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In front of A threat, the brain must act quickly, its neurons make new connections to find out what the difference between life and death might be. But in its response, the brain also raises the issue: As a recent troubling finding shows, in order to express learning and memory genes more quickly, brain cells divide DNA into fragments at many key points, and then reconstruct the broken genome later.
The findings do not provide information on the nature of brain plasticity. It also demonstrates that DNA breakdown may be the most common and important part of normal cellular processes. This has implications for the way scientists approach their opinion of aging and disease and how they approach the genomic facts they have just described as unlucky.
The most surprising finding is the breakdown of double-stranded DNA when the two rails of the helical ladder are cut at the same position in the genome because the genetic damage associated with cancer, neurodegeneration, and aging is particularly dangerous. It is more difficult for cells to repair double-strand breaks than other DNA damage, as there is no complete “template” left to drive the strands back together.
However, it has long been recognized that DNA rupture sometimes has a constructive role. When cells are dividing, double-strand fractures allow for the normal process of genetic recombination between chromosomes. In the developing immune system, they allow DNA fragments to be recombined and create a diverse repertoire of antibodies. Double-strand fractures are also involved in neuronal development and helps turn on some genes. Still, these functions seem to be the exceptions to unexpected and unwanted double-thread breaks.
But a turning point It came 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 were monitoring previous work linking Alzheimer’s disease to the accumulation of double-stranded fractures in neurons. Surprisingly, the researchers found that culture-stimulating neurons caused double-strand breaks in their DNA, and the breaks quickly increased the expression of a dozen fast-acting genes associated with synaptic activity in learning and memory.
Double-stranded fractures appeared to be essential for regulating gene activity that is important for neuronal function. Tsai and his collaborators hypothesized that the fractures essentially released enzymes that were stuck in the twisted pieces of DNA, releasing them to quickly transcribe important genes in the environment. But the idea “had a lot of skepticism,” Tsaik said. “People have a hard time imagining that double-strand fractures can be physiologically important.”
However, Paul Marshall, A postdoctoral researcher at the University of Queensland in Australia and his colleagues decided to follow up on the discovery. Their job, which It appeared in 2019, both confirmed and extended the remarks made by the Tsai group. He showed that the DNA rupture affected two waves of enhanced gene transcription, one immediately and the other a few hours later.
Marshall and his colleagues proposed a two-step mechanism to explain the phenomenon: when DNA is broken, some enzyme molecules are released for transcription (as suggested by Tsai’s team) and the site of fracture is also chemically labeled with a methyl group. called epigenetic marker. Later, when repair of the broken DNA begins, the marker is removed and, in the process, more enzymes can be released, starting the second round of transcription.
“Double-threaded fracture is not only considered an operator,” Marshall said, “it then becomes a marker, and that marker itself is functional when it comes to regulating and driving machinery to that location.”
Since then, other research has shown something similar. One, published last year, broken double-stranded threads are not only with the creation of the memory of fear, but also with the memory of it.
Now, a examine in the last month in PLOS ONE, Tsai and colleagues have shown that the counterintuitive mechanism of gene expression may be predominant in the brain. This time, instead of using cultured neurons, they studied the brain cells of living mice that were learning to link an environment to electric shock. When the group mapped genes that suffered double-strand fractures in the frontal cortex and shocked mice hippocampus, they found hundreds of fractures around genes, many of which were involved in memory-related synaptic processes.
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