Search bioRxiv⌕ Search

bioRxiv · 10.1101/523563

3D spatial organization and network-guided comparison of mutation profiles in Glioblastoma reveals similarities across patients

Abstract

Mutation profiles of Glioblastoma (GBM) tumors are very heterogeneous which is the main challenge in the interpretation of the effects of mutations in disease. Additionally, the impact of the mutations is not uniform across the proteins and protein-protein interactions. The pathway level representation of the mutations is very limited. In this work, we approach these challenges through a systems level perspective in which we analyze how the mutations in GBM tumors are distributed in protein structures/interfaces and how they are organized at the network level. Our results show that out of 14644 mutations, 4392 have structural information and ~13% of them form spatial patches. Despite a small portion of all mutations, 3D patches partially decrease the heterogeneity across the patients. Hub proteins adapt multiple patches of mutations usually with a very large one and connects mutations in multiple binding sites through the core of the protein. We reconstructed patient specific networks for 290 GBM tumors. Network-guided analysis of mutations completes the interaction components that mutated proteins potentially affect, and groups the patients according to the reconstructed networks. As a result, we found 4 tumor clusters that overcome the heterogeneity in mutation profiles, and reveal predominant pathways in each group. Additionally, the network-based similarity analysis shows that each group of patients carries a set of signature 3D mutation patches. We believe that this study provides another perspective to the analysis of mutation effects and a good training towards the network-guided precision medicine.\n\nAuthor SummaryGlioblastoma (GBM) is the most aggressive brain tumor type with a 15 months of survival on average. The mutation distribution of the GBM patients is very heterogeneous and standard treatments fail to consider the inter-tumor heterogeneity. In our study, we follow a systems level approach that integrates mutation profiles with protein-protein interaction networks. We hypothesized that although the mutations are heterogeneous, the mutations that are close in 3D of the same protein may affect the protein function similarly and this information can be used to get meaningful relation between disease state and mutations. Therefore, we spatially grouped these mutations as \"patches\" and reconstructed patient specific protein interaction networks. When we cluster these networks based on their pathway similarities, we found four patient groups in GBM. Then, the comparison of groups revealed overrepresentation of 3D patches. This finding can be used for patient specific therapy.

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Dincer, C., Kaya, T., Keskin, O., Gursoy, A., Tuncbag, N.. 2019-01-17. 3D spatial organization and network-guided comparison of mutation profiles in Glioblastoma reveals similarities across patients. https://doi.org/10.1101/523563

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

KEEP EXPLORING

Related preprints

A three-factor model can explain symmetry breaking and the n-1 rule during X-chromosome inactivation

X-chromosome inactivation (XCI) is a mammalian gene regulatory process that via chromosome-scale transcriptional silencing, leaves active a single X chromosome per diploid genome complement. The mechanisms that enable cells to select the appropriate number of X chromosomes to inactivate while leaving others active remain unclear. We demonstrate that all known chromosomal counting scenarios during XCI can be accounted for by a three-factor mathematical model that includes (1) Xist, the long noncoding RNA (lncRNA) responsible for gene silencing during XCI in eutherians, (2) an X-linked transcriptional activator of Xist, and (3) the autosomally-encoded SPEN, an Xist RNA-binding protein that is essential for gene silencing during XCI. In our model, symmetry between active X chromosomes is broken by stochastic differences in the number of Xist molecules that associate with the X chromosomes at the onset of XCI. Subsequently, integrated positive and negative feedback loops amplify then propagate superstoichiometric assemblies of SPEN complexed with Xist on the inactive chromosome(s), and select for levels of X-linked activator that enable only one X chromosome per diploid genome complement to remain active. Thus, asymmetric propagation of the SPEN-Xist ribonucleoprotein complex may play an essential role in symmetry breaking and chromosomal counting during XCI, independently of or in concert with cis-acting networks of DNA regulatory elements. Our results also have conceptual implications for gene regulatory circuits on autosomes.

systems biology↗

stem.MAP: Identification of cell-type-specific protein complexes in mammalian embryonic stem cells.

Protein complexes carry out critical functions during development. Mapping cell-type-specific protein complexes in early embryogenesis is essential for uncovering the molecular mechanisms of embryonic development. We unfortunately currently lack a catalog of protein complexes specific for embryogenesis including embryonic stem cells. Here we develop a proteomics-based machine learning workflow to predict protein complexes present in mouse embryonic stem cells (mESC). Our method integrates data from a cell-type agnostic protein complex resource with co-fractionation mass spectrometry (CF-MS) experiments on mESC. Our resource, stem.MAP, identifies 3,986 complexes encompassing ~133,000 unique interactions, and 8,616 proteins. stem.MAP captures variant complexes critical for stem cell function including the PRC2, BAF and NuRD complexes. stem.MAP also discriminates mutually exclusive interactions specific to embryonic stem cells (e.g. Eif4ebp2 - Eif4e). Finally we observe 1,388 high confidence stem.MAP interactions found only in mESC CF-MS data, many with support from AlphaFold modeling and a gastruloid coregulation network. We make stem.MAP protein complexes available through our web resource: stem.proteincomplexes.org. We anticipate stem.MAP will be beneficial to the study of early development and we expect our proteomics-based machine learning workflow to be applicable to the creation of any context-specific protein interaction network.

systems biology↗

Coarse-graining genome-scale metabolic models for dynamic, multi-scale simulations of Pseudomonas aeruginosa in gel environments

Microbial communities are shaped by coupled interactions between microenvironment conditions and the intracellular adaptations that emerge in response external metabolic cues. For pathogenic microbes such as Pseudomonas aeruginosa, these interactions can rapidly generate heterogeneous sub-populations that exhibit adaptations for sustaining host infection and resisting antibiotic treatment. Technological strides in -omics data collection, combined with robust computational tools like genome-scale metabolic models (GEM) for predicting cellular metabolism, have yielded promising multi-scale depictions of microbial population development in simulated spatial environments. These multi-scale model simulations help establish and evaluate mechanistic contexts for how infection-enhancing behaviors might emerge in the population or be influenced by variable perturbations in the biological system. However, the number and rigorous tuning of parameters influencing the connections between intracellular-extracellular events pose barriers when shaping simulations to different in vitro systems of interest. In this work, we present a genome-scale, metabolism-informed continuum model (GEM-CM), a computational framework for coupling a reaction-diffusion model to a surrogate GEM representation that generates metabolic rate predictions informed by flux balance analysis outputs. A key feature of GEM-CM is its application of random forest regression, or ensembles, to coarse-grain the interface connecting the GEM and reaction-diffusion models down to a small set of input metabolites methodically chosen through the random forests evaluation of feature importance. To demonstrate GEM-CMs utility, we evaluated simulation predictions against P. aeruginosa PA14 populations radially propagating in low weight percentage agar gels. In addition to biomass growth, we simulated PA14 populations producing the cytotoxic secondary metabolite pyocyanin (PCN). GEM-CM could capture PA14 growth dynamics in agar gels when ensembles were provided with three carbon source inputs describing the simulated growth media. Bacterial motility parameters and the random forest ensemble allowed GEM-CM simulations to accurately predict spatial biomass distributions for PA14 populations over time and probe their PCN production dynamics. Ensembles also demonstrated robust performance for single gene knockout conditions with GEM-CM simulation accurately capturing the partial or total biomass and PCN inhibition observed in transposon mutant screenings. When evaluating transposon mutant population development, the GEM-CM framework additionally suggested that metH may be a promising target to inhibit the spatial propagation of PA14. This works proof-of-concept applications illustrated GEM-CM utility as an early stage multi-scale modeling tool for interrogating in vitro metabolic behavior in microbial populations.

systems biology↗