Extracellular proteins OSM-7 and OSM-8 are required for stress response gene regulation at all post-embryonic stages.

Nematode cuticles are extracellular matrices (ECMs) that function as structural support and permeability barriers. Genetic disruption of specific cuticle collagen structures or secreted epidermal proteins in C. elegans activates stress response genes in epithelial cells suggesting the presence of an extracellular damage signaling mechanism. Cuticles are replaced during development via molting but investigations of extracellular signaling to stress responses have focused on adults. In our current study, we measured cuticle phenotypes and stress response gene expression in all post-embryonic stages of mutant strains for a collagen and two secreted epidermal proteins to gain insights into developmental patterns.

Compensation for hypercapnia by a euryhaline elasmobranch: effect of salinity and roles of gills and kidneys in fresh water.

Specimens of the euryhaline elasmobranch, Dasyatis sabina were acclimated to seawater and fresh water, and exposed to normocapnic (air) and hypercapnic (1% CO2 in air) environmental water. Blood pH, PCO2, and [HCO3-], as well as whole-animal net-acid excretion, were measured for up to 24 h of hypercapnia. In a separate experimental series, urine was collected from freshwater acclimated stingrays during 8 h of normocapnia and hypercapnia. Stingrays in both salinities at least partially compensated for the respiratory acidosis by accumulating HCO3- in their extracellular spaces. The degree of compensation for blood pH was 88.5% in seawater, but only 31.0% in fresh water after 24 h of hypercapnia. Whole-animal net-acid excretion was also greater in seawater than in fresh water, as was the increase in extracellular fluid [HCO3-]. Mean urinary net-acid excretion rates were slightly negative, and never increased above normocapnic control rates during hypercapnia. Since whole-animal net-acid excretion rates increased with blood [HCO3-], and urinary excretion was always negative, the gills were probably the primary organ responsible for compensation from environmental hypercapnia. The faster, and more complete, compensation for hypercapnia in seawater than in fresh water for this euryhaline elasmobranch is consistent with data for euryhaline teleosts, and probably reflects Na+-dependent mechanisms of branchial acid excretion.