Researchers at Queen Mary University of London have shown that zebrafish can provide genes baz1b Evidence for the evolution of social behaviors in humans and domesticated species.
Research published in iScienceI looked at transgenic zebrafish that fail to make baz1b protein. The results indicate that the gene is not only at the center of physical and behavioral changes in fish and other domesticated species, but potentially also the social relationships of humans.
Domesticated species—such as dogs and cats—show genetic differences compared to their wild-type counterparts, including a difference in baz1b gene. These genetic changes are associated with physical and behavioral traits including smaller facial features such as skulls and teeth, as well as being more sensitive to society, less aggressive, and less fearful.
However, studies have also indicated that modern humans resumed themselves after splitting from their extinct relatives, the Neanderthals and Denisovans. In doing so, we went through similar physical and behavioral changes.
All of these changes have been linked to the fact that pets have fewer of a certain type of stem cell, called neural stem cells.
Research led by the Queen Mary team builds on this by examining the effect of removal baz1b Gene function, and impact on neural crest development and social behaviour.
The mutant zebrafish studied were found to be more socially vulnerable than their functional counterparts baz1b. They showed an increased tendency to interact with members of the same species, although the differences between the two zebrafish species were no longer noticeable once the fish were three weeks old.
In addition to being more social, the mutant zebrafish showed distinctive facial changes later in life. These included changes in eye length and width, a prominent forehead, and a shorter snout. This was accompanied by a decrease in anxiety-related behaviours.
To measure this, the researchers examined the zebrafish’s response to a short flash of light, specifically the distance traveled over a five-minute period after the flash, as well as their response to acoustic startle and their response when exposed to a novel environment. . In all cases, the mutant zebrafish recovered more quickly after the change in state, indicating less fear-related reactivity.
The mutant zebrafish also showed a slight impairment of neural crest development at the larval stages.
Research determined that in zebrafish baz1b The gene affects both the morphological and behavioral characteristics associated with the domestication syndrome in other species.
José Vicente Torres Perez, co-author from Queen Mary University of London and the University of Valencia, said: “Since the process of self-domestication, which allowed modern humans to form larger social groups, among other characteristics, is similar to this process of domestication in other ‘domesticated’ species, our research It has the potential to help us uncover the biological roots that govern these behaviours.
“Our research supports the current hypothesis that the behavioral and morphological changes that came with domestication in animals and humans can be traced back to the underdevelopment of neural crest stem cells.”
This study offers an interesting perspective on the origins of how we interact with others. While transferring inferences from zebrafish to other vertebrates can be challenging, comparative studies like this one give insights into the evolution of human cognition.”
Professor Caroline Brennan, lead author and Professor of Molecular Genetics at Queen Mary University of London
Zebrafish were chosen in part for the research because about 80% of genes associated with human disease have a corresponding recomponent — a gene in a different species that evolved from a common ancestor — making zebrafish an ideal model for studying the underlying genetics and neural circuits. Behavior.
Torres Perez, JV, et al. (2022) Loss of baz1b function in zebrafish results in phenotypic changes consistent with the domestication syndrome. iScience. doi.org/10.1016/j.isci.2022.105704.