Hydra Watch What They Eat

A picture of a hydra, from the Encyclopedia of Life

Upon first glance, hydra seem like remarkably simple creatures. The basic description of a hydra would be a tube closed at one end with tentacles surrounding a mouth on the other, made of fragile tissue that can be as slim as two cells thick. No gills, no heart, no brain, no eyes – of course, it would be hard to pack all those organs into a creature a few millimeters long, and hydra certainly seem to do well enough without them. These small relatives of jellyfish are found worldwide, and are some of the only members of the phylum Cnidaria to be found in fresh water.

Yet their modest body plan is misleading. Hydra have fascinated scientists for centuries, for they have a phenomenal capacity to regenerate and may even be immortal. In 1744, Swiss naturalist Abraham Trembly was one of the first to be entranced by these simple animals and reflected, “It seemed to me from the start of my observations that knowledge of the remarkable properties of the polyps could bring pleasure to the inquisitive and contribute something to the progress of natural history.”

The hydra’s simple nature is also belied by their tentacles, which inject a potent neurotoxin into unsuspecting prey using extremely sophisticated cells called cnidocytes. For decades, scientists have sought to understand how these specialized attack cells are triggered. Now, evidence published in BMC Biology suggests these primitive creatures may ‘see’ more than we realized, as the firing of these prey-catching stinging cells is regulated by the same chemical pathway used in our eyes.

Ever since the genome for Hydra magnipapillata was published in 2010, it was known that hydra possess the genes for opsins, the photosensitive protein family found in all animals that can see, but no one knew exactly what they do with them. Unlike other animals, hydra don’t have eyes or eye spots, or any kind of centralized visual sensory area, although they have behavioral responses to light. When David Plachetzki teamed up with Caitlin Fong and Todd Oakley’s lab at UC Santa Barbara, they found that these light-sensitive proteins were clustered on the hydra’s tentacles and around the hydra’s mouth, suggesting that they might be involved in feeding behavior.

Fluorescent picture of hydra tentacle bulbs; Musculature is stained green, neurons, including cnidocytes, are stained red and nuclei are stained blue

In hydra, potent stinging cells are grouped with other neurons in what are called “battery complexes” on the hydra’s tentacles, forming one of the most intricate systems of neurons in an organism that lacks a central nervous system. Using fluorescent molecular probes, the researchers were able to show that opsins are expressed in the same locations. They also discovered that other proteins that are part of the response to light, cyclic nucleotide gated (CNG) ion channel and arrestin, are found in these battery complexes, too. In other words, the stinging arsenals are completely equipped to react to changes in light.

Just because they have the parts, however, doesn’t mean they use them. So to see if the stinging cells themselves, the cnidocytes, are regulated by light, the researchers exposed hydra to LED lights of different intensities, then prodded the animals’ tentacles with gelatin-coated fishing wire as if they were being touched by potential prey. After, the team was able to count how many cnidocytes were embedded in the line as a way of measuring whether the stinging cells were triggered.

They found that bright light decreased the firing of stinging cells – which makes sense, really. “Cnidocytes are expensive to make for a hydra; a significant proportion of their cellular mass is comprised by these cell types. Therefore, it is important these austere animals to discharge them in an economical manner,” explains Plachetzki. Hydra and their relatives in the phylum Cnidaria are known to feed in daily patterns, becoming especially active at dawn or dusk, so it’s logical that they would be less inclined to feed in bright light, which might be perceived as day. Of course, there is an even more straightforward explanation as to why cnidocytes fire when the lights go out – shadows. “It could be that hydra use this sensory function to detect the shadows cast by prey on feeding tentacles, just when the moment is right to strike.” The researchers were able to directly connect the opsin signaling cascade to this change in feeding behavior by introducing a blocker of opsin signaling, cis-diltiazem. In the presence of the blocker, light had no affect, confirming that opsin-based signaling is required for this light-mediated change in cnidocyte firing.

Since hydra have been extensively studied for centuries, it is a bit surprising that we are only now learning how light affects their feeding. “It is strange that nobody had discovered this before,” remarked Plachetzki. “Folks have been playing around with hydra and their photobehavior for greater than 200 years, why didn’t they notice this?” But, he says, when you look at some of the older observations of these creatures, “you get the impression that others might have had this hypothesis as well, but there were until now never any data to support it.”

These findings reveal one of the earliest uses of the chemical pathways that were co-opted to create vision. By learning more about these signaling cascades, we can begin to glimpse back at the very beginnings of sight, and slowly learn more about the evolutionary steps that led to our eyes. Aside from the interesting evolutionary implications, this research may also lead to more direct benefits to humans. Cnidarians, including hydra, jellies and corals, are responsible for tens of thousands of stings every year, a handful of which are fatal. The more we know about how these stinging cells are triggered, the better we can prevent these stings, or even develop a way of protecting swimmers against them.

Reference: David C Plachetzki, Caitlin R Fong and Todd H Oakley (in press). Cnidocyte discharge is regulated by light and opsin-mediated phototransduction. BMC Biology

The Sweet Taste of Fear

Lots of animals use chemical cues to avoid danger. Mice will run from the smell of cat urine, for example. But one particular instance of chemical fear signaling has been stumping scientists for 70 years; the release of Schreckstoff by schooling fish.

For some species of fish, when a predator swoops in and injures one fish in a school, the rest will take off in fear. This much we know. In 1938, Austrian ethologist Karl von Frisch claimed that at the root of this behavior was a chemical alarm signal which he referred to as “Schreckstoff,” which means “scary stuff” in German. Since von Frisch’s seminal work, over 100 published studies concerning Schreckstoff have demonstrated that certain fishes have some substance in their skin cells which is released when that fish is injured and causes other fish to scatter. That much, we know, too.

This has perplexed scientists because it seems strange that any animal could evolve to give off that kind of chemical alarm. The other fish aren’t fleeing from blood or any clear signals of death, so what are they so afraid of? And if it’s not a signal of death but instead a signal of danger, as many scientists have argued, where is the benefit to the dying fish? You see, as much as we love the idea of altruism, it’s not very common in the natural world – at least not in its pure form. Doing something purely for the sake of others is of little benefit to an individual from an evolutionary perspective. So, hypotheses have been thrown around wildly to explain this kind of altruistic signaling – perhaps the alarm is to protect close kin, or, somehow, the chemical actually attracts the would-be-predator’s predators, thus giving the injured fish a chance to escape. Despite years of laboratory research, no hypothesis seems to be able to explain the presence of Schreckstoff. Furthermore, though some scientists have offered up potential compounds, what exactly Schreckstoff is has remained a mystery.

Now, a team from Singapore has identified that the elusive Schreckstoff as the same compound that we take to improve our joints and treat osteoporosis: chondroitin sulfate.

Structure of Chondroitin Sulfate (c/o Wikipedia)
Structure of Chondroitin Sulfate (c/o Wikipedia)

Chondroitin sulfate is a specialized chain of sugars that is a major component of fish skin, just like it’s a major component of our cartilage. Using zebrafish, a common laboratory organism, the research team found chondroitin from zebrafish tissues caused other fish to turn fin and run. They even took chondroitin from shark skin – the kind we take as supplements – and found that the zebrafish were terrified by it. The fish were also more afraid when the chondroitin was broken down by an enzyme first. The team hypothesized that when a fish is injured, enzymes released by the wounding break down chondroitin sulfate into smaller sugary chunks, and these bits and pieces, as well as the larger chondroitin molecules released by the wounded cells, are the smell that serves as a chemical alarm signal.

The best part of this discovery is that it solves evolutionary issue that scientists have had with the existence of Schreckstoff. The burden of producing a fear signal while dying doesn’t make sense unless that signal is something the fish already produced for other reasons which is only released in the case of injury – akin to some being afraid of the smell of blood. That way, the evolutionary impetus isn’t on the fish producing Schreckstoff to produce an alarm, it’s on other individuals to detect a sign of danger or death to save their own tails.

Here’s how it goes: once upon an evolutionary time, fish that were sensitive to Schreckstoff were the first to run in the face of danger, and thus were more likely to survive. Over time this would lead to an entire lineage of Schreckstoff-sensitive fish. Since chondroitin is a known component of fish skin for other reasons, but wouldn’t be released into the water unless that skin is ruptured, it perfectly fits this evolutionary scenario.

Brain scans showing chondroitin-stimulated brains in comparison to controlsBecause young zebrafish are see-through, researchers were also able to specifically examine what parts of the zebrafish brain are turned on by chondroitin fragments. They found that a specialized part of the brain called the mediodorsal posterior region was responsible for the fearful reaction. What is particularly interesting about this chunk of brain matter is that it is packed with a group of neurons called crypt cells which have no other known function. Scientists have been trying to uncover what these strange neurons do for awhile, and this new discovery may hold the key. Co-author Suresh Jesuthasan thinks that these cells are a part of a special brain circuit which mediates the fish’s innate fear response.

Together, the new findings, published in Current Biology, are the pieces to the Schreckstoff puzzle that scientists have been trying to fit for decades. There are still questions to be answered, of course – how do certain species only respond to injuries by their own species and not those of others, for example? – but this new study has provided valuable insight into fear responses in fish, and perhaps opened up new doors in our understanding of how fear originates and is processed in animal brains.

Article Link: Mathuru et al., Chondroitin Fragments Are Odorants that Trigger Fear Behavior in Fish, Current Biology (2012), doi:10.1016/j.cub.2012.01.06

Here’s the researchers’ video of the fear response:

Zebrafish fear response to Schreckstoff