To Learn Quickly, Brain Cells Break Down Their DNA

Faced with a threat, the brain has to move fast, the neurons making new connections to figure out what might be in exchange for the difference between life and death. But in response to this, the brain also raises the stakes: As demonstrated by the unconventional that has now been discovered, in order to more easily express generations of learning and memory, brain cells have pasted their DNA into many main points, and then construct their broken genome later.

The search not only provides insight into the nature of brain plasticity. It also shows that DNA breakdown can be a normal and important part of normal cellular processes – with implications for how scientists think about aging and disease, and how they approach genomic events. which they often write as not really luck.

The discovery is even more surprising because the duplications of the double strand of DNA, in which the same helical ladder metal is cut in the same position along the genome, pose a specific risk of genetic damage. associated with cancer, neurodegeneration and aging. It is more difficult for cells to repair double-strand breaks than other types of DNA damage because there is no unwanted “template” left to facilitate the reachachment of the strands.

Although it has long been recognized that DNA breakdown sometimes also plays an important role. When cells separate, double-strand breaks allow the normal process of genetic reunification between chromosomes. In the evolving immune system, they activate pieces of DNA to combine and produce different repertoires of antibodies. Breaking the double strand is also done in neuronal development and to help turn on some gen. However, such functions as exceptions to the rule that double strand break are not accidental and unwanted.

but a turning point arrived in 2015. Li-Huei Tsai, a neuroscientist and director of the Picower Institute for Learning and Memory at the Massachusetts Institute of Technology, and his colleagues follow previous work involving Alzheimer’s disease in the accumulation of double strand breaks in neurons. To their surprise, the researchers found that the stimulation of cultural neurons caused a double strand break in their DNA, and the breakdowns rapidly increased the expression of a dozen fast -moving activity -related genes. synaptic learning and memory.

Double strand breaks as important for controlling gene activity essential to the functioning of neurons. Tsai and his colleagues think that the breakdown essentially releases enzymes attached to the twisted pieces of DNA, which are released to easily identify related genes. But the idea “met with a lot of skepticism,” Tsai said. “People have a hard time thinking that double-strand breaks can be physically significant.”

However, Paul Marshall, a postdoctoral researcher at the University of Queensland in Australia, and his colleagues decided to follow the search. Their job, that is appeared in 2019, both confirmed and expanded on Tsai’s team’s observations. This showed that DNA breakdown affected two waves of enhanced gene transcription, one immediately and one a few hours later.

Marshall and his colleagues proposed a two-step mechanism to explain the phenomenon: When DNA is damaged, certain enzyme molecules are released for writing (as suggested by Tsai’s group) and the resting area is also transferred to the chemical group methyl. Called epigenetic marker. Afterwards, when the repair of the broken DNA begins, the marker is removed-and in the process, many more enzymes can be freed, beginning the second phase of translation.

“It’s not just the breaking of the double strand that’s involved as a trigger,” Marshall said, “after it becomes a marker, and the marker itself can be used in terms of controlling and guiding location machinery.”

Since then, other studies have shown something similar. In one, published last year, associated with double strand break not only in the formation of a memorable fear, but with its memory.

Now, in a study last month on PLOS USA, Tsai and his colleagues have shown that this counter -mechanism of gene expression may predominate in the brain. This time, instead of using neuron cultures, they looked at the brain cells of living mice that had learned to coexist in an environment with electric shock. When the group mapped genes that underwent double strand breaks in the prefrontal cortex and hippocampus of shocked mice, they found breaks occurring in nearly a hundred genes, most of which were involved in memory -related synaptic processes.

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