Clonal and colonial organisms ranging from herbaceous angiosperms to early-evolving animals show similar organization. Ramets, which are nutrient-gathering and reproductive entities, are connected by some sort of vascular system. Colonial cnidarians epitomize this organization, with feeding and reproductive polyps connected by gastrovascular stolons. Characteristic colonial variation also exists within the cnidarians: some species or genotypes show widely spaced polyps and long stolonal connections, while others show closely spaced polyps and short stolonal connections. The former are usually termed “runners” and the latter “sheets.” A host of organisms illustrate this basic pattern.1 Generative processes such as rates of stolon elongation relative to rates of polyp formation are usually thought to underlie this morphological variation. Increasingly, the importance of regressive processes is being recognized in developmental biology, so it is sensible to consider the possible influence of regressive processes on the formation of runners and sheets. To this end, we have characterized the process of stolon regression. Clearly, if such a process occurs at a high rate, a runner-like colony may turn into a sheet-like one and conversely.

Podocoryna (= Podocoryne) carnea, a well-studied colonial hydroid, was used to investigate stolon regression. This process occurs naturally in colonies; at any given time, a few of the tens or even hundreds of stolon tips in a colony might be regressing. To characterize this process further, pharmacological manipulations were used to induce the majority of the stolons of a colony to regress. Depending on the concentration, vitamin C, peroxide and nitric oxide donors all trigger high levels of regression. The data suggest that stolon regression involves: (1) cessation of gastrovascular flow, (2) accumulation of high levels of peroxide and nitric oxide in the regressing stolon, and (3) physical regression of the tissue within the perisarc accompanied by morphological indications of cell death.2–4

The initiation of stolon regression by perturbations of gastrovascular flow provides an intriguing connection to environmental factors that regulate colony growth and development.4 Gastrovascular flow seems to act as a colony-wide system by which local conditions (e.g., pressure, shear, redox state) are set; these local conditions in turn lead to patterns of gene activity that result in either further development or regression.5 Environmental perturbations seem to be integrated by the entire system, and subsequently transduced into local signals.6 The relationship between stolon regression and gastrovascular flow suggests that a wide range of environmental effects may trigger this process. The effects of temperature are particularly worth considering in this context. In a related species of hydractiniid hydroid, sudden temperature increases resulted in chaotic gastrovascular dynamics.7 Preliminary data suggest that such temperature perturbations also lead to stolon regression. For instance, in Podocoryna carnea colonies cultured at roughly 20.5°C, exposure to 2 h of ≈23°C resulted in clear evidence of regression (Fig. 1).

Coral bleaching is one of the most pressing issues that cnidarian biologists must currently confront. Typically, in response to environmental perturbation, which is often temperature related, bleaching coral release their symbiotic algae with subsequent detrimental effects.8 While hydroid colonies lack such symbionts and show other clear differences in their gastrovascular system as compared to corals,9 some parallels may still be found.7 In particular, temperature-related gastrovascular perturbations resulting in fluxes of ROS and RNS, tissue regression, and cell death pose intriguing connections to what is known of coral bleaching from anemone model systems.10,11 Nevertheless, the physiology of coral bleaching remains poorly characterized.8 Clearly, better laboratory models are needed to remedy this.