When someone on the street delivers a high-pitched scream, it changes the behavior of those nearby—some may flee, while others may approach to render help. This mechanism of ‘warning the herd’ works for creatures that can vocalize, but what about those that cannot, like fish?
It turns out that fish have their own means of signaling danger, which goes by the term Schreckstoff. The word, coined by Nobel laureate Karl von Frisch, originates from the German words ‘schreck’ (appropriately meaning ‘fright’ or ‘terror’) and ‘stoff’ (meaning ‘substance’). How Schreckstoff evolved in fish is a mystery, one that A*STAR researchers, working in collaboration with scientists from Nanyang Technological University, Singapore, and the University of Oregon, US, are attempting to unravel.
“When injured, fish release substances from their skin that cause fear in other members of their shoal,” explained Suresh Jesuthasan, a Principal Investigator at the Institute of Molecular and Cell Biology (IMCB), A*STAR. “These substances are detected by the fish’s olfactory system (responsible for the sense of smell), and lead to a dramatic change in swimming behavior, which can include high-speed escape, freezing or hiding.”
In this study, Jesuthasan’s team demonstrated that bacteria are a component of Schreckstoff in zebrafish. When the group introduced bacteria into tanks containing zebrafish, they noted alarm behavior in the fish.
But bacteria are just one part of the equation—the group’s findings also indicate that Schreckstoff is a by-product of the fish immune response. “Fish are in constant contact with bacteria. To prevent these bacteria from causing an infection, fish have an immune system in the skin,” Jesuthasan said.
A type of cell, known as a club cell, is responsible for consuming these bacteria and alerting the immune system in the skin. If a fish suffers an injury to the skin, the club cells present at the site of injury burst, releasing the accumulated bacteria into their immediate environment.
“In this case, bacteria can produce something that triggers fear. The findings are also relevant to the field of mucosal immunity—that is, immunity in the gut or airway epithelium—as they point to the existence of a surveillance mechanism that has not been reported in other vertebrates yet,” Jesuthasan said.
He added that the findings not only reinforce the growing view that bacteria influence behavior, but also suggest an evolutionary advantage for Schreckstoff: any fish that is able to link the release of bacteria with danger would be more likely to survive.
Jesuthasan now wants to explore the implications of the mechanism behind Schreckstoff. “It would be interesting to see how the immune mechanisms uncovered in this study are relevant to the gut and airway, and in other species,” he concluded.
The A*STAR-affiliated researchers contributing to this research are from the Institute of Molecular and Cell Biology (IMCB).
