A newly identified protein plays a key role in selecting enzymes that either cut or unwind DNA during the replication phase.
Researchers have recently identified a protein critical for determining which enzymes are involved in cutting or unwinding DNA during replication.
According to a recent study published in Nature Communications, an international team of scientists has discovered that the protein USP50 aids in the DNA replication process by helping to manage the appropriate use of nucleases and helicases. These enzymes are essential for facilitating the replication process and for addressing issues that arise when the copying machinery encounters obstacles.
The research team, led by Professor Jo Morris from the University of Birmingham’s Department of Cancer and Genomic Sciences, has found that USP50 plays a crucial role in determining which helicases and nucleases are utilized during ongoing replication, fork restarts, and the upkeep of telomeres, which are the DNA-rich structures at the ends of chromosomes. The recognition of USP50’s function offers new insights into DNA replication and may enhance our understanding of the development of certain hereditary conditions.
Jo Morris, a Professor of Molecular Genetics at the University of Birmingham and the study’s corresponding author, stated:
“Our research examines how cells selectively employ specific enzymes to regulate DNA replication effectively. We discovered that, due to the variety of enzymes available for cleaving and unwinding, cells must carefully control which ones they deploy to ensure proper replication. Our findings indicate that the protein USP50 is integral to this regulation.
“This discovery could be an essential milestone in comprehending how certain hereditary gene alterations can lead to early-onset aging and cancer.”
Attempted workaround
The study also revealed that in the absence of USP50 during replication, cells resorted to using various nucleases and helicases in a disorganized manner, resulting in defects in replication.
Professor Morris further added: “We were surprised to find that cellular nucleases and helicases can halt the replication of specific DNA segments — this indicates that cells meticulously coordinate the use of their DNA-processing enzymes to ensure accurate DNA replication.”
Professor Simon Reed, Co-Director of the Division of Cancer and Genetics at Cardiff University and a co-founder of Broken String Biosciences, who co-authored the paper, commented:
“I am genuinely honored to be a co-author of this study published in Nature Communications, which investigates the essential role of USP50 in maintaining genome stability. This research provides valuable insights into the intricate mechanisms that protect our cells from DNA damage and emphasizes how these findings could influence future therapies. I am grateful to my collaborators — together, we have made significant progress in understanding cell function and how we might leverage this knowledge to enhance medical science.”
