Possible answer:

Stalled DNA replication fork checkpoint

When DNA replication is arrested due to obstacles in the template DNA strand or depletion of nucleotides or other factors, cells need to activate checkpoints to prevent progression into mitosis with incomplete or damaged DNA replication intermediates. Depending on the severity and duration of the replication stress, different checkpoint pathways can be engaged, but the predominant one is the intra-S checkpoint in the G1/S transition of the cell cycle.

Intra-S checkpoint

The intra-S checkpoint monitors the integrity and progression of DNA replication during S phase, which involves the duplication of the genome. Several proteins and pathways contribute to this checkpoint, which can sense DNA damage, replication fork collapse, or nucleotide depletion. One of the key effectors of the intra-S checkpoint is the ATR kinase, which phosphorylates substrates involved in DNA repair, replication restart, or cell cycle arrest.

Activation of the intra-S checkpoint can slow down or stop cell cycle progression, allowing cells to repair and resume DNA replication before entering mitosis. If the damage is too severe, cells can undergo apoptosis or senescence as part of the DNA damage response. However, if the checkpoint is defective or overwhelmed, cells can proceed with cell division despite having incomplete or abnormal DNA replication, which can lead to genomic instability and cancer.

Conclusion

Therefore, when a cell has a stalled DNA replication fork, the predominantly activated checkpoint is the intra-S checkpoint, which monitors S phase and engages various DNA damage response pathways to ensure that DNA replication is complete and accurate before cells enter mitosis. The other checkpoints (G1/S, G2/M, and M) can also be activated if the stress persists or if other factors are involved, but they are less specific to DNA replication problems.