Calcium signaling explained in new model

A new research proposes a model for how calcium signaling is able to activate distant effectors, without raising its own levels throughout the cell by extension.

Cells perceive their environment and communicate with other cells by exchanging chemical messages. These are received and interpreted by other cells and initiate a cascade of secondary intracellular messengers that direct specific cellular responses.

Calcium (Ca²⁺) is an important secondary messenger involved in a wide range of physiological processes, from muscle contraction to fertilization. It was not clear how some mid-range Ca²⁺ signals are able to specifically activate distant effectors, without a rise in Ca²⁺ levels that would activate other effectors in the cell as well.

In their model, Raphaël Courjaret and Khaled Machaca of the Weill Cornell Medical College in Qatar suggest that Ca²⁺ ions entering the cell through an influx pathway known as store-operated Ca²⁺ entry (SOCE) are pumped into the cell’s endoplasmic reticulum, and then re-released at a location farther away that is closer to the effector¹. This way, Ca²⁺ journeys to the location where it brings about its effect, without increasing global Ca²⁺ levels throughout the cell.

The team used electrophysiological techniques and observed the localization of components of their proposed pathway by confocal microscopy to validate their model, which was published in Nature Communications.

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