The role of polyp-stolon junctions in the redox signaling of colonial hydroids
An encrusting colonial hydroid can be regarded as a network of polyps or ‘mouths’ connected by tube-like stolons. The success of the colony crucially depends on putting these mouths where the available food is. Feeding-related perturbations may provide important signals in this regard. After feeding, polyps contract regularly, dispersing food throughout the colony via the gastrovascular fluid. Mitochondrion-rich epitheliomuscular cells concentrated near polyp-stolon junctions likely drive these contractions. Putatively, the redox state of these cells may influence colony-level form. For instance, the metabolic demand associated with feeding-related contractions results in mitochondria that have relatively oxidized electron carriers and produce lesser amounts of reactive oxygen species (ROS). ROS or other redox-sensitive molecules emitted from polyp-stolon junctions into the gastrovascular fluid may provide stolons with signals influencing elongation, branching, and regression. Treatments of colonies with anti-oxidants cause peripheral stolon tips to rapidly regress. This regression appears to be an active process involving a flux of locally produced peroxides and cell and tissue death. At the same time, polyps and stolon tips in the center of treated colonies remain healthy. ‘Sheet-like’ growth of short, branched stolons ensues. Signals that inhibit the outward growth of stolons may lead by default to the concentrated growth of stolons and polyps in food-rich areas. ROS may mediate signaling mechanisms involving nitric oxide, programmed cell death, a variety of redoxregulated proteins, or all of these.
Key words: epitheliomuscular cell, mitochondria, Podocoryna, Podocoryne, reactive oxygen species
KeywordsRedox Signaling Catalytic Cysteine Treated Coloni Colonial Hydroid Outward Growth
Unable to display preview. Download preview PDF.