Intercellular calcium waves and Ca2+ signalling

George and Bates (2022) review calcium waves in developing animals. In Drosophila melanogaster, the larval wing epithelium propagates calcium waves both after wounding and spontaneously in vivo.² They report that disrupting these waves, by drugs or by mutations in the ion channels they need, is associated with faulty wing development.² In blue pansy butterflies, calcium waves and transients occur during pupal wing development. Disrupting the oscillations leads to malformed scales and eye spots.³ Many oscillations appear to start at the future eye spot. The authors suggest they may instruct development of that structure.³

Tung and colleagues (2024) used a genetically encoded calcium reporter, GCAMP6S, to watch Xenopus embryos after acute mechanical injury. They note that such damage is well known to induce calcium waves within one organism, aiding cell-cell coordination and wound closure.⁵ The team then asked whether uninjured embryos in the same medium respond. They defined transfer time as the delay from injury until the mean calcium signal exceeded the maximum of spontaneous activity.⁶ Trewavas (2026) reports a parallel in plants. Touching a single pavement cell induces a directional calcium wave, and insect damage induces a wave that depends on glutamate-dependent channels.⁸

Ariazi and colleagues (2017) collect reports that Ca2+ signals pass between distant cells through tunneling nanotubes. They say these reports suggest some form of membrane or cytosolic continuity along the nanotubes, or active gap junction channels at the end of the process.¹ They also note that in lymphocytes the nanotubes are not permeable to Ca2+, so the properties of these structures vary.¹ George and Bates list mechanical stress as an inducer of calcium waves in many cell types.⁴ Chen and colleagues (2025) describe a different trigger. Electrical potentials at a piezoelectric scaffold surface can activate voltage-gated calcium channels and produce calcium transients in stem cells.⁷

George and Bates ask how calcium oscillations are coordinated across a whole tissue. One hypothesis they raise is that mechanical forces between cells guide the ionic signalling.⁴ Acharya and colleagues (2026) propose that loss of gap junction communication acts on the Hippo-YAP node partly through calcium waves. They predict that connexin-stabilising drugs would restore wave propagation in oral cancer stem cell models. They state that this has not yet been tested.⁹ Trewavas treats calcium waves as part of information transfer leading to tissue learning in plants.⁸