Contribution of endoplasmic reticulum to Ca(2+) signals in Dictyostelium depends on extracellular Ca(2+).
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 microM and then remains constant at extracellular Ca(2+) concentrations up to at least 250 microM. 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+).
Department of Microbiology, La Trobe University, Victoria, Australia. P.Fisher@latrobe.edu.au
Paul R
PR
Fisher
Zofia
Z
Wilczynska
D000818:Animals; D002118:Calcium / Q000378:metabolism* / Q000494:pharmacology; D020013:Calcium Signaling; D000242:Cyclic AMP / Q000494:pharmacology; D004023:Dictyostelium / Q000187:drug effects / Q000378:metabolism*; D004721:Endoplasmic Reticulum / Q000378:metabolism*
D000242:Cyclic AMP; D002118:Calcium