Programmed Cell Death is Inhibited by Nitric Oxide in the Apical Ganglion during the Metamorphosis of the Marine Mollusc Ilyanassa obsoleta

GIFONDORWA, D.J.; LEISE, E.M.; Univ. of North Carolina Greensboro; Univ. of North Carolina Greensboro: Programmed Cell Death is Inhibited by Nitric Oxide in the Apical Ganglion during the Metamorphosis of the Marine Mollusc Ilyanassa obsoleta

The central nervous system of a competent larva of Ilyanassa obsoleta contains an unpaired apical ganglion (AG) of approximately 25 neurons which include the apical sensory organ (ASO). The AG innervates the velum, the larval swimming and feeding organ, and lies atop the dorsal commissure connecting the paired cerebral ganglia. Evidence from a related mollusc suggests that the ASO is a site for the reception of metamorphic cues (Hadfield et al., Biol. Bull. 2000, 198:67-76). In I. obsoleta, by three days after metamorphic induction, the AG disappears. In competent larvae, the AG displays nitric oxide synthase (NOS)-like immunoreactivity in most of its neuronal somata (Thavardhara and Leise, J. Neurocytol. 2001, 30:449-456). Previous work in our laboratory has demonstrated that inhibition of NOS induces competent larvae to metamorphose. Because nitric oxide (NO) can prevent cells from undergoing apoptosis, a form of programmed cell death (PCD), we hypothesize that inhibition of NOS induces metamorphosis by initiating the loss of the AG. Results of a Terminal deoxynucleotidyl transferase dUTP Nick End Labeling (TUNEL) assay on sections of the AG taken from metamorphosing larvae support this hypothesis and show the presence of nuclei containing fragmented DNA. At 24 hours post induction, stained sections of the AG display pyknotic nuclei, phagocytic cells, and cellular fragments, all features of the early stages of PCD.

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