bioRxiv ScienceSearch

bioRxiv · 10.1101/012955

Predicting X-ray Diffuse Scattering from Translation Libration Screw Structural Ensembles

Abstract

Identifying the intramolecular motions of proteins and nucleic acids is a major challenge in macromolecular X-ray crystallography. While Bragg diffraction describes the average positional distribution of crystalline atoms, many different models can fit this distribution equally well. Diffuse X-ray scattering can reduce this degeneracy by directly reporting on correlated atomic displacements. Although recent technological advances are increasing the potential to accurately measure diffuse scattering, computational modeling and validation tools are still needed to quantify the agreement between experimental data and different parameterizations of crystalline disorder. A new tool, phenix.diffuse, addresses this need by employing Guiniers equation to calculate diffuse scattering from Protein Data Bank (PDB)-formatted structural ensembles. As an example case, phenix.diffuse is applied to Translation-Libration-Screw (TLS) refinement, which models rigid body displacement for segments of the macromolecule. To enable calculation of diffuse scattering from TLS refined structures, phenix.tls_models builds multi-model PDB files that sample the underlying T, L and S tensors. In the glycerophosphodiesterase GpdQ, alternative TLS group partitioning and different motional correlations between groups yield markedly dissimilar diffuse scattering maps with distinct implications for molecular mechanism and allostery. These methods demonstrate how X-ray diffuse scattering can extend macromolecular structural refinement, validation, and analysis.\n\nSynopsisA method of simulating X-ray diffuse scattering from multi-model PDB files is presented. Despite similar agreement with Bragg data, different Translation-Libration-Screw refinement strategies produce unique diffuse intensity patterns.

Source connections

Explore related subjects

Keep this discovery

BibTeXRIS

Andrew Van Benschoten, Pavel Afonine, Thomas Terwilliger, Michael Wall, Colin Jackson, Nicholas Sauter, Paul Adams, Alexandre Urzhumtsev, James Fraser. 2015-01-02. Predicting X-ray Diffuse Scattering from Translation Libration Screw Structural Ensembles. https://doi.org/10.1101/012955

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

TatA complexes exhibit a marked change in organisation in response to expression of the TatBC complex

The twin arginine translocation (Tat) system is an integral membrane protein complex that accomplishes the remarkable feat of transporting large, fully-folded polypeptides across the inner membrane of bacteria, into the periplasm. In Escherichia coli Tat is comprised of three membrane proteins: TatA, TatB and TatC. How these proteins arrange themselves in the inner membrane to permit passage of Tat substrates, whilst maintaining membrane integrity, is still poorly understood. TatA is the most abundant component of this complex and facilitates assembly of the transport mechanism. We have utilised immunogold labelling in combination with array tomography to gain insight into the localisation and distribution of the TatA protein in E. coli cells. We show that TatA exhibits a uniform distribution throughout the inner membrane of E. coli and that altering the expression of TatBC shows a previously uncharacterised distribution of TatA in the inner membrane. Array tomography was used to provide our first insight into this altered distribution of TatA in 3D space, revealing that this protein forms linear clusters in the inner membrane of E. coli upon increased expression of TatBC. This is the first indication that TatA organisation in the inner membrane alters in response to changes in Tat subunit stoichiometry.\n\nSummary statementThe volumetric electron-microscopy technique, array tomography, revealed a novel distribution of TatA protein (from the twin arginine translocase complex), in Escherichia coli.

Biophysics

A unified coarse-grained theory of bacterial physiology explains the relationship between cell size, growth rate and proteome composition under various growth limitations

Universal observations in Biology are sometimes described as "laws". In E. coli, experimental studies performed over the past six decades have revealed major growth laws relating ribosomal mass fraction and cell size to the growth rate. Because they formalize complex emerging principles in biology, growth laws have been instrumental in shaping our understanding of bacterial physiology. Here, we discovered a novel size law that connects cell size to the inverse of the metabolic proteome mass fraction and the active fraction of ribosomes. We used a simple whole-cell coarse-grained model of cell physiology that combines the proteome allocation theory and the structural model of cell division. The model captures all available experimental data connecting the cell proteome composition, ribosome activity, division size and growth rate in response to nutrient quality, antibiotic treatment and increased protein burden. Finally, a stochastic extension of the model explains non-trivial correlations observed in single cell experiments including the adder principle. This work provides a simple and robust theoretical framework for studying the fundamental principles of cell size determination in unicellular organisms.

Biophysics

Identification of a Zika NS2B-NS3pro pocket susceptible to allosteric inhibition by small molecules including qucertin rich in edible plants

It has been recently estimated that one-third of the world population will be infected by Zika virus, but unfortunately so far there is no vaccine or medicine available. In particular, the special concern on the vaccine treatment to Zika and Dengue arising from antibody-dependent enhancement strongly emphasizes the irreplaceable role of its NS2B-NS3 protease (NS2B-NS3pro) as a target for anti-Zika drug discovery/design due to its absolutely-essential role in viral replication. Very recently we identified two small molecules inhibit Zika NS2B-NS3pro in non-competitive mode, with Ki values of 0.57 and 2.02 {micro}M respective for p-Nitrophenyl-p-guanidino benzoate and qucertin. Here, by molecular docking, we show that although one is designed compound while another is a natural product, both molecules bind to the same pocket on the back of the substrate-binding pocket of Zika NS2B-NS3pro. As the two inhibitors fundamentally differ from cn-716, the only known peptidomimetic boronic acid inhibitor in both structure scaffolds and inhibitory modes, our discovery might open up a new avenue for the future development of allosteric inhibitors, which is highly demanded to achieve therapeutic inhibition of flaviviral NS2B-NS3pro complexes. Furthermore, as qucertin is abundant in many vegetables and fruits such caper, lovage, tea and red onion, our results should benefit the public to immediately fight Zika virus.

Biophysics