways play a more critical role in the control This is supported by recent findings from our and other labs, which shed new light on how repair and checkpoint control are coordinated [4,5,6]
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