Polyphosphoinositlde metabolism during the fertilization wave in sea urchin eggs

Abstract

A transient increase in intracellular free calcium is believed to be the signal responsible for the stimulation of the egg metabolism at fertilization and the resumption of the cell cycle. We have studied how the polyphosphoinositides (PPI) turn over at fertilization in sea urchin eggs, in order to determine the relationship between the metabolism of these lipids and the calcium signal. We compare the patterns of PPI turnover that occur during the first minute following fertilization in eggs in which PPI are labelled to steady state with [3H]inositol or [3H]arachidonate with that in which PPI are labelled for a shorter period with [3H]inositol. When eggs are labelled to apparent isotopic equilibrium with either [3H]inositol or [3H]arachidonate, no early increase in [3H]PtdInsP2 occurs while PtdIns decreases slightly. On the contrary, when not labelled to isotopic equilibrium, all [3H]PPI increase during the first 15 seconds following fertilization. We find that, within seconds, fertilization triggers a 600-fold increase in the turnover of PPI, producing an amount of InsP3 apparently sufficient to trigger calcium release. We suggest that phosphoinositidase C and PtdInsP kinase, responsible respectively for the hydrolysis and synthesis of PtdInsP2, are both stimulated to a comparable degree in the first 30 seconds following fertilization and that net changes in the amount of PtdInsP2 at fertilization are very sensitive to the relative levels of activation of the two enzymes. Activating the eggs with the calcium ionophore A23187 showed that both these enzymes are sensitive to calcium, suggesting that calcium-dependent InsP3 production might play a role in the initiation and/or the propagation of the fertilization calcium wave.(ABSTRACT TRUNCATED AT 250 WORDS)

The cortical reaction and development of activation competence in mammalian oocytes

“…In sea urchin eggs, fertilization results in a stimulation of PIP 2 turnover and the production of second messengersinositol 1,4,5-trisphosphate (IP 3 ) and diacylglycerol (DAG) (Ciapa et al, 1992). PIP 2 appears to play a role in the amount of Ca released in activated amphibian eggs (Larabell and Nuccitelli, 1992).…”

New insights into the mechanism of egg activation in fish

“…For example, if binding of IP 3 to the IP 3 -receptor is blocked by injecting the IP 3 antagonist heparin, or a functionally inhibitory IP 3 -receptor antibody, Ca 2+ release at fertilisation and egg activation is also blocked (Miyazaki et al, 1993). Furthermore, there appears to be an increased turnover of phosphoinositide lipids and increase in IP 3 levels in sea urchin and frog eggs at fertilisation (Nuccitelli, 1991;Ciapa et al, 1992;Snow et al, 1996;Lee and Shen, 1998) and Ca 2+ release at egg activation can be inhibited in both species with the PLC inhibitor U73122 (Dupont et al, 1996;Lee and Shen, 1998). However, we must not dismiss nor neglect the possible involvement of other naturally-occurring calcium releasing agents and their respective signalling pathways; cyclic ADP-ribose (cADPR), nicotinic acid adenine dinucleotide phosphate (NAADP), nitric oxide (NO), and cyclic GMP (cGMP) pathways all play crucial roles in Ca 2+ release in various physiological signalling mechanisms (Lee, 1977;Galione et al, 2000;Bootman et al, 2001;Leckie et al, 2003).…”