Format

Send to

Choose Destination
Sci Rep. 2018 Mar 5;8(1):4002. doi: 10.1038/s41598-018-22397-4.

Sea urchin histamine receptor 1 regulates programmed cell death in larval Strongylocentrotus purpuratus.

Author information

1
University of Guelph, Integrative Biology, Guelph, ON, N1G 2W1, Canada.
2
Department of Biology, University of Ottawa, Ottawa, ON, K1N 6N5, Canada.
3
University of Guelph, Integrative Biology, Guelph, ON, N1G 2W1, Canada. aheyland@uoguelph.ca.

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.

PMID:
29507306
PMCID:
PMC5838261
DOI:
10.1038/s41598-018-22397-4
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central
Loading ...
Support Center