Untitled

Abstract

Production of nitric oxide (NO), an evolutionarily conserved, intercellular signaling molecule, appears to be required for the maintenance of the larval state in the gastropod mollusc Ilyanassa obsoleta. Pharmacological inactivation of endogenous nitric oxide synthase (NOS), the enzyme that generates NO, can trigger metamorphosis in physiologically competent larvae of this species. Neuropils in the brains of these competent larvae display histochemical reactivity for NADPH diaphorase (NADPHd), an indication of neuronal NOS activity. The intensity of NADPHd staining is greatest in the neuropil of the apical ganglion (AG), a region of the brain that contains the apical sensory organ and that innervates the bilobed ciliated velum, the larval swimming and feeding organ. Once metamorphosis is initiated, the intensity of NADPHd staining in the AG and presumably, concomitant NO production, decline. The AG is finally lost by the end of larval metamorphosis, some 4 days after induction. To determine if the neurons of the AG are a source of larval NO, we conducted immunocytochemical studies on larval Ilyanassa with commercially available antibodies to mammalian neuronal NOS. We localized NOS-like immunoreactivity (NOS-IR) to 3 populations of cells in competent larvae: somata of the AG and putative sensory neurons in the edge of the mantle and foot. Immunocytochemistry on pre-competent larvae demonstrated that numbers of NOS-IR cells in the AG increase throughout the planktonic larval stage.

Developmental expression of COE across the Metazoa supports a conserved role in neuronal cell-type specification and mesodermal development

“…Prior to settlement and metamorphosis, many species must identify a suitable substrate upon which to attach (Jackson et al 2002). It is believed that apical organs are involved in recognising metamorphosis-inducing cues via chemoreception (Hadfield et al 2000; Leise et al 2001; Thavaradhara and Leise 2001). Elucidating the evolutionary origins of these structures across a variety of metazoan phyla has the potential to address questions of larval homology and more broadly whether the ancestor of the Metazoa developed indirectly or directly.…”

In Haliotis, NO means YES

“…As put forward by Ueda and Degnan, the three different regulatory roles for NO in controlling the metamorphosis of marine larvae appear to be in operation in gastropod molluscs. In one role as a negative regulator, as reported for instance in Ilyanassa obsoleta and Crepidula fornicata, NOS expression occurs in the apical sensory organ, a larvalspecific sensory organ that is degraded by programmed cell death immediately after metamorphosis (Thavaradhara and Leise, 2001;Gifondorwa and Leise, 2006;Hens et al, 2006;Pechenik et al, 2007). As a negative modulator in the nudibranch Phestilla sibogae, NOS expression occurs outside of the apical sensory organ in the cerebral ganglia, pedal ganglia and sensory cells of the foot which become also part of the adult nervous system after metamorphosis (Bishop et al, 2008).…”

Nitric oxide is not a negative regulator of metamorphic induction in the abalone Haliotis asinina

“…Immunohistochemistry assays in molluscs have detected NOS protein activity localized to the apical sensory organ (ASO) of I. obsoleta (Thavaradhara and Leise, 2001) and C. fornicata (Pechenik et al, 2007) veliger larvae, and in putative sensory neurons in the edge of the mantle and foot in I. obsolete veligers (Thavaradhara and Leise, 2001). The ASO is a larval-specific sensory structure that is thought to function as a sensory structure to detect inductive cues (Hadfield et al, 2000); it is lost during or immediately after metamorphosis (Croll and Dickinson, 2004;Gifondorwa and Leise, 2006;Croll, 2009).…”