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Dna replication in mitosis vs meiosis9/16/2023 As a result, a greater proportion of RepID-depleted cells than RepID-containing cells underwent apoptosis. In other words, malfunctioning DNA replication checkpoints may actually help kill cancer cells because they render them more sensitive to this class of drugs.Īladjem and her team tested one such drug, and they found that the drug triggered severe excess DNA replication in cells depleted of RepID. The ultimate result is programmed cell death, or apoptosis. This places an excessive burden on the cancer cells, leading to improper separation of their chromosomes when they divide. A number of drugs under investigation inhibit the remaining functional checkpoints in these cells, triggering excessive DNA replication. Oftentimes, portions of DNA replication checkpoints are disrupted in cancer cells. If CRL4 is not working properly, though, a buildup of CDT1 can occur, allowing DNA replication to proceed unchecked, resulting in excess replication of segments of the genome. Once CRL4 is bound to chromatin, it causes a protein called CDT1 to break down, keeping it from kick-starting replication more than once each time cells divide. They showed that RepID recruits the enzyme CRL4 to chromatin before DNA replication begins. This can lead to cancer, primarily by making it more likely that fragments of chromosomes rearrange themselves, activating genes that lead to uncontrollable cell division.Ī team led by Mirit Aladjem, Ph.D., Senior Investigator in CCR’s Developmental Therapeutics Branch, and Sang-Min Jang, Ph.D., a postdoctoral researcher in Aladjem’s lab, reported in Nature Communications that the RepID protein sets off a chain reaction of protein signaling and recruitment to prevent DNA replication from getting out of control. As a result, cells can become cancerous through a variety of mechanisms, such as increased copies of genes that drive cancer growth or through uncontrollable cell division, which is a hallmark of cancer.ĭNA replication errors, especially those occurring at regions that are hard to replicate, called fragile sites, can cause breaks in DNA. Occasionally, these checkpoints get disrupted. Now, CCR scientists have added to this understanding by describing novel aspects of DNA replication that involve a protein called RepID.Ĭells have a number of molecular checkpoints in place to prevent DNA replication from going awry, including some to ensure that cells replicate their DNA only once before each division. Because defects in this process can cause mutations that eventually lead to cancer, understanding the details of how replication works could point to possible cancer treatments. Each time a cell divides, it must first duplicate its genetic material in a process called DNA replication.
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