Summary: A new study reveals that human accelerated regions ( HARs ) —segments of DNA that evolved much faster than expected—may be key to the brain’s advanced cognitive abilities. Researchers compared the neuronal communication between humans and chimpanzees, finding that HARs promote the growth of several neural projections.
When people HARs were introduced into primate neurons, they furthermore grew more forecasts, suggesting a strong link between HARs and neurological complexity. These same hereditary changes, however, may also be a cause of developmental disorders like autism, highlighting the fragile balance of human brain development.
Essential Information
- Fast-Evolving DNA: Human accelerated regions ( HARs ) evolved 10 times faster than expected, shaping neural development.
- Enhanced Brain Connectivity: HARs drive the development of several neurites in mortal cells, improving communication between brain tissue.
- Chance for Brain Disorders: While HARs support mental complexity, their upheaval may lead to conditions like autism.
Origin: UCSF
How did people develop brains capable of complicated language, culture, and more?  ,  ,  ,
The solution might be in genetic diversity. Our genes have developed at record-breaking rates, according to researchers at UC San Francisco, giving us a faster rate of mental development than apes. However, it might also place us at risk for mental disorders that are unique to humans.  ,  ,
The review, which was supported by offers from the National Institutes of Health, appears in , Nature , on Feb. 26.  ,
The research focused on chromosomes known as human accelerated regions ( HARs ), which have changed ten times more quickly than the expected rate of evolution in mammals since humans split from chimpanzees on the evolutionary tree.  ,  ,
The researchers studied the effects of HARs in artificial cells made of human and primate cell lines under the direction of Yin Shen, PhD, doctor at the UCSF Weill Institute for Neurosciences and Yen Shen, PhD.  ,  ,  ,
The people and primate genomes are 99 % related. The 1 % difference in human and chimpanzee neurons can be significantly different because of the HARs, which account for a large portion of the difference.
The human cells developed numerous slender projections, or neurites, to aid in the transmission and reception of signals. However, one neurites were only produced by the chimpanzee neurons. When animal HARs were made into synthetic chimp neurons, the chimp neurons produced many more of these cables.  ,  ,  ,
Shen said,” More neurites during advancement may mean more difficulty in our neural network.
” These sites facilitate the transmission of signals in our higher cognitive works,” writes the author. However, developmental delays in their growth may cause developmental disorders like autism.
Authors: Another UCSF scholars are Xiekui Cui, PhD, Han Yang, PhD, Charles Cai, Cooper Beaman, Xiaoyu Yang, PhD, Hongjiang Liu, Xingjie Ren, PhD, Zachary Amador, Ian R. Jones, Kathleen C. Keough, PhD, Meng Zhang, PhD, MS, Tyler Fair, PhD, Zhen Ye, Alex A. Pollen, PhD, and Katherine S. Pollard, PhD. for all artists to see the report.  ,
Funding: This work was supported by the US National Institutes of Health ( NIH) grants U01DA052713, UM1HG009402, R21DA056293, R21HG010065, R01MH109907, U01MH116438, DP2MH122400-01, P30DK063720, and S101S10OD021822-01, the Schmidt Futures Foundation, the Chan Zuckerberg Biohub, and the Gladstone Institutes. For all cash, please refer to the article.  ,  ,  ,
About this news item about consciousness and genetics
Author: Levi Gadye
Source: UCSF
Contact: Levi Gadye – UCSF
Image: The image is credited to Neuroscience News
Original Research: Closed entry.
Yin Shen and colleagues ‘” Comparative characterization of individual accelerated parts in neurons.” Character
Abstract
Quantitative description of neurons with human accelerated areas
Human accelerated regions ( HARs ) are conserved genomic loci that have experienced rapid nucleotide substitutions following chimpanzee divergence.
In potential regulatory regions close to developmental genes, HARs are enriched, suggesting that they play a role in protein legislation. However, their goal genes and useful contributions to human mind development remain largely unstudied.
Here we describe the , cis-regulatory features of HARs in people and primate induced adult stem (iPS) cell-induced activating cells. Using genomic , and protein looping data, we prioritized 20 HARs and their primate orthologues for practical characterization via single-cell CRISPR disturbance, and demonstrated their species-specific protein regulatory features.
Our findings reveal various practical outcomes of HAR-mediated , cis-regulation in human neurons, including attenuated , NPAS3 , appearance by altering the conditional affinities of many transcription factors in HAR202 and maintaining iPS body pluripotency and cerebral differentiation capacities through the upregulation of , PUM2 , by 2xHAR. 319.
Finally, we used prime editing to demonstrate differential enhancer activity caused by several HAR26, 2xHAR. 178 variants. In particular, we link one variant in HAR26, 2xHAR. 178 to elevated , SOCS2 , expression and increased neurite outgrowth in human neurons.
Our study provides new insight into the endogenous gene regulatory roles of HARs and their potential contribution to human brain evolution.
