David Cortez (Vanderbilt University)

Cells continuously divide as the body grows and renews. Before a cell divides, it copies its DNA so that both resulting cells have their own complete genome. The area along the DNA’s double strand where helix is unwound to replicate the genetic sequence is called the replication fork.
Occasionally, DNA replication is slowed or stalled by damage. Replication is also challenged when an oncogene—a gene that can transform a cell into a tumor cell—is activated. A common response to DNA replication stress is called “replication fork reversal.” “Fork reversal is thought to be a backward movement of the fork, in which the parental DNA strands rejoin, and a new daughter strand duplex is formed,” Cortez said. “Despite years of research, how this type of DNA gymnastics happens is unclear.”

Wenpeng Liu 
The research, led by postdoctoral fellow Wenpeng Liu, discovered a mechanism that allows cells to accomplish healthy DNA reversal while tolerating replication stress. The mechanism, dependent on the protein RAD51, answers long-standing questions in the field and completely changes the fork reversal model.
This new model says that the DNA “fork” that is reversed isn’t even the replication fork generated by the enzyme that unwinds the double-stranded DNA. “Our conclusions explain how cells can copy their DNA during every cell division cycle without generating errors that lead to diseases like cancer,” Cortez said.

Source: https://news.vanderbilt.edu/2023/05/02/research-snapshot-dna-replication-discovery-opens-pathways-to-understanding-and-treating-cancer-aging-and-degenerative-disease/