The classical target for NO is the enzyme guanylyl cyclase (GC) that produces the intracellular second messenger cGMP. To determine if NO in larval Tritia acts in a cGMP-dependent fashion, Nathaniel Durham – MS degree 2002 conducted several different types of investigations, including pharmacological experiments, radioimmunoassays, enzyme-linked immunoassays and immunocytochemistry (Leise et al., 2004). A number of Nathan’s experiments were successful and demonstrated that modulation of larval levels of cGMP could affect levels of metamorphosis. One such example is depicted in the graph (Below). If our hypothesis is correct, inhibition of cGMP activity should induce metamorphosis by repressing the interaction of NO and GC (Durham, 2002, M.S. Thesis, UNCG). Supported by NSF grant IBN-9604516.
Above: NS-2028, an inhibitor of soluble guanylyl cyclase activity, promoted serotonergically-induced metamorphosis after 24 hours of incubation.
