The role of polyp-stolon junctions in the redox signaling of colonial hydroids

摘要

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 redox-regulated proteins,or all of these.