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To ensure normal fetal development and prevent disease, it is crucial that certain genes are turned on or off at the right time during cell division. Researchers in Professor Kristian Helin's group at the University of Copenhagen, have now shown how the TET1 enzyme controls this activity. The results have just been published in the journal Nature.
The complete human genetic code was mapped in 2000. However, it has become clear that the genetic code can only partly answer how an individual develops and is protected against disease.
What is also instrumental is how our genes are controlled - what genes are turned on or off and at what times. This timing is partly regulated by specific enzymes that attach small chemical groups called methyl groups, along our DNA strands.
"The methyl group can turn off the gene that lies in a stretch of DNA where it becomes attached. TET1 is a type of enzyme that can fine tune the signals that control gene activity by changing the methyl groups which thereafter are removed," says Kristian Helin.
"Our most important finding is that TET1 acts like a safe guard and prevents methyl groups being attached to genes that need to be active for normal growth and development of our cells. Crucial for normal fetal development for example" PhD student Kristine Williams.
Selected genes also need to be active in our stem cells before those cells can become specialized to one of the more than 200 cell types that exist in our body. Other genes need only be active in very specific cells - for example liver, muscle or nerve cells.
The research results also contribute to our understanding of what goes wrong when some cells accidently develop into cancer cells. The functions of our body are dependent on constant cellular renewal through the division of cells. A large, interconnected cellular machinery ensures that our DNA is intact and copied correctly when our cells divide, crucial for their normal development and function. In a worst case scenario, changes in the DNA, so called mutations, can result in the development of cancer.
Some specialised genes act as tumor suppressors and are especially important for fighting cancer: "If methyl groups are deployed to genes that are usually active in normal cells, the genes are turned off and this can be detrimental. If it happens to tumor suppressor genes, it can be a step towards cancer development as the genes no longer can protect against unintended cell growth," Kristian Helin.
So TET1 fights cancers by controlling the activity and protective function of tumor suppressor genes. Our cells also contain a close relative to TET1, the TET2 enzyme, which is the most frequently mutated gene in blood cancers. BRIC researches have discovered that TET2 also controls gene activity by facilitating removal of methyl groups from DNA.
The scientists are currently extending their research to cellular models for cancer development. Results will supply insight into the mechanisms leading to blood cancers and can potentially lead to development of new therapies.
Original article: http://news.ku.dk/all_news/2011/2011.4/stem_cells_cancer_bric_nature/
Published paper: "TET1 and hydroxymethylcytosine in transcription and DNA methylation fidelity", Williams et al., Nature April 13, 2011
Biotech Research and Innovation Centre (BRIC) is a research center at University of Copenhagen.