In our previous reports, wehave verified the involvement of G protein, Ca2+ channel in plasma memband CDPK in extracellular calmodulin(CaM) signal transduction chain for theinitiatory effects of extracellular CaM onpollen germination and pollen tubegrowth . In this paper, both normal andexogenous CaM-enhanced pollen germination and tube growth were completelyinhibited by the phospholipase C inhibitor U-73122 (Fig. 1 ). The enhancement of pollen germination and tubegrowth by the G protein agonist choleratoxin were also completely inhibited byU-73122 (Fig. 2), whereas the inhibition of pollen germination and tubegrowth by the G protein antagonist pertussis toxin was reversed by IP3 (Fig. 2).Heparin, an antagonist Of IP3 receptor,inhibited pollen germination and tubegrowth (Fig. 3 ), while thapsigargin increased cytosolic Ca2+ by inhibiting theIP3-specific Ca2+ pump in endoplasmicreticulum, and thereby increased pollengermination and tube growth (Fig. 4).The above results suggest that phosphoinositide signaling pathway might be involved in the extracellular CaM signaltransduction chain in the initiatory effectsof extracellular CaM on pollen germination and tube growth.
