Transient responses during hyperosmotic shock in the filamentous fungus Neurospora crassa.

Fungal cells maintain an internal hydrostatic pressure (turgor) of about 400-500 kPa. In the filamentous fungus Neurospora crassa, the initial cellular responses to hyperosmotic treatment are loss of turgor, a decrease in relative hyphal volume per unit length (within 1 min) and cell growth arrest; all recover over a period of 10-60 min due to increased net ion uptake and glycerol production. The electrical responses to hyperosmotic treatment are a transient depolarization of the potential (within 1 min), followed by a sustained hyperpolarization (after 4 min) to a potential more negative than the initial potential (a driving force for ion uptake). The nature of the transient depolarization was explored in the context of other transient responses to hyperosmotic shock, to determine whether activation of a specific ion permeability or some other rapid change in electrogenic transport was responsible. Changing the ionic composition of the extracellular medium revealed that K(+) permeability increases and H(+) permeability declines during the transient depolarization. We suggest that these changes are due to concerted inhibition of the electrogenic H(+)-ATPase, and an increase in a K(+) conductance. Knockout mutants of known K(+) (tok, trk, trm-8, hak-1) and Cl(-) (a clc-3 homologue) channels and transporters had no effect on the transient depolarization, but trk and hak-1 do play a role in osmoadaptation, as does a homologue of a serine kinase regulator of H(+)-ATPase in yeast, Ptk2.