Sending out tendrils to cover any surface that they settle on, an individual Podocoryna carnea polyp can eventually grow into a large hydroid colony with many individuals linked by tube-like stolons. Neil Blackstone and colleagues from Northern Illinois University, USA, explain that these colonies adjust growth by changing stolon growth and altering the distribution of polyps along the stolon network. However, tissue regression – where regions of stolon recede – also plays a key role in shaping P. carnea structures. Intrigued by the factors and mechanisms that influence colony regression, Blackstone and his team decided to investigate the effect of stolon regression on P. carnea morphology ().
Knowing that hydrogen peroxide triggers stolon regression, the team simulated the cyclic pattern of stressors that P. carnea colonies are exposed to in shallow-marine environments with brief exposures to different concentrations of hydrogen peroxide. Monitoring the colonies over 3 months, the team saw that colonies exposed to high levels of hydrogen peroxide (1 mmol l–1) formed dense sheets instead of the lacy structures formed by colonies exposed to dilute hydrogen peroxide (0.1 mmol l–1). They suspect that increased levels of stolon regression in the treated colonies force polyps to develop close together to form the denser sheet-like structures.
Blackstone and colleagues then monitored the effect of three stressors – confinement, rising temperatures and starvation – on the colonies and found a complicated set of interactions, where some combinations of stressors resulted in regression while others protected against it.
Next, the team investigated the effects of a group of chemicals, known as caspase inhibitors, on colony morphology. Explaining that a form of cell death, known as apoptosis, appears to occur during stolon regression and that caspases are key proteins in the apoptotic process, the researchers tested the effect of several caspase inhibitors on P. carnea colonies and found that the inhibitors reduced the amount of stolon regression, as well as the presence of damaging reactive oxygen species. However, instead of following a neat apoptotic cell death pathway, the stolon cells had taken on some of the features of cells undergoing the messier necrotic form of death.
Drawing together their observations, Blackstone and colleagues suggest that stolon regression could be the trigger that switches colonies from lacy to sheet-like structures. They also suspect that stolon regression has a lot in common with the way that other cnidarians deal with the stress response when they produce reactive oxygen species and kill off cells.
