Growth and morphogenesis transformation in Polyporus umbellatus were examined in the presence of various pharmacological compounds, to investigate signal transduction pathways that influence the development of sclerotia. Both the calcium channel blocker nifedipine and the calcium ionophor A23187 reduced sclerotial production in P. umbellatus; four classes of Ca(2+) signal agent-including calcium chelators, calcium channel blockers, calcium ionophors and calmodulin inhibitors-were further studied. Among them, EGTA and BAPTA, as calcium chelators, exhibited a complete inhibitory effect on sclerotial formation, among the levels tested. Calcium channel blockers and calcium ionophors at the concentrations used in this study could not eliminate sclerotia formation completely, but did greatly reduce sclerotial production. Notoginsenoside in dosages >250 microg/ml produced a significant negative effect on mycelial growth, and it prevented sclerotial formation entirely at a dosage of 500 microg/ml; no other drug influenced vegetative growth at all. The calcium ionophor A23187 did not decrease sclerotial mean weight at low doses (20 nM); at higher doses (200 nM), however, sclerotial development was significantly reduced, albeit not completely halted. The CaM inhibitors (W-7 and chlorpromazine) could each completely stop sclerotial formation. Using Fluo-3/AM as the indicator of cytosolic free calcium, the Ca(2+) content in the cytoplasm was found to have decreased significantly when hyphae were treated with different drugs, and there was no active Ca(2+) signal in the sclerotial mycelium. In general, the results suggest that Ca(2+) signal transduction may play an important role in sclerotial formation in P. umbellatus.