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© The Rockefeller University Press, 0021-9525/1998//1235 $5.00
The Journal of Cell Biology, Volume 142, Number 5, , 1998 1235-1243

Articles

Ca2+ Homeostasis in the Agonist-sensitive Internal Store: Functional Interactions Between Mitochondria and the ER Measured In Situ in Intact Cells



Barbara Landolfi*, Silvana Curci*, Lucantonio Debellis*, Tullio Pozzan{ddagger}, and Aldebaran M. Hofer{ddagger}

* Istituto di Fisiologia Generale, Università degli Studi di Bari, Via Amendola 165/A, I-70126 Bari, Italy; and {ddagger} University of Padova, Consiglio Nazionale delle Ricerche Center for Biomembranes, Viale G. Colombo 3, I-35121 Padova, Italy

Mitochondria have a well-established capacity to detect cytoplasmic Ca2+ signals resulting from the discharge of ER Ca2+ stores. Conversely, both the buffering of released Ca2+ and ATP production by mitochondria are predicted to influence ER Ca2+ handling, but this complex exchange has been difficult to assess in situ using conventional measurement techniques. Here we have examined this interaction in single intact BHK-21 cells by monitoring intraluminal ER [Ca2+] directly using trapped fluorescent low-affinity Ca2+ indicators. Treatment with mitochondrial inhibitors (FCCP, antimycin A, oligomycin, and rotenone) dramatically prolonged the refilling of stores after release with bradykinin. This effect was largely due to inhibition of Ca2+ entry pathways at the plasma membrane, but a significant component appears to arise from reduction of SERCA-mediated Ca2+ uptake, possibly as a consequence of ATP depletions in a localized subcellular domain. The rate of bradykinin-induced Ca2+ release was reduced to 51% of control by FCCP. This effect was largely overcome by loading cells with BAPTA-AM, highlighting the importance of mitochondrial Ca2+ buffering in shaping the release kinetics. However, mitochondria-specific ATP production was also a significant determinant of the release dynamic. Our data emphasize the localized nature of the interaction between these organelles, and show that competent mitochondria are essential for generating explosive Ca2+ signals.

Key Words: metabolic microdomains • calcium homeostasis • organelle interactions • mitochondrial uncouplers • signal transduction

Abbreviations used in this paper: BK, bradykinin; FCCP, carbonyl cyanide p-trifluoromethoxy-phenylhydrazone; InsP3, inositol 1,4,5-trisphosphate; tBHQ, 2, 5-Di(tert-butyl)hydroquinone.

Address all correspondence to Aldebaran M. Hofer, University of Padova, CNR Center for Biomembranes, Viale G. Colombo 3, I-35121 Padova, Italy. Tel.: +39-49-827-6065. Fax: +39-80-5443388. E-mail: wim{at}civ.bio.unipd.it


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