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Gene for neat repair of DNA discovered
January 24, 2002Researchers from the Erasmus University in Rotterdam have demonstrated that a gene helps in the neat repair of DNA. Without this gene the body would repair damaged DNA in a careless manner more often. This causes new damage, which can lead to cancer.
The careless repair of damaged DNA can cause mutations and can result in cancer. Cell biologists from the Erasmus University in Rotterdam studied the repair of double strand breaks. Such breaks can for example arise following radiotherapy.
The researchers simulated radiotherapy by specifically damaging the DNA of mouse cells. Mouse cells in which the gene Rad54 was first inactivated, more often chose a careless means of repairing the damaged DNA. In normal mouse cells no more than 60% of the repairs are done in a careless manner, whereas in cells with an inactivated Rad54 gene this figure was about 80%.
The results show that the Rad54 gene is important for repairing breaks in a neat manner and for preventing mutations. The scientists hope that their findings combined with future research will lead to improvements in the treatment of cancer. In the meantime the researchers are examining patients who overreact to radiotherapy. The idea is that physicians could for example give milder radiotherapy to patients who lack the Rad54 gene.
In another experiment the cell biologists examined the repair of cross-links. This type of damage arises after chemotherapy with, for example, melphalan, mitomycin C or cisplatin. The researchers inactivated the Snm1 gene in mice. After this the mice were given a small quantity of mitomycin.
Mice with a inactivated Snm1 gene died at a lower dose of mitomycin than mice with an intact Snm1 gene. This was probably because the mice with a inactivated Snm1 could not adequately repair the cross-links. Future research in patients who strongly react to chemotherapy must demonstrate whether this also involves a disrupted Snm1 gene.
DNA breaks can be repaired in three ways. The neat manner, homologous recombination, restores the break by copying information from an intact DNA molecule to the broken DNA molecule. The careless manner is called "sticking" recombination. This repair mechanism comes into play when the same piece of DNA is present slightly further along the same DNA molecule. The cell removes the undamaged intermediate piece of DNA. This costs less time than the neat manner but carries the risk that information will be lost. In the third manner, which is the simplest and most careless, the ends around a break are simply stuck together.
NWO (Netherlands Organization for Scientific Research)
DNA Current Events and DNA News RSSHuman genomics in China
Ten years ago, the Chinese National Human Genome Center at Shanghai (South Center, hereafter) was established in the Zhangjiang HiTech Park of Pudong District in Shanghai. To commemorate this important event, which marks the beginning of the Genomics Era in China, we specially organize a series of mini-reviews for this special issue.
Lost in translation
The enzyme machine that translates a cell's DNA code into the proteins of life is nothing if not an editorial perfectionist.
Converting adult somatic cells to pluripotent stem cells using a single virus
A Boston University School of Medicine-led research team has discovered a more efficient way to create induced Pluripotent Stem (iPS) cells, derived from mouse fibroblasts, by using a single virus vector instead of multiple viruses in the reprogramming process.
Looking through Galileo's eyes
In 1609, exactly four centuries ago, Galileo revolutionised humankind's understanding of our position in the Universe when he used a telescope for the first time to study the heavens, which saw him sketching radical new views of the moon and discovering the satellites orbiting Jupiter.
Protein's essential role in repairing damaged cells revealed
University of Michigan researchers have discovered that a key protein in cells plays a critical role in not one, but two processes affecting the development of cancer.
Genetic mutation causes familial susceptibility for degenerative brain disease
Mutation of a gene that helps proteins migrate in and out of the cell's genetic command center - the nucleus - puts some families at higher risk for the degenerative brain disease acute necrotizing encephalopathy (ANE).
NYU scientists discover dangerous new method for bacterial toxin transfer
Scientists have discovered a new way for bacteria to transfer toxic genes to unrelated bacterial species, a finding that raises the unsettling possibility that bacterial swapping of toxins and other disease-aiding factors may be more common than previously imagined.
Plant polymerases IV and V are special forms of Polymerase II
It's a little like finding out that Superman is actually Clark Kent. A team of biologists at Washington University in St. Louis has discovered that two vital cellular components, nuclear RNA Polymerases IV and V (Pol IV and V), found only in plants, are actually specialized forms of RNA Polymerase II, an essential enzyme of all eukaryotic organisms, including humans.
Evolution in action: Our antibodies take 'evolutionary leaps' to fight microbes
With cold and flu season in full swing, the fact that viruses and bacteria rapidly evolve is apparent with every sneeze, sniffle, and cough. A new report in the January 2009 issue of The FASEB Journal, explains for the first time how humans keep up with microbes by rearranging the genes that make antibodies to foreign invaders. This research fills a significant gap in our understanding of how the immune system helps us survive.
Team finds breast cancer gene linked to disease spread
A team of researchers at Princeton University and The Cancer Institute of New Jersey has identified a long-sought gene that is fatefully switched on in 30 to 40 percent of all breast cancer patients, spreading the disease, resisting traditional chemotherapies and eventually leading to death.
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