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J. Cell Biol.,
Volume 142, Number 5, September 7, 1998 1235-1243
* Istituto di Fisiologia Generale, Università degli Studi di Bari, Via Amendola 165/A, I-70126 Bari, Italy; and 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.
University of
Padova, Consiglio Nazionale delle Ricerche Center for Biomembranes, Viale G. Colombo 3, I-35121 Padova, Italy
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