Circulation of Fluids in the Gastrovascular System of a Stoloniferan Octocoral

Cilia-based transport systems characterize sponges and placozoans. Cilia are employed in cnidarian gastrovascular systems as well, but typically function in concert with muscular contractions. Previous reports suggest that anthozoans may be an exception to this pattern, utilizing only cilia in their gastrovascular systems. With an inverted microscope and digital image analysis, we used stoloniferan octocoral colonies growing on microscope cover glass to quantitatively describe the movement of fluids in this system for the first time. Flow in stolons (diameter ≈300 μm) is simultaneously bidirectional, with average velocities of 100–200 μm/s in each direction. Velocities are maximal immediately adjacent to the stolon wall and decrease to a minimum in the center of the stolon. Flow velocity is unaffected by stolonal contractions, suggesting that muscular peristalsis is not a factor in propelling the flow. Stolon intersections (diameter ≈500 μm) occur below polyps and serve as traffic roundabouts with unidirectional, circular flow. Such cilia-driven transport may be the plesiomorphic state for the gastrovascular system of cnidarians

Structure and signaling at hydroid polyp-stolon junctions, revisited

The gastrovascular system of colonial hydroids is central to homeostasis, yet its functional biology remains poorly understood. A probe (2′,7′-dichlorodihydrofluorescein diacetate) for reactive oxygen species (ROS) identified fluorescent objects at polyp-stolon junctions that emit high levels of ROS. A nuclear probe (Hoechst 33342) does not co-localize with these objects, while a mitochondrial probe (rhodamine 123) does. We interpret these objects as mitochondrion-rich cells. Confocal microscopy showed that this fluorescence is situated in large columnar cells. Treatment with an uncoupler (2,4-dinitrophenol) diminished the ROS levels of these cells relative to background fluorescence, as did removing the stolons connecting to a polyp-stolon junction. These observations support the hypothesis that the ROS emanate from mitochondrion-rich cells, which function by pulling open a valve at the base of the polyp. The open valve allows gastrovascular fluid from the polyp to enter the stolons and vice versa. The uncoupler shifts the mitochondrial redox state in the direction of oxidation, lowering ROS levels. By removing the stolons, the valve is not pulled open, metabolic demand is lowered, and the mitochondrion-rich cells slowly regress. Transmission electron microscopy identified mitochondrion-rich cells adjacent to a thick layer of mesoglea at polyp-stolon junctions. The myonemes of these myoepithelial cells extend from the thickened mesoglea to the rigid perisarc on the outside of the colony. The perisarc thus anchors the myoepithelial cells and allows them to pull against the mesoglea and open the lumen of the polyp-stolon junction, while relaxation of these cells closes the lumen