Metamorphosis induction of larvae

Larval settlement responses of the ribbed mussel, Aulacomya maoriana Iredale 1915, were investigated after exposure to various chemicals and mono-species bacteria. Identification of settlement inductive compounds assists in the elucidation of intermediary biochemical mechanisms involved in the neuronal control of settlement behaviour downstream from primary cue reception. Neuroactive compounds and amino acids (potassium ions, GABA, acetylcholine, l-Phenylalanine, l-Tyrosine, dopamine, epinephrine, l-Tryptophan, and 5-HTP) and planktonic bacteria, biofilms and biofilm exudates of Macrococcus sp. AMGM1, Bacillus sp. AMGB1, and Pseudoalteromonas sp. AMGP1 were tested for their abilities to induce larval settlement. Toxicity effects of each treatment also were simultaneously identified by recording larval mortalities. Results indicate that all chemicals used induced larvae to settle, with acetylcholine being the most effective (~ 24% at 10−6 M compared to < 2% in control assays). Toxicities of treatment compounds were low at optimal settlement inducing concentrations, except for l-Tryptophan (~ 32%) and GABA (~ 59%). Our data suggest that catecholamines (and their precursors) play an important role in the biochemical mechanisms of settlement for A. maoriana. While serotonin precursors did induce low levels of larval settlement at some concentrations, high toxicity responses to 5-HTP at 10−5 M, combined with complete settlement inhibition indicate that the mechanism of action may be more complex than can be elucidated in this study. Larval settlement responses to bacterial treatments were low for planktonic and biofilm phases across all three strains, and settlement inhibition was observed when larvae were exposed to biofilm exudates of all bacterial strains. Comparisons of A. maoriana responses to other endemic and worldwide distributed mussel species are provided as a means to highlight potential evolutionary differences in chemoreception mechanisms.

Herein, we present the first laboratory study on the effects of pharmacologically active compounds on larval settlement of the green-lipped mussel, Perna canaliculus. Competent hatchery-reared larvae were exposed to seawater containing excess K+ in the form of KCl and K2SO4 and the neurotransmitters γ-aminobutyric acid (GABA) and acetylcholine. Both KCl and K2SO4 were identified as active inducers of larval settlement with maximum inductions occurring after exposures to 10 and 7.5 mM, respectively. Peak settlement response to KCl was higher (> 64%) than that achieved with K2SO4 (> 41%). GABA did not induce larval settlement and displayed toxic and settlement inhibitive effects at 10−4 and 10−3 M. Acetylcholine induced larval settlement (> 49%) at 10−4 M with minimal acute toxic effects (LC < 10%). To gain insight into the class of acetylcholine receptors involved, atropine was used to block the muscarinic-type receptors. Atropine treatment alone did not inhibit settlement compared to control assays, indicating that muscarinic-type receptors are not involved in settlement behavior. Furthermore, results showed that atropine did not significantly decrease acetylcholine induced settlement responses, which suggests an active role of the nicotinic-type receptors in the biochemical pathways of mussel settlement. Results of this study provide new insights on the mechanism of settlement behavior in P. canaliculus, which may have direct application to the growing New Zealand aquaculture industry.

Herein, we present the first laboratory study on the effects of pharmacologically active compounds on larval settlement of the green-lipped mussel, Perna canaliculus. Competent hatchery-reared larvae were exposed to seawater containing excess K+ in the form of KCl and K2SO4 and the neurotransmitters γ-aminobutyric acid (GABA) and acetylcholine. Both KCl and K2SO4 were identified as active inducers of larval settlement with maximum inductions occurring after exposures to 10 and 7.5 mM, respectively. Peak settlement response to KCl was higher (&gt; 64%) than that achieved with K2SO4 (&gt; 41%). GABA did not induce larval settlement and displayed toxic and settlement inhibitive effects at 10−4 and 10−3 M. Acetylcholine induced larval settlement (&gt; 49%) at 10−4 M with minimal acute toxic effects (LC &lt; 10%). To gain insight into the class of acetylcholine receptors involved, atropine was used to block the muscarinic-type receptors. Atropine treatment alone did not inhibit settlemen...