Calcium oscillations are one of the most universal signals in biology. Yet we still know surprisingly little about how these periodic (or aperiodic) events arise.
Happy to present our lab's latest work:
doi.org/10.1098/rsob.250220
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In the 1970s, before calcium oscillations were visualized (in 1984), they were already known to exist. Two classes of models were proposed: one based on periodic events at the plasma membrane, the other on intracellular mechanisms.
doi.org/10.1242/jeb.81.1.217
Mar 18, 2026 · 2:56 PM UTC
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In the late 1980s, two classes of models emerged: one based on IP₃ signaling, presumably generated at the plasma membrane, and the other on calcium-induced calcium release from the ER.
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Note Goldbeter trained with Ilya Prigogine, and the basic idea of CICR (an autocatalytic reaction driving ER calcium depletion) is similar to the Brusselator model for glycolysis. nobelprize.org/prizes/chemis…
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While Ca²⁺ release models were developed in the spirit of searching for minimal systems, the key prediction that ER calcium refill limits the interval between spikes could not be tested until ER calcium could be measured directly.
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I learned a tremendous amount from Goldbeter's work. I am also deeply influenced by the writings from the main advocate of these models (Sir Michael Berridge). That said, as you will see, we ultimately disagree with the conclusion.
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We’re neither the first nor, hopefully, the last to argue for the plasma membrane oscillation model.
For a long time, I’ve been puzzled why this model, which to a novice sounds far more intuitive, has been almost completely ignored by the field.
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Reading this excellent memoriam, i then realize the phosphoinositides field predates the calcium field, so when they were young, they were the rebels that challenge the dogma of their time, and now, their models became the dogma doi.org/10.1016/j.ceca.2020.…
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