High resolution

Module 5: Figure mitochondria and Ca2+ entry

Mitochondrial modification of Ca2+ entry.

In this study on Jurkat leukaemic T cells, thapsigargin (TG) added in a Ca2+-free solution (0 Ca) emptied the internal Ca2+ store by blocking the sarco/endo-plasmic reticulum Ca2+-ATPase (SERCA) pumps. This empty store then activated a store-operated channel (SOC), as evident by the marked increase in Ca2+ that occurred when 2 mM Ca2+ was added back to the bathing medium (black bar). In cells that had been treated with carbonyl cyanide m-chlorophenylhydrazone (CCCP) to inhibit the mitochondria (dotted line), the initial peak was the same, indicating that the entry channel was fully activated, but this response then declined to a much lower level. This lower plateau probably results from the fact that the mitochondria lying close to the entry channels remove Ca2+, thereby negating its inhibitory effect on entry (Module 9: Figure T-cell Ca2+ signalling). Reproduced from The Journal of Cell Biology, 1997, vol. 137, pp. 633–648 by copyright permission of The Rockefeller University Press; see Hoth et al. 1997.