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Mol. Cell. Biol., Nov 1997, 6339-6347, Vol 17, No. 11
M Paidhungat and S Garrett
Previous studies attributed the yeast (Saccharomyces cerevisiae) cdc1(Ts)
growth defect to loss of an Mn2+-dependent function. In this report we show
that cdc1(Ts) temperature-sensitive growth is also associated with an
increase in cytosolic Ca2+. We identified two recessive suppressors of the
cdc1(Ts) temperature-sensitive growth which block Ca2+ uptake and
accumulation, suggesting that cytosolic Ca2+ exacerbates or is responsible
for the cdc1(Ts) growth defect. One of the cdc1(Ts) suppressors is
identical to a gene, MID1, recently implicated in mating
pheromone-stimulated Ca2+ uptake. The gene (CCH1) corresponding to the
second suppressor encodes a protein that bears significant sequence
similarity to the pore-forming subunit (alpha1) of plasma membrane,
voltage-gated Ca2+ channels from higher eukaryotes. Strains lacking Mid1 or
Cch1 protein exhibit a defect in pheromone- induced Ca2+ uptake and
consequently lose viability upon mating arrest. The mid1delta and cch1delta
mutants also display reduced tolerance to monovalent cations such as Li+,
suggesting a role for Ca2+ uptake in the calcineurin-dependent ion stress
response. Finally, mid1delta cch1delta double mutants are, by both
physiological and genetic criteria, identical to single mutants. These and
other results suggest Mid1 and Cch1 are components of a yeast Ca2+ channel
that may mediate Ca2+ uptake in response to mating pheromone, salt stress,
and Mn2+ depletion.
Copyright © 1997, American Society for Microbiology
A homolog of mammalian, voltage-gated calcium channels mediates yeast pheromone-stimulated Ca2+ uptake and exacerbates the cdc1(Ts) growth defect
Department of Molecular Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710, USA.
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