QUICK SEARCH:   [advanced] Author: Keyword(s):
Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents

doi: 10.1242/10.1242/jcs.00372

This Article Figures Only Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kellermayer, R. Articles by Bedwell, D. M. Search for Related Content PubMed PubMed Citation Articles by Kellermayer, R. Articles by Bedwell, D. M.

Extracellular Ca²⁺ sensing contributes to excess Ca²⁺ accumulation and vacuolar fragmentation in a pmr1 mutant of S. cerevisiae

¹ Department of Microbiology, University of Alabama at Birmingham, Birmingham, AL 35294, USA
² Department of Clinical Chemistry, University Medical School, 7624 Peçs, Hungary

^* Author for correspondence (e-mail: dbedwell{at}uab.edu)

Accepted 16 January 2003

Previous studies have suggested that yeast strains lacking the Ca²⁺-ATPase Pmr1p are unable to maintain an adequate level of Ca²⁺ within the Golgi apparatus. It is thought that this compartmental store depletion induces a signal that causes an increased rate of Ca²⁺ uptake and accumulation in a manner similar to the capacitative Ca²⁺ entry (CCE) response in non-excitable mammalian cells. To explore this model further, we examined cellular Ca²⁺ uptake and accumulation in a pmr1 strain grown in the presence of a reduced level of divalent cations. We found that the level of Ca²⁺ uptake and accumulation in a pmr1 strain increased as the concentration of divalent cations in the growth medium decreased. These results are inconsistent with a model in which cellular Ca²⁺ uptake and accumulation are determined solely by the depletion of Ca²⁺ in an intracellular compartment. Instead, our results suggest that a second regulatory mechanism couples cellular Ca²⁺ uptake to the availability of Ca²⁺ in the extracellular environment. Furthermore, we found that various conditions that increase the level of cytosolic Ca²⁺ correlate with vacuolar fragmentation in wild-type (WT), pmr1 and pmr1/pmc1 yeast strains. This suggests that vacuolar fragmentation might function as a normal physiological response to Ca²⁺ stress that increases the vacuolar surface/volume ratio, thereby maximizing the sequestration of this important signaling molecule.

Key words: Yeast, Pmr1p, Ca²⁺ homeostasis, Vacuole

This article has been cited by other articles:

				V. S. Anil, P. Rajkumar, P. Kumar, and M. K. Mathew A Plant Ca2+ Pump, ACA2, Relieves Salt Hypersensitivity in Yeast: MODULATION OF CYTOSOLIC CALCIUM SIGNATURE AND ACTIVATION OF ADAPTIVE Na+ HOMEOSTASIS J. Biol. Chem., February 8, 2008; 283(6): 3497 - 3506. [Abstract] [Full Text] [PDF]

				E. M. Rees, J. Lee, and D. J. Thiele Mobilization of Intracellular Copper Stores by the Ctr2 Vacuolar Copper Transporter J. Biol. Chem., December 24, 2004; 279(52): 54221 - 54229. [Abstract] [Full Text] [PDF]

				V.-K. Ton and R. Rao Functional expression of heterologous proteins in yeast: insights into Ca2+ signaling and Ca2+-transporting ATPases Am J Physiol Cell Physiol, September 1, 2004; 287(3): C580 - C589. [Abstract] [Full Text] [PDF]