bioRxiv Science⌕ Search

bioRxiv · 10.1101/2019.12.18.880534

Computer-aided Binding Mode Prediction and Affinity Maturation of LRR Protein Binder without Structural Determination

Abstract

Precise binding mode identification and subsequent affinity improvement without structure determination remain a challenge in the development of therapeutic proteins. However, relevant experimental techniques are generally quite costly, and purely computational methods have been unreliable. Here, we show that integrated computational and experimental epitope localization followed by full-atom energy minimization can yield an accurate complex model structure which ultimately enables effective affinity improvement and redesign of binding specificity. As proof-of-concept, we used a leucine-rich repeat (LRR) protein binder, called a repebody (Rb), that specifically recognizes human IgG1 (hIgG1). We performed computationally-guided identification of the Rb:hIgG1 binding mode and leveraged the resulting model to reengineer the Rb so as to significantly increase its binding affinity for hIgG1 as well as redesign its specificity toward multiple IgGs from other species. Experimental structure determination verified that our Rb:hIgG1 model closely matched the co-crystal structure. Using a benchmark of other LRR protein complexes, we further demonstrated that the present approach may be broadly applicable to proteins undergoing relatively small conformational changes upon target binding. Author SummaryIt is quite challenging for computational methods to determine how proteins interact and to design mutations to alter their binding affinity and specificity. Despite recent advances in computational methods, however, in silico evaluation of binding energies has proven to be extremely difficult. We show that, in the case of protein-protein interactions where only small structural changes occur upon target binding, an integrated computational and experimental approach can identify a binding mode and drive reengineering efforts to improve binding affinity or specificity. Using as a model system a leucine-rich repeat (LRR) protein binder that recognizes human IgG1, our approach yielded a model of the protein complex that was very similar to the subsequently experimentally determined co-crystal structure, and enabled design of variants with significantly improved IgG1 binding affinity and with the ability to recognize IgG1 from other species.

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Choi, Y., Jeong, S., Choi, J.-M., Ndong, C., Bailey-Kellogg, C., Griswold, K. E., Kim, H.-S.. 2019-12-19. Computer-aided Binding Mode Prediction and Affinity Maturation of LRR Protein Binder without Structural Determination. https://doi.org/10.1101/2019.12.18.880534

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

KEEP EXPLORING

Related preprints

Accelerating discovery and integration from RNA to Protein with R2T2P

Integrating transcriptomics and proteomics data remains an unmet challenge in the post-genomics era, discouraging researchers from pursuing integrative approaches to molecular biology research. Leveraging the power of translation profiling, we present RNA to Translation to Protein (R2T2P), a computational platform integrating genome-guided transcriptome assembly with identification of translation and proteins, including a tailored differential analysis framework and support for multiple reference transcriptomes. We applied R2T2P to investigate a cellular model of facioscapulohumeral muscular dystrophy (FSHD), where ectopic expression of the DUX4 retrogene in skeletal muscle triggers significant alterations in transcription and RNA metabolism. We uncovered hundreds of uncharacterized, highly overexpressed RNAs, including antisense and alternative transcripts, and quantified their contribution to translatome and proteome. Re-analysis of expression datasets from patient-derived myotubes and muscle biopsies validated this alternative transcriptome in FSHD patients, adding a reservoir of bona-fide novel molecular actors in a rare disease. Available at https://github.com/nfdata-omics/R2T2P/, R2T2P is a flexible and powerful workflow in modern integrative biology.

bioinformatics↗

MorphoANOVA: Dissecting Histology-Gene Expression Relationships in Spatial Transcriptomics

Spatial transcriptomics (ST) measures the expression of hundreds to thousands of genes within tissue architecture, often accompanied by histology images. However, it remains challenging to systematically characterize which genes exhibit associations with tissue morphology, whether these associations vary spatially, and which genes show additional spatial expression patterns beyond those captured by morphology. Here we introduce MorphoANOVA, a gene-wise statistical framework for characterizing morphology--expression relationships across genes measured by ST. Using nested spatially varying coefficient models and sequential ANOVA, MorphoANOVA assesses slide-wide associations with an H\&E-derived morphology feature, location-specific changes in these associations, and additional spatial variation after accounting for the selected feature. The resulting statistics enable gene prioritization and pathway enrichment analysis, while spatial component maps support the interpretation of individual genes. Simulations demonstrate MorphoANOVA's ability to distinguish the modeled components and recover their spatial patterns. Applications to human cortex and breast cancer identify biological programs associated with different morphology--expression patterns and reveal distinct relationships with cell composition. Across three HER2-positive breast cancer patients, invasive-cancer marker genes consistently exhibit stronger evidence of location-specific morphology associations. MorphoANOVA thus provides a framework for systematically interpreting spatial gene-expression patterns in relation to tissue morphology.

bioinformatics↗

Evaluation effects can rival reported concordance gains in cross-cancer survival prediction

Studies of cross-cancer learning for survival prediction from tumour omics have reported concordance gains of 0.020 and 0.045, but how such gains compare with evaluation effects remains unclear. We examined these effects across 13 TCGA cancers (5,761 patients, 1,526 disease-specific deaths), using five repeats of five-fold cross-validation and paired bootstrap intervals. When model selection did not use test data, our borrowing model gained 0.009 (95% interval 0.001 to 0.016) over its target-fitted reference when cancers received equal weight (post hoc). Random-effects pooling gave a gain of 0.002 (-0.002 to 0.006), with most weight assigned to cancers where the model made little use of the pretrained score. Choosing the fusion weight on test splits raised the apparent equal-weight gain to 0.017. We reimplemented a published method, VAECox, which showed no pretraining gain over random initialisation at the last or validation-selected training step. Choosing each network's best test step, as the published code does, raised concordance by 0.03 to 0.05 across the 13-cancer and ten-cancer overall-survival settings, but barely changed the difference between networks. In a constructed post hoc experiment, choosing the best test step only for the pretrained network changed the equal-weight mean difference from -0.004 to +0.045 (+0.035 to +0.054). Across seven multi-omics comparisons, estimates from single five-fold runs differed from their cancer's five-run mean by at least 0.02 in 11% to 42% of runs. Concordance was about 0.02 lower at held-out tissue source sites. Interpreting a reported gain therefore requires each model's selection rule, variation across repeated partitions, the weighting of cancers and the evaluation population.

bioinformatics↗