There are only parts of DNA that evolution dares not change, such as valuable recipes passed down from generation to generation. For example, mammals have a variety of coded sequences that have remained unchanged for millions of years.

Humans are the odd exception to this club. For some reason, recipes long preserved by our ancient ancestors were suddenly “spiced” within a short evolutionary period.

Because we are the only species in which these regions are replicated so quickly, they are called “human accelerated regions” (or HARs). In addition, scientists believe that at least some HARs may be behind many of the features that distinguish humans from their close relatives, such as chimpanzees and bonobos.

A research team led by computational biologist Cathy Pollard, director of the Gladstone Institute for Data and Biotechnology in the US, discovered HAR nearly two decades ago by comparing human and chimpanzee genomes.

In a new study, Pollard’s team has found that the three-dimensional folding of human DNA in the nucleus is a key factor at this crucial moment for our species.

Think of a piece of DNA from our last common chimpanzee ancestor as a long scarf wrapped around your neck, with stripes of different colors throughout.

Now imagine someone trying to make the same scarf but not following the original pattern. Some bands are narrower, some wider, and some are in a different order from the original.

When you wrap the new scarf around your neck in the same way as the original, the strips next to each other in the loop are no longer the same.

Like this scarf, the major difference between human and chimpanzee DNA is structural: Large DNA building blocks have been inserted, deleted, or rearranged into the human genome. This is why human DNA in the nucleus is folded differently from the DNA of other primates.

Pollard’s team investigated whether these structural changes in human DNA and its altered three-dimensional folding lead to the “hijacking” of certain genes in HAR and link them to protein-coding genes other than those in which they were originally used.

Many genes in HAR are linked to other genes by acting as enhancers (ie, they increase transcription of associated genes/genes).

“Developers can influence the activity of any nearby gene, and this can vary depending on how the DNA is folded,” Pollard said. Said.

In a study published earlier this year, Pollard’s team created a model that suggests that rapid changes in HAR in early humans often neutralized each other and shifted reinforcing activity up and down in a unique genetic setting – a model supported by their new research.

In their latest study, the team compared the genomes of 241 mammalian species, using machine learning to deal with large amounts of data.

They identified 312 HARs and studied where they were located in the three-dimensional “regions” of helical DNA. About 30 percent of HARs were located in regions of DNA where structural variation causes the genome to fold differently in humans compared to other primates.

The team also found that the HAR-containing neighborhood is rich in genes that distinguish humans from our closest relatives, chimpanzees.

In an experiment comparing DNA in growing human and chimpanzee stem cells, one-third of the HARs identified were specifically transcribed during the development of the human neocortex.

Many HARs play important roles in embryonic development, particularly in the formation of neural pathways related to intelligence, reading, social skills, memory, attention, and focus that we know in humans to differ significantly from other animals.

In HAR, these enhancer genes, unchanged for millions of years, may have had to adapt to their different target genes and regulatory domains.

“Imagine you’re a booster that controls hormone levels in the blood, and then the DNA is folded in a new way and suddenly you’re sitting next to a neurotransmitter gene and you have to regulate the levels of chemicals in the brain and not in the blood,” Pollard said.

“Something big happens like this big change in genome folding, and our cells have to fix it quickly to avoid an evolutionary disadvantage.”

We do not yet fully understand how these changes affect certain aspects of our brain development and how they have become an integral part of our species’ DNA. Pollard and his team are already planning to delve into these questions.

But their research shows how unique and unlikely the evolution of the human brain is.

This study was published in Science.