Experiments have shown that a major role is played here by the enzyme topoisomerase IIβ.
Cellular DNA is usually quite complicated thing and twisted in superhelix so that the proteins that carry out its replication (ie a doubling) before dividing or transcription (RNA synthesis), simply can not with such confusing and twisted DNA work. And here they are needed topoisomerase, which make the DNA double-stranded breaks or single and then stitch them back, thus unraveling the complex space in the DNA. When neurons of topoisomerase II? turned off, the amount of damage-breaks in DNA rapidly decreased, but at the same time silent genes necessary for neuronal response to a stimulus.
Near these genes are located specific sequences of nucleotides to lure to his protein CTCF.
- It serves as an inhibitor of transcription, i.e. in the presence of its RNA gene can be synthesized. Activation of multiple genes begins with the fact that proteins are sitting on a regulatory region of DNA called a promoter interact with proteins on a regulatory domain called an enhancer. However, CTCF create DNA loops and curves, because of which the promoter and enhancer (and proteins that sit on them) can not get close and interact. And here comes to the aid of topoisomerase, which, by cutting the DNA, helps it to change shape so that the sequence of converged regulators, in spite of the protein CTCF. Then begins the synthesis of RNA on the gene necessary for strengthening the synapse and neuron can now securely integrate into a storage chain.
- Of course, then the gap will be embedded in the DNA. But it is quite possible that with the age of the proteins that make tears, stop working as it should, and leave such damage uncorrected. So that this molecular mechanism is necessary for memory formation, it contributes to the aging of cells. That is precisely the ability to learn and remember becomes a major cause of age-related cognitive disorders – in full accordance with the Solomon expression “in much wisdom is much grief” (though King Solomon had in mind here still something other than neurophysiological disorders).
It follows that in order to prevent age-related troubles (up to Alzheimer’s disease), arising from the problems in the genome, we need to take care not only about the fact that the DNA is generally no breaks were not – they just need, and lots of it – and the fact that such breaks promptly healed repariruschimi systems. While before we talk about the prospects of new clinical data, test them on human cells.