Image: Jenna Hambrick / La Jolla Institute for Immunology
Scientists at the Institute of immunology in La JOLLA, California have identified the mechanism that prevents catastrophic genome instability and cancer. About it reported in a press release on MedicalXpress.
The researchers found that a key role is played by the process of methylation, that is, joining the methyl group CH3 to cytosine — nitrogen base, which is part of the DNA. Such modification is related to epigenetic regulation contributes to the activation or deactivation of specific genes. A methylated form of cytosine — 5-methylcytosine is formed with the participation of enzymes DNMT, however, scientists did not know what contributes to the demethylation.
It turned out that TET proteins convert 5-methylcytosine 5-hydroxymethylcytosine, which goes to the normal cytosine. In addition, the dysfunction such as TET and DNMT closely associated with many types of cancer, including malignant blood diseases. In each of these cases, the instability of the genome in which genes accumulate deleterious mutations.
Experiments on mice have demonstrated that mutations in the TET lead to an increase in the level of methylation of the genome of T-cells, however, this large region of DNA, on the contrary, lose the methyl group. It turned out that the molecules that contribute to the attaching of methyl groups to cytosine, moved to another part of genetic material outside of the heterochromatin region of DNA, located in a tightly Packed condition and with inactive genes. A reduced level of methylation in the heterochromatin is a common symptom of cancer.
Heterochromatin contains genes that should be inactive in the cells of a certain type, but “selfish” DNA elements, as well as a repeating sequence. They do not encode proteins like normal genes, but are able to move and multiply within the genome, disrupting its integrity.
Video, photo All from Russia.