Abstract
Settlement is a rapid process in many marine invertebrate species, transitioning a planktonic larva into a benthic juvenile. In indirectly developing sea urchins, this ecological transition correlates with a morphological, developmental and physiological transition (metamorphosis) during which apoptosis is essential for the resorption and remodelling of larval and juvenile structures. While settlement is initiated by environmental cues (i.e. habitat-specific or benthic substrate cues), metamorphosis is regulated by developmental endocrine signals, such as histamine (HA), thyroid hormones (THs) and nitric oxide (NO). In the purple sea urchin, Strongylocentrotus purpuratus, we found that suH1R mRNA levels increase during larval development and peak during metamorphic competence. SuH1R positive cell clusters are prominently visible in the mouth region of sea urchin larvae, but the protein appears to be expressed at low levels throughout the larval arms and epidermis. SuH1R knock-down experiments in larval stages show that the function of suH1R is in inhibiting apoptosis. Our results therefore suggest that suH1R is regulating the metamorphic transition by inhibiting apoptosis. These results provide new insights into metamorphic mechanisms and have implications for our understanding of settlement and metamorphosis in the marine environment.
Highlights
Marine invertebrate phyla display a diverse array of life history strategies
Metamorphosis is a rapid process in sea urchin larvae that involves apoptosis and our results suggest that HA signaling functions as a potent inhibitor of apoptosis during this process
The results presented here demonstrate that suH1R is expressed throughout larval development and that expression mirrors expected levels of apoptosis at different stages of development. suH1R expression is low in earlier stages of development, and increases exponentially as these larvae reach metamorphic competence
Summary
Marine invertebrate phyla display a diverse array of life history strategies. Many of them develop to adulthood via a distinct larval stage, which transitions into the juvenile through a dramatic metamorphosis. In indirectly developing sea urchins a broad array of endocrine and neuroendocrine molecules has been shown to affect metamorphosis. These include dopamine[2,3], L-DOPA (L-3,4-dihydroxyphenylalanine), glutamine, glutamic acid[2,4], nitric oxide[5], thyroxine[6] and histamine (HA)[7]. Extensive cell death in larval tissues during echinoderm metamorphosis leaves the juvenile rudiment to develop into an adult; few studies have looked at the mechanisms and timing of apoptosis during sea urchin development[7,12,13]. The mechanism underlying arm retraction appears to be caspase mediated[7] These data suggest that the histamine signalling system is essential to the maintenance of metamorphic competence. Histaminergic cells are found in the lateral arm clusters (important ganglia implicated in sensory perception) and the apical organ (the “central nervous system” of these larvae – implicated in sensory perception as well as settlement and metamorphosis)[15]
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