Both calcium-sensing receptor intracellular C-terminal domains support homodimer signaling

Extracellular calcium-sensing receptors (CaSRs) are required for whole-body calcium homeostasis and operate as homodimers, shown structurally to bind only one heterotrimeric G protein at a time. Whether the intracellular domain (ICD) of the other, uncoupled monomer is functionally redundant or still required for optimal CaSR signaling remains unknown. Cotransfection of human embryonic kidney 293 cells with receptors containing both extracellular (CaSR<sub>1</sub><sup>S170A</sup>) and intracellular (CaSR<sub>2</sub><sup>F801A</sup>) mutations, which are nonfunctional when transfected individually, partially rescues function via trans-activation in CaSR<sub>1</sub><sup>S170A</sup>:CaSR<sub>2</sub><sup>F801A</sup> heterodimers. Further, mutation of an inhibitory, intracellular protein kinase C site T888 permits gain-of-function in CaSR. Therefore, we disabled phosphorylation of this residue (CaSR<sup>T888A</sup>) by mutating one, and then both monomers in the CaSR<sub>1</sub><sup>S170A</sup>:CaSR<sub>2</sub><sup>F801A</sup>trans-activation-enabled heterodimers. The extracellular Ca<sup>2+</sup>-induced intracellular Ca<sup>2+</sup> mobilization elicited by CaSR<sub>1</sub><sup>S170A</sup>:CaSR<sub>2</sub><sup>F801A</sup> was significantly enhanced by disabling one T888 inhibitory phosphorylation site in either CaSR<sub>1</sub><sup>S170A/T888A</sup>:CaSR<sub>2</sub><sup>F801A</sup> or CaSR<sub>1</sub><sup>S170A</sup>:CaSR<sub>2</sub><sup>F801A/T888A</sup>, and further enhanced in cells in which both T888 sites had been removed in CaSR<sub>1</sub><sup>S170A/T888A</sup>:CaSR<sub>2</sub><sup>F801A/T888A</sup>. The results demonstrate that both ICDs of CaSR dimers contribute independently to receptor signaling. Further, in the presence of N-(3-[2-chlorophenyl]propyl)-(R)-alpha-methyl-3-methoxybenzylamine (NPS R-568; CaSR positive allosteric modulator), extracellular Ca<sup>2+</sup>-stimulated signaling from the nonfunctional CaSR<sup>S170A</sup> mutant was rescued to wild-type levels by removal of the inhibitory T888 phosphorylation site in CaSR<sup>S170A/T888A</sup> homodimers. Therefore, although CaSR<sup>S170A</sup> destabilizes the closed (active) form of the Venus fly trap in wild-type homodimers, receptor function can be rescued by relieving intracellular C-terminal domain-dependent inhibition of signaling. SIGNIFICANCE STATEMENT: Despite the homodimeric calcium-sensing receptor coupling to only one G protein at a time, disinhibiting both intracellular domains elicits a greater increase in intracellular Ca<sup>2+</sup> mobilization than disinhibiting only one, suggesting a positive functional contribution from both subunits.

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Journal
Molecular Pharmacology
Published
2025-09-25
DOI
https://doi.org/10.1016/j.molpha.2025.100077
Primary Topic
Ion channel regulation and function
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article
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article

Both calcium-sensing receptor intracellular C-terminal domains support homodimer signaling

Arthur D. Conigrave, Lenah S. Binmahfouz, Eleanor Barker, Donald T. Ward et al.
Molecular Pharmacology
Ion channel regulation and function
article

Both calcium-sensing receptor intracellular C-terminal domains support homodimer signaling

Arthur D. Conigrave, Lenah S. Binmahfouz, Eleanor Barker, Donald T. Ward, Mahvash A. Goolam
article en

Abstract

Extracellular calcium-sensing receptors (CaSRs) are required for whole-body calcium homeostasis and operate as homodimers, shown structurally to bind only one heterotrimeric G protein at a time. Whether the intracellular domain (ICD) of the other, uncoupled monomer is functionally redundant or still required for optimal CaSR signaling remains unknown. Cotransfection of human embryonic kidney 293 cells with receptors containing both extracellular (CaSR<sub>1</sub><sup>S170A</sup>) and intracellular (CaSR<sub>2</sub><sup>F801A</sup>) mutations, which are nonfunctional when transfected individually, partially rescues function via trans-activation in CaSR<sub>1</sub><sup>S170A</sup>:CaSR<sub>2</sub><sup>F801A</sup> heterodimers. Further, mutation of an inhibitory, intracellular protein kinase C site T888 permits gain-of-function in CaSR. Therefore, we disabled phosphorylation of this residue (CaSR<sup>T888A</sup>) by mutating one, and then both monomers in the CaSR<sub>1</sub><sup>S170A</sup>:CaSR<sub>2</sub><sup>F801A</sup>trans-activation-enabled heterodimers. The extracellular Ca<sup>2+</sup>-induced intracellular Ca<sup>2+</sup> mobilization elicited by CaSR<sub>1</sub><sup>S170A</sup>:CaSR<sub>2</sub><sup>F801A</sup> was significantly enhanced by disabling one T888 inhibitory phosphorylation site in either CaSR<sub>1</sub><sup>S170A/T888A</sup>:CaSR<sub>2</sub><sup>F801A</sup> or CaSR<sub>1</sub><sup>S170A</sup>:CaSR<sub>2</sub><sup>F801A/T888A</sup>, and further enhanced in cells in which both T888 sites had been removed in CaSR<sub>1</sub><sup>S170A/T888A</sup>:CaSR<sub>2</sub><sup>F801A/T888A</sup>. The results demonstrate that both ICDs of CaSR dimers contribute independently to receptor signaling. Further, in the presence of N-(3-[2-chlorophenyl]propyl)-(R)-alpha-methyl-3-methoxybenzylamine (NPS R-568; CaSR positive allosteric modulator), extracellular Ca<sup>2+</sup>-stimulated signaling from the nonfunctional CaSR<sup>S170A</sup> mutant was rescued to wild-type levels by removal of the inhibitory T888 phosphorylation site in CaSR<sup>S170A/T888A</sup> homodimers. Therefore, although CaSR<sup>S170A</sup> destabilizes the closed (active) form of the Venus fly trap in wild-type homodimers, receptor function can be rescued by relieving intracellular C-terminal domain-dependent inhibition of signaling. SIGNIFICANCE STATEMENT: Despite the homodimeric calcium-sensing receptor coupling to only one G protein at a time, disinhibiting both intracellular domains elicits a greater increase in intracellular Ca<sup>2+</sup> mobilization than disinhibiting only one, suggesting a positive functional contribution from both subunits.

Molecular PharmacologyVol. 107(11)
King Abdulaziz University (SA), Manchester Academic Health Science Centre (GB), University of Manchester (GB), UNSW Sydney (AU)
Openalex Percentile: Top 77%
Ion channel regulation and function
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