Effect of Ca

Area of Science:

• Marine Biology
• Reproductive Endocrinology
• Cell Signaling

Background:

• Starfish follicle cells mediate oocyte maturation through the production of 1-methyladenine (1-MeAde).
• Gonad-stimulating substance (GSS) is a key hormone regulating 1-MeAde production in starfish.
• The role of extracellular calcium (Ca2+) in GSS-mediated signaling in starfish follicle cells remains incompletely understood.

Purpose of the Study:

• To investigate the effect of calcium-free seawater (CaFSW) treatment on 1-MeAde production by starfish follicle cells.
• To elucidate the role of extracellular calcium in GSS-induced cyclic AMP (cAMP) production and subsequent 1-MeAde synthesis.
• To explore the potential impact of calcium depletion on G-protein coupled receptor signaling pathways in starfish follicle cells.

Main Methods:

• Starfish follicle cells were treated with Ca2+-free seawater (CaFSW).
• 1-methyladenine (1-MeAde) and cyclic AMP (cAMP) production were measured in response to gonad-stimulating substance (GSS).
• ADP-ribosylation assays using [α-32P]NAD+ with cholera and pertussis toxins were performed on membrane preparations.

Main Results:

• CaFSW treatment significantly reduced 1-MeAde production in response to GSS.
• cAMP levels in CaFSW-treated cells were lower and showed only a minimal increase with GSS, insufficient for 1-MeAde production.
• 1-MeAde and cAMP production were dependent on extracellular Ca2+ concentration, with significant reduction below 1 mM Ca2+.
• ADP-ribosylation revealed the presence of stimulatory and inhibitory G-proteins, but adenylyl cyclase activity was not affected by GSS.

Conclusions:

• The reduced 1-MeAde production in CaFSW-treated starfish follicle cells is attributed to diminished cAMP levels.
• Extracellular calcium is crucial for effective GSS signaling, likely by facilitating GSS receptor binding or downstream cAMP production.
• These findings suggest that GSS may be unable to bind to its receptor in follicle cells after washing with CaFSW, impacting the signaling cascade.