Barnabas Szakal

The genetic information stored in DNA is under continuous threat by endogenous and environmental sources of DNA damage. Cells have evolved multiple DNA repair pathways that function in overlapping manners, with principles shared across species. Here, we depict the main DNA repair pathways cells rely on, with the primary lesions they are tackling, along with key players and main DNA transactions. To view this SnapShot, open or download the PDF.

Completion of DNA replication relies on the ability of replication forks to traverse various types of DNA damage, actively transcribed regions, and structured DNA. The mechanisms enabling these processes are here referred to as DNA damage tolerance pathways. Here, we depict the stalled DNA replication fork structures with main DNA transactions and key factors contributing to the bypass of such blocks, replication restart, and completion. To view this SnapShot, open or download the PDF.

In our previous study of systematically generated mutant strains, we observed that combining mutations affecting SWR-C or its substrate, Htz1, and the replication fork progression proteins Mrc1, Tof1 or Csm3 resulted in synergistic increases in dGCR rate, as assessed by semi-qualitative patch scores6. To understand these interactions, we performed GCR rate measurements with newly reconstructed mrc1Δ, swr1Δ, and mrc1Δ swr1Δ strains containing the dGCR, sGCR, or uGCR assay (Fig. 1a, b).