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Compartmentalisation in cAMP Signalling: A Phase Separation Perspective
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Cells rely on precise spatiotemporal control of signalling pathways to
ensure functional specificity. The compartmentalisation of cyclic AMP
(cAMP) and protein kinase A (PKA) signalling enables distinct cellular
responses within a crowded cytoplasmic space. Traditionally,
compartmentalisation has been attributed to PKA anchoring,
phosphodiesterase-mediated cAMP degradation, and restricted cAMP
diffusion. Emerging evidence suggests that liquid-liquid phase
separation (LLPS) might play a significant role in organising cAMP
signalling. LLPS has been implicated in receptor clustering, cyclic
nucleotide synthesis, effector activation, and signal termination,
offering a dynamic mechanism for spatially restricting cAMP activity.
Notably, PKA RIα condensates appear to act as cAMP reservoirs,
modulating local cAMP availability and phosphodiesterase-mediated
degradation. Disrupting LLPS-mediated condensation of cAMP/PKA pathway
components has been linked to cancer and neurodegeneration, pointing to
physiological relevance. This review explores current evidence on LLPS
in cAMP signalling, highlighting the implications for signal
compartmentalisation and functional specificity.
Title: Compartmentalisation in cAMP Signalling: A Phase Separation Perspective
Description:
Cells rely on precise spatiotemporal control of signalling pathways to
ensure functional specificity.
The compartmentalisation of cyclic AMP
(cAMP) and protein kinase A (PKA) signalling enables distinct cellular
responses within a crowded cytoplasmic space.
Traditionally,
compartmentalisation has been attributed to PKA anchoring,
phosphodiesterase-mediated cAMP degradation, and restricted cAMP
diffusion.
Emerging evidence suggests that liquid-liquid phase
separation (LLPS) might play a significant role in organising cAMP
signalling.
LLPS has been implicated in receptor clustering, cyclic
nucleotide synthesis, effector activation, and signal termination,
offering a dynamic mechanism for spatially restricting cAMP activity.
Notably, PKA RIα condensates appear to act as cAMP reservoirs,
modulating local cAMP availability and phosphodiesterase-mediated
degradation.
Disrupting LLPS-mediated condensation of cAMP/PKA pathway
components has been linked to cancer and neurodegeneration, pointing to
physiological relevance.
This review explores current evidence on LLPS
in cAMP signalling, highlighting the implications for signal
compartmentalisation and functional specificity.
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