Rr. Preston et Ja. Hammond, Correlation between loss of a Mg2+ conductance and an adaptation defect ina mutant of Paramecium tetraurelia, J EUKAR MIC, 46(3), 1999, pp. 290-297
Paramecium tetraurelia responds to chronic KCl-induced depolarization by sw
imming backward, but the ciliate recovers within seconds and then undergoes
a prolonged adaptation period during which sensitivity to external stimuli
is altered radically. We examined the role of Mg2+ in this phenomenon. pro
mpted by finding that mutations in the eccentric-A gene both suppressed a M
g2+-specific conductance and prevented adaptation. Adaptation of the wild t
ype proceeded normally when extracellular Mg2+ was varied from 0-20 mM, how
ever, suggesting that channel-mediated Mg2+ fluxes were not involved. In se
eking alternative explanations for the eccentric mutant phenotype, we ascer
tained that there was an osmotic component to adaptation but that K+-induce
d depolarization was the primary stimulus. We also noted that wild-type and
eccentric mutant cells depolarized by equivalent amounts in KCl, suggestin
g that the genetic lesion must lie downstream of membrane-potential change.
We also examined whether the adaptation-induced behavioral changes and, in
deed, the defect in eccentric might be explained in terms of Mg2+ and Na+ e
fflux during behavioral resting, but experimental observations failed to su
pport this notion. Finally, we consider the possibility that eccentric gene
mutation prevents adaptation by interfering with intracellular free Mg2+ h
omeostasis in Paramecium.