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Wegner, S.

Publications and source records attributed to Wegner, S..

2 recordsLinked to original sources

Capturing the Conformational Heterogeneity of HSPB1 Chaperone Oligomers at Atomic Resolution

Small heat shock proteins (sHSPs), including HSPB1, are essential regulators of cellular proteostasis that interact with unfolded and partially folded proteins to prevent aberrant misfolding and aggregation. These proteins fulfill a similar role in biological condensates, where they interact with intrinsically disordered proteins to modulate their liquid-liquid and liquid-to-solid phase transitions. Characterizing sHSP structure, dynamics, and client interactions is challenging due to their partially disordered nature, their tendency to form polydisperse oligomers, and their diverse range of clients. In this work, we leverage various biophysical methods, including fast 1H-based magic angle spinning (MAS) NMR spectroscopy, molecular dynamics (MD) simulations and modeling, to shed new light on the structure and dynamics of HSPB1 oligomers. Using split-intein mediated segmental labeling, we provide unambiguous evidence that in the oligomer context the N-terminal domain (NTD) of HSPB1 is rigid and adopts an ensemble of heterogenous conformations, the -crystallin domain (ACD) forms dimers and experiences multiple distinct local environments, while the C-terminal domain (CTD) remains highly dynamic. Our computational models suggest that the NTDs participate in extensive NTD-NTD and NTD-ACD interactions and are sequestered within the oligomer interior. We further demonstrate that HSPB1 higher order oligomers disassemble into smaller oligomeric species in the presence of a client protein and that an accessible NTD is essential for HSPB1 partitioning into condensates and interactions with client proteins. Our integrated approach provides a high-resolution view of the complex oligomeric landscape of HSPB1 and sheds light on the elusive network of interactions that underly HSPB1 function in biological condensates. Significance statementHSPB1 is a ubiquitous cellular chaperone that helps prevent the aberrant aggregation of intrinsically disordered proteins involved in biological condensates and neurodegenerative diseases. Despite its central role in this process, many aspects of HSPB1s structure and interactions with clients are not well understood due to its tendency to form polydisperse oligomeric structures and to function in heterogeneous condensate environments. Here, we present an integrated approach that includes segmental labeling, fast MAS NMR spectroscopy, and computational tools to characterize the structure and dynamics of HSPB1 in its oligomeric form and within client condensates at high resolution. Our approach, which is applicable to other complex biological systems, highlights the important role of HSPB1s N-terminal domain in oligomeric assembly and interactions with clients.

biophysics↗

Circadian control of intrinsic heart rate via a sinus node clock and the pacemaker channel

In the human, there is a circadian rhythm in the resting heart rate and it is higher during the day in preparation for physical activity. Conversely, slow heart rhythms (bradyarrhythmias) occur primarily at night. Although the lower heart rate at night is widely assumed to be neural in origin (the result of high vagal tone), the objective of the study was to test whether there is an intrinsic change in heart rate driven by a local circadian clock. In the mouse, there was a circadian rhythm in the heart rate in vivo in the conscious telemetrized animal, but there was also a circadian rhythm in the intrinsic heart rate in denervated preparations: the Langendorff-perfused heart and isolated sinus node. In the sinus node, experiments (qPCR and bioluminescence recordings in mice with a Per1 luciferase reporter) revealed functioning canonical clock genes, e.g. Bmal1 and Per1. We identified a circadian rhythm in the expression of key ion channels, notably the pacemaker channel Hcn4 (mRNA and protein) and the corresponding ionic current (funny current, measured by whole cell patch clamp in isolated sinus node cells). Block of funny current in the isolated sinus node abolished the circadian rhythm in the intrinsic heart rate. Incapacitating the local clock (by cardiac-specific knockout of Bmal1) abolished the normal circadian rhythm of Hcn4, funny current and the intrinsic heart rate. Chromatin immunoprecipitation demonstrated that Hcn4 is a transcriptional target of BMAL1 establishing a pathway by which the local clock can regulate heart rate. In conclusion, there is a circadian rhythm in the intrinsic heart rate as a result of a local circadian clock in the sinus node that drives rhythmic expression of Hcn4. The data reveal a novel regulator of heart rate and mechanistic insight into the occurrence of bradyarrhythmias at night.

physiology↗