Key result
Alanine replacement demonstrated that PLB e-position residues and SLN V14, L21, and a novel heptad repeat contribute to self-association affinity and stoichiometry, forming stable hexamers.
Why the study?
The structural determinants of phospholamban and sarcolipin self-assembly and their effects on oligomer stoichiometry and affinity were not fully characterized.
Identifies specific transmembrane zipper motifs in PLB and SLN that control their self-assembly and stoichiometry, providing structural insights into SERCA regulation.
We characterized the structural determinants of phospholamban (PLB) and sarcolipin (SLN) self-assembly, using experimental and computational assays. PLB and SLN are transmembrane peptides that regulate contractility via phosphorylation-dependent regulation of the sarcoplasmic reticulum Ca2+-ATPase (SERCA). The physiological role of PLB and SLN has been proposed to be important as a reservoir for fine-tuning SERCA activity and to act as ion-selective channels. Structural studies of PLB and SLN transmembrane domains have indicated stabilization of higher-order oligomers by leucine/isoleucine zippers in a heptad-repeat motif (a–g residue positions), requiring residue C41. Here we have modeled and tested the additional residues responsible for self-assembly using alanine replacement. We demonstrate that PLB e-position residues in the cleft between subunits contribute to self-association affinity and stoichiometry. For SLN, we identified two residues (V14, L21) and a novel heptad repeat (a-position) that contribute to self-association affinity and stoichiometry. This is in addition to the d-position that we previously identified for SLN oligomerization. Our molecular models demonstrate stable hexamer assemblies, but without the likelihood of a hydrated pore. We propose that PLB and SLN populate a distribution of oligomeric forms in sarcoplasmic reticulum membranes (monomer through pentamer and hexamer) and suggest that pore formation requires increased toroidal stoichiometry.
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Svensson et al. (2026) studied this question. Alanine replacement was evaluated on Structural determinants of PLB and SLN self-assembly. Alanine replacement demonstrated that PLB e-position residues and SLN V14, L21, and a novel heptad repeat contribute to self-association affinity and stoichiometry, forming stable hexamers.
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