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Schreiber, G.

Publications and source records attributed to Schreiber, G..

27 records · Page 2Linked to original sources

The effects of protein crowders on small molecule drug diffusion

Crowded environments are known to affect the diffusion of macromolecules but their effects on the diffusion of small molecules, such as drugs, are largely uncharacterized. Here, we investigate how three macromolecular protein crowders, bovine serum albumin (BSA), hen egg-white lysozyme and myoglobin, influence the translational diffusion rates and interactions of four low molecular-weight compounds: the diagnostic marker fluorescein, and three drugs, doxorubicin, glycogen synthase kinase-3 inhibitor SB216763 and quinacrine. Using Fluorescence Recovery After Photo-bleaching in Line mode (Line- FRAP), Brownian dynamics simulations and molecular docking, we find that the diffusive behavior of the small molecules is highly affected by self-aggregation, interactions with the proteins, and surface adhesion. The diffusion of fluorescein is decreased by protein crowders due to its interactions with the proteins and their surface adsorption. In contrast, the presence of protein crowders increases the diffusion rate of doxorubicin by reducing surface interactions. SB216763 shows a third scenario, where BSA, but not lysozyme or myoglobin , reduces self-aggregation, resulting in faster diffusion. Quinacrine was the only compound whose diffusion was not affected by the presence of protein crowders. The mechanistic insights gained here into the effects of interactions of small molecules with proteins and surfaces on the translational diffusion of small molecules can assist in optimizing the design of compounds for higher mobility and lower occlusion in complex macromolecular environments.

biochemistry↗

Receptor binding and escape from Beta antibody responses drive Omicron-B.1.1.529 evolution

On the 24th November 2021 the sequence of a new SARS CoV-2 viral isolate spreading rapidly in Southern Africa was announced, containing far more mutations in Spike (S) than previously reported variants. Neutralization titres of Omicron by sera from vaccinees and convalescent subjects infected with early pandemic as well as Alpha, Beta, Gamma, Delta are substantially reduced or fail to neutralize. Titres against Omicron are boosted by third vaccine doses and are high in cases both vaccinated and infected by Delta. Mutations in Omicron knock out or substantially reduce neutralization by most of a large panel of potent monoclonal antibodies and antibodies under commercial development. Omicron S has structural changes from earlier viruses, combining mutations conferring tight binding to ACE2 to unleash evolution driven by immune escape, leading to a large number of mutations in the ACE2 binding site which rebalance receptor affinity to that of early pandemic viruses.

microbiology↗

Chaperones drive in vitro evolution of uracil glycosylase towards misfolded states

Natural evolution is driven by random mutations that improve fitness. In vitro evolution mimics this process, however, on a short time-scale and is driven by the given bait. Here, we used directed in vitro evolution of a random library of Uracil glycosylase (eUNG) displayed on yeast surface to select for binding to chaperones GroEL, DnaK+DnaJ+ATP (DnaKJ) or E.coli cell extract (CE). Using binding to the eUNG inhibitor Ugi as probe for native foldedess, the CE selected population was further divided to Ugi binders (+U) (native) or non-binders (-U). We found that GroEL, DnaKJ and CE-U select and enrich for mutations causing eUNG to misfold, with the three being enriched in mutations in buried and conserved positions, with a tendency to increase positive charge. Still, each selection, as well as CE+U and natural evolution of eUNG has its own trajectory. While GroEL and CE-U selected for mutants highly sensitive to protease cleavage, DnaKJ selected for partially structured misfolded species with a tendency to refold, making them less sensitive to proteases. CE+U selected for more neutral mutations than natural evolution. In a more general context, our results show that GroEL has a higher tendency to purge promiscuous misfolded protein mutants from the system, while DnaKJ binds mutants misfolding-prone species that are, upon chaperone release, more likely to natively refold. CE-U shares some of the properties of GroEL and DnaKJ selected populations, while harboring also unique properties, explained by the existence of additional chaperones in CE, such as Tig, HtpG and ClpB.

evolutionary biology↗

SARS-CoV-2 convergent evolution as a guide to explore adaptive advantage

Much can be learned from 1.2 million sequences of SARS-CoV-2 generated during the last 15 months. Out of the overwhelming number of mutations sampled so far, only few rose to prominence in the viral population. Many of these emerged recently and independently in multiple lineages. Such a textbook example of convergent evolution at the molecular level is not only curiosity but a guide to uncover the basis for adaptive advantage behind these events. Focusing on the extent of the convergent evolution in the spike (S) protein, our report confirms that the most concerning SARS-CoV-2 lineages carry the heaviest burden of convergent S-protein mutations, suggesting their fundamental adaptive advantage. The great majority (21/25) of S-protein sites under convergent evolution tightly cluster in three functional domains; N-terminal domain, receptor-binding domain, and Furin cleavage site. We further show that among the S-protein receptor-binding motif mutations, ACE2 affinity-improving substitutions are favored. While the probed mutation space in the S protein covered all amino-acids reachable by single nucleotide changes, substitutions requiring two nucleotide changes or epistatic mutations of multiple-residues have only recently started to emerge. Unfortunately, despite their convergent emergence and physical association, most of these adaptive mutations and their combinations remain understudied. We aim to promote research of current variants which are currently understudied but may become important in the future.

evolutionary biology↗

An emerging SARS-CoV-2 mutant evading cellular immunity and increasing viral infectivity

During the current SARS-CoV-2 pandemic that is devastating the modern societies worldwide, many variants that naturally acquire multiple mutations have emerged. Emerging mutations can affect viral properties such as infectivity and immune resistance. Although the sensitivity of naturally occurring SARS-CoV-2 variants to humoral immunity has recently been investigated, that to human leukocyte antigen (HLA)-restricted cellular immunity remains unaddressed. Here we demonstrate that two recently emerging mutants in the receptor binding domain of the SARS-CoV-2 spike protein, L452R (in B.1.427/429) and Y453F (in B.1.298), can escape from the HLA-24-restricted cellular immunity. These mutations reinforce the affinity to viral receptor ACE2, and notably, the L452R mutation increases protein stability, viral infectivity, and potentially promotes viral replication. Our data suggest that the HLA-restricted cellular immunity potentially affects the evolution of viral phenotypes, and the escape from cellular immunity can be a further threat of the SARS-CoV-2 pandemic. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=198 SRC="FIGDIR/small/438288v1_ufig1.gif" ALT="Figure 1"> View larger version (45K): org.highwire.dtl.DTLVardef@153428forg.highwire.dtl.DTLVardef@136ca5aorg.highwire.dtl.DTLVardef@1ee490org.highwire.dtl.DTLVardef@2fe478_HPS_FORMAT_FIGEXP M_FIG C_FIG

microbiology↗

SARS-CoV-2 RBD in vitro evolution follows contagious mutation spread, yet generates an able infection inhibitor

SARS-CoV-2 is continually evolving, with more contagious mutations spreading rapidly. Using in vitro evolution to affinity maturate the receptor-binding domain (RBD) of the spike protein towards ACE2 resulted in the more contagious mutations, S477N, E484K, and N501Y, to be among the first selected, explaining the convergent evolution of the "European" (20E-EU1), "British" (501.V1),"South African" (501.V2), and Brazilian" variants (501.V3). Plotting the binding affinity to ACE2 of all RBD mutations against their incidence in the population shows a strong correlation between the two. Further in vitro evolution enhancing binding by 600-fold provides guidelines towards potentially new evolving mutations with even higher infectivity. For example, Q498R epistatic to N501Y. Nevertheless, the high-affinity RBD is also an efficient drug, inhibiting SARS-CoV-2 infection. The 2.9[A] Cryo-EM structure of the high-affinity complex, including all rapidly spreading mutations, provides a structural basis for future drug and vaccine development and for in silico evaluation of known antibodies.

biochemistry↗

An enhanced yeast display platform demonstrates the binding plasticity under various selection pressures

Yeast surface display is popular in vitro evolution method. Here, we enhanced the method by multiple rounds of DNA and protein engineering, resulting in increased protein stabilities, surface expression, and enhanced fluorescence. The pCTcon2 yeast display vector was rebuild, introducing surface exposure tailored reporters - eUnaG2 and DnbALFA, creating a new platform of C and N terminal fusion vectors. In addition to gains in simplicity, speed, and cost, new applications were included to monitor protein surface exposure and protein retention in the secretion pathway. The enhanced methodologies were applied to investigate de-novo evolution of protein-protein interaction sites. Selecting binding from a mix of 6 protein-libraries towards two targets using high stringency selection led to the isolations of single high-affinity binders to each of the targets, without the need for high complexity libraries. Conversely, low-stringency selection resulted in the creation of many solutions for weak binding, demonstrating the plasticity of weak de-novo interactions.

biochemistry↗

Line-FRAP, a versatile method based on fluorescence recovery after photobleaching to measure diffusion rates in vitro and in vivo

A cell is a densely packed conglomerate of macromolecules, where diffusion is essential for their function. The crowded conditions may affect diffusion both through hard (occluded space) and soft (weak, non-specific) interactions. Multiple-methods have been developed to measure diffusion rates at physiological protein concentrations within cells, however, each of them has its limitations. Here, we introduce Line-FRAP, a method based on measuring recovery of photobleaching under a confocal microscope that allows diffusion rate measurements for fast diffusing molecules to be measured in versatile environments using standard equipment. Implementation of Line mode to the classical FRAP technique greatly improves the time resolution in data acquisition, from 20-50 Hz in the classical mode to 800 Hz in the line mode. We also introduce an updated method for data analysis to obtain diffusion coefficients in various environments, with the number of pixels bleached at the first frame after bleaching being a critical parameter. We evaluated the method using different proteins either chemically labelled or by fusion to YFP. The calculated diffusion rates were comparable to literature data as measured in vitro, in HeLa cells and in E.coli. Diffusion coefficients in HeLa was ~2.5-fold slower and in E. coli 15-fold slower than measured in buffer. Moreover, we show that increasing the osmotic pressure on E.coli further decreases diffusion, till a point where proteins stop to move. The method presented here is easy to apply on a standard confocal microscope, fits a large range of molecules with different sizes and provides robust results in any conceivable environment and protein concentration for fast diffusing molecules.

biochemistry↗

Constitutively active RAS in S. pombe causes persistent Cdc42 signalling but only transient MAPK activation

The small GTPase RAS is a signalling hub for many pathways and oncogenic human RAS mutations are assumed to over-activate all of its downstream pathways. We tested this assumption in fission yeast, where, RAS-mediated pheromone signalling (PS) activates the MAPKSpk1 and Cdc42 pathways. Unexpectedly, we found that constitutively active Ras1.G17V induced immediate but only transient MAPKSpk1 activation, whilst Cdc42 activation persisted. Immediate but transient MAPKSpk1 activation was also seen in the deletion mutant of Cdc42-GEFScd1, a Cdc42 activator. We built a mathematical model using PS negative-feedback circuits and competition between the two Ras1 effectors, MAPKKKByr2 and Cdc42-GEFScd1. The model robustly predicted the MAPKSpk1 activation dynamics of an additional 21 PS mutants. Supporting the model, we showed that a recombinant Cdc42-GEFScd1 fragment competes with MAPKKKByr2 for Ras1 binding. Our study has established a concept that the constitutively active RAS propagates differently to downstream pathways where the system prevents MAPK overactivation. HighlightsO_LIConstitutively active Ras1.GV prolongs Cdc42 activation in S. pombe pheromone signalling C_LIO_LIRas1.GV results in an immediate but only transient MAPKSpk1 activation C_LIO_LIThe RAS effector pathways MAPKSpk1 and Cdc42 compete with each other for active Ras1 C_LIO_LIPredictive modelling explains MAPKSpk1 activation dynamics in 24 signaling-mutants C_LI eTOC BlurbS. pombe Ras1 activates the MAPKSpk1 and Cdc42 pathways. Kelsall et al. report that the constitutively active Ras1.G17V mutation, which causes morphological anomalies, induces prolonged Cdc42 activation but only a transient MAPKSpk1 activation followed by attenuation. Mathematical modelling and biochemical data suggest a competition between the MAPKSpk1 and Cdc42 pathways for active Ras1.

molecular biology↗