Open AccessContribution of endoplasmic reticulum to Ca 2+ signals in Dictyostelium depends on extracellular Ca 2+
Author(s) -
Fisher Paul R.,
Wilczynska Zofia
Publication year - 2006
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1111/j.1574-6968.2006.00180.x
Subject(s) - extracellular , endoplasmic reticulum , calreticulin , intracellular , calnexin , cytosol , microbiology and biotechnology , mutant , chemotaxis , biology , thapsigargin , stim1 , biophysics , chemistry , biochemistry , receptor , enzyme , gene
We recently reported the first molecular genetic evidence that Dictyostelium Ca 2+ responses to chemoattractants include a contribution from the endoplasmic reticulum (ER) – responses are enhanced in mutants lacking calreticulin or calnexin, two major Ca 2+ ‐binding proteins in the ER, even though the influx of Ca 2+ into the mutants is reduced. Compared with wild‐type cells, the ER in the mutants contributes at least 30–70 nM additional Ca 2+ to the responses. Here we report that this additional ER contribution to the cytosolic Ca 2+ signal depends upon extracellular Ca 2+ – it does not occur in the absence of extracellular Ca 2+ , increases to a maximum as the extracellular Ca 2+ levels rise to 10 μM and then remains constant at extracellular Ca 2+ concentrations up to at least 250 μM. These results suggest that Ca 2+ influx causes the intracellular release, in the simplest scenario by a mechanism involving Ca 2+ ‐induced Ca 2+ release from the ER. By way of contrast, we show that Ca 2+ responses to mechanical stimulation are reduced, but still occur in the absence of extracellular Ca 2+ . Unlike the responses to chemoattractants, mechanoresponses thus include contributions from the ER that are independent of extracellular Ca 2+ .