In all species, fertilization triggers in the egg a rapid and transient increase of intracellular free calcium (Cai), but how this signal is generated following sperm and egg interaction has not been clearly characterised yet. In sea urchin, a signalling pathway involving tyrosine kinase and PLCΓ has been proposed to be at the origin of the fertilization Cai signal. We report here that injection of src homology-2 (SH2) domains of the sea urchin PLCΓ inhibits in a competitive manner the endogenous PLCΓ, alters both the amplitude and duration of the fertilization Cai wave, but does not abrogate it. Our results suggest that PLCΓ acts in conjunction with a cADPr pathway and G-proteins of the... More
In all species, fertilization triggers in the egg a rapid and transient increase of intracellular free calcium (Cai), but how this signal is generated following sperm and egg interaction has not been clearly characterised yet. In sea urchin, a signalling pathway involving tyrosine kinase and PLCΓ has been proposed to be at the origin of the fertilization Cai signal. We report here that injection of src homology-2 (SH2) domains of the sea urchin PLCΓ inhibits in a competitive manner the endogenous PLCΓ, alters both the amplitude and duration of the fertilization Cai wave, but does not abrogate it. Our results suggest that PLCΓ acts in conjunction with a cADPr pathway and G-proteins of the Gαq type to trigger the fertilization Cai wave, and reinforce a crucial role for PLCΓ at mitosis and cytokinesis.
