Abstract
Cellular function is highly dependent on genomic stability, which is mainly ensured by two cellular mechanisms: the DNA damage response (DDR) and the Spindle Assembly Checkpoint (SAC). The former provides the repair of damaged DNA, and the latter ensures correct chromosome segregation. This review focuses on recently emerging data indicating that the SAC and the DDR proteins function together throughout the cell cycle, suggesting crosstalk between both checkpoints to maintain genome stability.
Highlights
The eukaryotic cell has developed several surveillance mechanisms to ensure genome integrity throughout the cell cycle
Its role in DNA Damage Response (DDR) has been well studied; in human colon cancer cells, it has been reported that in the absence of damage, BRCA1 is phosphorylated by CHK2 at Serine 988 at centrosomes; this phosphorylation is important for the PP6CSAPS3 phosphatase complex to be recruited to kinetochores and to interact with BRCA1, preventing, on the one hand, the binding of AURORA A to BRCA1 and on the other hand, inhibiting the activity of AURORA A, favoring a proper assembly of the mitotic spindle (Figure 2) promoting adequate chromosome segregation
Despite the studies performed on BRCA2 and its participation in mitosis, the involvement of this protein in this phase of the cell cycle and the determination of whether BRCA2 is fundamental in the completion of cytokinesis is just beginning to be understood
Summary
Cellular function is highly dependent on genomic stability, which is mainly ensured by two cellular mechanisms: the DNA damage response (DDR) and the Spindle Assembly Checkpoint (SAC). The former provides the repair of damaged DNA, and the latter ensures correct chromosome segregation. This review focuses on recently emerging data indicating that the SAC and the DDR proteins function together throughout the cell cycle, suggesting crosstalk between both checkpoints to maintain genome stability
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