English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Intracellular Ca signals represent a universal mechanism of cell function.Messages carried by Ca are local, rapid, and powerful enough to be deliveredover the thermal noise. A higher signal to noise ratio is achieved by acooperative action of Ca release channels such as IP3 receptors or ryanodinereceptors arranged in clusters or release units containing a few to severalhundred release channels. The release channels synchronize their openings viaCa-induced-Ca-release, generating high-amplitude local Ca signals known aspuffs in neurons or sparks in muscle cells. Despite the high release amplitudeand positive feedback nature of the activation, Ca signals are strictlyconfined in time and space by an unexplained termination mechanism. Here weshow that the collective transition of release channels from an open to aclosed state is identical to the phase transition associated with the reversalof magnetic field in an Ising ferromagnet. We demonstrate this mechanism usingnumerical model simulations of Ca sparks over a wide range of cluster sizesfrom 25 to 169 release channels. While prior studies suggested contributions ofstochastic attrition and Ca store depletion, our new simple quantitativecriterion closely predicts the depletion level required for spark terminationfor each cluster size. We further formulate exact requirements for a cluster ofrelease channels to follow the Ising model in any cell type. Thus we describedeterministically the behaviour of a system on a coarser scale (release unit)which is random on a finer scale (release channels), bridging the gap betweenscales. Our results provide the first exact mapping of a nanoscale biologicalsignalling model to an interacting particle system in statistical physics,making the extensive mathematical apparatus available to quantitative biology.

Clusters of calcium release channels harness the Ising phase transition to confine their elementary intracellular signals