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Biology subjects

Morton, W. S.

Publications and source records attributed to Morton, W. S..

2 recordsLinked to original sources

Quantifying (de)Mixing of Disordered Proteins in Molecular Dynamics Simulations

Biomolecular condensates control the spatial and temporal organization of cellular biochemistry. Their architectures often arise from complex, multicomponent mixtures governed by weak, multivalent interactions between intrinsically disordered regions (IDRs) of proteins. However, current approaches lack generalizable metrics to determine whether IDRs will mix or segregate within condensates. Here, we present a domain decomposition method (DDM) that accurately determines phase concentrations without identifying condensate interfaces. When tested against 399 IDR simulations, the DDM recovers dense- and dilute-phase concentrations within 1% agreement of established surface-based methods. By calculating spatial variances to map three-dimensional organization, this approach successfully distinguishes homogeneous mixing from surface enrichment, core--shell architectures, and complete segregation. Applying this continuous metric to 2,068 binary mixtures of 32 distinct IDRs, we demonstrate that physicochemical similarity strongly promotes mixing. Hydrophobic IDRs mixed promiscuously across all partner chemistries, whereas charged sequences mixed in a way highly sensitive to charge complementarity, forming the most stable condensates as net charge approached zero. Compared with experimental networks, our IDR-only simulations predicted the partitioning preferences for 10 of 13 proteins, with discrepancies accurately isolating cases where colocalization strictly requires RNA or folded domains. Quantifying mixing in this way provides a robust and reproducable method for predicting IDR interactomes and understanding the composition of complex cellular condensates.

biophysics↗

Mechanisms of transcription attenuation and condensation of RNA polymerase II by RECQ5

The elongation rates of RNA polymerase II (RNAPII) require precise control to prevent transcriptional stress, which can impede co-transcriptional pre-mRNA processing and contribute to many age- or disease-associated molecular changes (e.g., loss of proteostasis)1-5. Additionally mesoscale organization of transcription is thought to control the transcriptional rates6 and multiple factors have been reported to form biomolecular condensates and integrate RNAPII through the interaction with the C-terminal domain (CTD) of the largest subunit, RPB17-10. However, the structural organization of these condensates remains uncharacterized due to their small size and inherently dynamic nature. Here, we investigated the molecular mechanisms by which a general transcription factor - RECQ5 - associates with hyperphosphorylated RNAPII elongation complex (P-RNAPII EC) and controls translocation of RNAPII along genes. We combined biochemical reconstitution, electron cryomicroscopy, cryotomography, and coarse-grained simulations. We report two mechanisms by which RECQ5 modulates RNAPII transcription. At the atomic level, we demonstrate that RECQ5 uses the brake helix as a doorstop to control RNAPII translocation along DNA, attenuating transcription. At the mesoscale level, RECQ5 forms a condensate scaffold matrix, integrating P-RNAPII EC through a network of site-specific interactions, reinforcing the condensates structural integrity. Our integrative, multi-scale study provides insights into the structural basis of transcription attenuation and into the molecular architecture and biogenesis of a model RNAPII condensate.

biochemistry↗