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Search indexed bioRxiv preprints in genomics, neuroscience, cell biology and bioinformatics. Read source abstracts and check manuscript versions; preprints are not peer reviewed.

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Metabolomics-informed coarse-grained model enables prediction of cell-free protein expression dynamics

Cell-free expression systems have gained considerable attention for their potential in biomanufac-turing, biosensing, and circuit prototyping. All these endeavors make use of the innate metabolic activity of cell lysates. However, our knowledge of the underlying nature of cell-free metabolism remains lacking. In this work, we use non-targeted mass spectrometry to generate time-course measurements of small molecules in E. coli cell lysates (metabolomics) during cell-free protein synthesis (CFPS) to show that the majority of E. colis metabolism is active in cell lysate. Fur-thermore, these data indicate that protein synthesis is a relatively small metabolic burden on cell lysates compared to the background metabolism, and that the build-up of multiple metabolic waste products is fundamentally responsible for stopping cell-free protein expression as opposed to depletion of fuel sources. We use these insights coupled with high-throughput CFPS experiments to develop a foundational coarse-grained mechanistic model of CFPS which we show can be easily recalibrated using Bayesian parameter inference techniques to provide accurate models across hundreds of novel experimental conditions. This work provides new experimental insights into the effects of cell-free metabolism on CFPS and establishes a novel framework for leveraging existing CFPS models in new experimental contexts, opening the avenue to future cell-free applications aimed at building complex systems, from multilayered biological circuits to synthetic biological cells.

synthetic biology↗

Magnetosome organelles are organized through interactions between McaA and McaB that alter the dynamics of the bacterial actin-like protein MamK

Magnetotactic bacteria (MTB) are a group of Gram-negative species that produce a lipid-bounded organelle, the magnetosome, in which a magnetic crystal is biomineralized. MTB use magnetosomes to align with the geomagnetic field for improved navigation of their environment. To optimize this alignment, these species organize their magnetosomes in a linear fashion using a handful of factors including the bacterial actin-like protein MamK. Despite these shared features, there is a broad diversity of species-specific linear magnetosome chain arrangements within MTB, but the molecular mechanisms behind these phenotypic variations are unclear. Recently, genetic analyses showed that two proteins McaA and McaB interface with the chain organization machinery of Magnetospirillum magneticum AMB-to arrange magnetite crystals in a series of subchains rather than the single cohesive chains found in closely related MTB. Here, we use in vivo co-immunoprecipitation in AMB-1 to demonstrate protein-protein interactions between McaA, McaB, and MamK. Experiments with McaA truncation mutants and conditional control of McaB localization determined that McaA-McaB interactions are dependent on amino acids 530-665 of McaA and McaB localization to the magnetosome chain. We further show that disrupting the McaA-McaB interaction alters the spatial dynamics of MamK in vivo We present a model in which protein-protein interactions between McaA, McaB, and MamK drive changes in MamK behavior to establish AMB-1s magnetosome chain organization. IMPORTANCEMagnetosomes model for understanding the cell biology of bacterial organelles and the mechanisms of bacterial cell organization. MamK, one of the best-studied bacterial actins, is a notable player in magnetosome chain assembly. This work explores how MamK dynamics are altered by two potential bacterial actin binding proteins, McaA and McaB. This system illustrates how changes in bacterial cytoskeleton regulation result in different organization of subcellular compartments. The conclusions from this research also have implications for understanding the broader evolutionary strategies for regulation of actin-like proteins and compartment organization diversification in bacteria.

microbiology↗

Spatial moment description of birth-death-movementprocesses incorporating the effects of crowding andobstacles

Birth-death-movement processes, modulated by interactions between individuals, are fundamental to many cell biology processes. A key feature of the movement of cells within in vivo environments are the interactions between motile cells and stationary obstacles. Here we propose a multi-species model of individual-level motility, proliferation and death. This model is a spatial birth-death-movement stochastic process, a class of individual-based model (IBM) that is amenable to mathematical analysis. We present the IBM in a general multi-species framework, and then focus on the case of a population of motile, proliferative agents in an environment populated by stationary, non-proliferative obstacles. To analyse the IBM, we derive a system of spatial moment equations governing the evolution of the density of agents and the density of pairs of agents. This approach avoids making the usual mean-field assumption so that our models can be used to study the formation of spatial structure, such as clustering and aggregation, and to understand how spatial structure influences population-level outcomes. Overall the spatial moment model provides a reasonably accurate prediction of the system dynamics, including important effects such as how varying the properties of the obstacles leads to different spatial patterns in the population of agents.

biophysics↗

The Markov link method: a nonparametric approach to combine observations from multiple experiments

This paper studies measurement linkage. An example from cell biology helps explain the problem: imagine for a given cell we can either sequence the cells RNA or we can examine its morphology, but not both. Given a cells morphology, what do we expect to see in its RNA? Given a cells RNA, what do we expect in its morphology? More broadly, given a measurement of one type, can we predict measurements of the other type? This measurement linkage problem arises in many scientific and technological fields. To solve this problem, we develop a nonparametric approach we dub the \"Markov link method\" (MLM). The MLM makes a conditional independence assumption that holds in many multi-measurement contexts and provides a way to estimate the link, the conditional probability of one type of measurement given the other. We derive conditions under which the MLM estimator is consistent and we use simulated data to show that it provides accurate measures of uncertainty. We evaluate the MLM on real data generated by a pair of single-cell RNA sequencing techniques. The MLM characterizes the link between them and helps connect the two notions of cell type derived from each technique. Further, the MLM reveals that some aspects of the link cannot be determined from the available data, and suggests new experiments that would allow for better estimates.\n\nSignificance StatementNovel experimental techniques are developing quickly, and each technique gives new perspectives. Ideally we would build theories that account for many perspectives at once. This is not easy. One challenge is that many experiments use measurement techniques that alter or destroy the subject, making it impossible to measure the same subject with both techniques and difficult to combine data from different experiments. In this paper we develop the Markov Link Method, a new tool that overcomes this challenge.

bioinformatics↗

Cell autonomous inflammation in VEXAS is mediated by cGAS-STING

VEXAS (vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic) is a severe adult-onset inflammatory disease caused by somatic mutations that reduce cytoplasmic activity of UBA1, the primary initiating enzyme for ubiquitylation. How this hypomorphic state drives cell-intrinsic immune activation in mature myeloid cells is unknown. Using unbiased multi-omic, biochemical, and cell biological analyses of model systems and patient-derived cells, we show that loss of cytoplasmic UBA1 activity convergently disrupts endoplasmic reticulum- associated degradation (ERAD) and mitochondrial homeostasis. ERAD failure arises from preferential under-charging of ERAD E2 enzymes, explaining hallmark VEXAS features, including ER-derived vacuoles and unfolded protein response activation, and promotes accumulation of the ERAD substrate STING. Simultaneously, mitochondrial dysfunction drives cytosolic leakage of mitochondrial DNA, inducing cGAS-dependent STING signaling and inflammatory cytokine production. STING inhibition or reversal of mitochondrial DNA leakage resolves multi-cytokine inflammation in VEXAS models and patient myeloid cells, establishing the cGAS-STING pathway as a therapeutically actionable vulnerability.

genetics↗

Limitations of EBV transformed human Raji B cells as a model for measuring canonical NF-κB activation

Autoimmune diseases, such as systemic lupus erythematosus (SLE), are underscored by dysregulated B cell function including the production of autoantibodies, skewed population ratios, and aberrant signaling. Given that the family of nuclear factor kappa B (NF-{kappa}B) transcription factors govern responses to stimuli, survival, differentiation, and so forth understanding the intricate regulatory network of NF-{kappa}B in B cell biology is paramount for unraveling treatments for B cell-linked autoimmune diseases. Here, we focus on a negative regulator of NF-{kappa}B signaling, A20 (TNFAIP3), that deactivates NF-{kappa}B transcription factor translocation through the ubiquitination and deubiquitination of target proteins. Haploinsufficiency in A20 results in an autoimmune phenotype and mutations to A20 have been associated with SLE, suggesting implications to B cell function. To investigate the role of A20 in NF-{kappa}B in human B cells, we generated a TNFAIP3 knockout (KO) Raji cell line. Cells were stimulated with either anti-IgM or Resiquimod (R848) to activate distinct NF-{kappa}B signaling pathways. Using qRT-PCR, western blotting, and flow cytometry, we assessed differences in gene expression, protein production, and NF-{kappa}B activation. We observed key limitations in using Epstein-Barr virus transformed B cell lines to model inducible NF-{kappa}B signaling.

immunology↗

Cell-TIMP: Cellular Trajectory Inference based on Morphological Parameter

Cellular morphology, shaped by various genetic and environmental influences, is pivotal to studying experimental cell biology, necessitating precise measurement and analysis techniques. Traditional approaches, which rely on geometric metrics derived from stained images, encounter obstacles stemming from both the imaging and analytical domains. Staining processes can disrupt the cells natural state and diminish accuracy due to photobleaching, while conventional analysis techniques, which categorize cells based on shape to discern pathophysiological conditions, often fail to capture the continuous and asynchronous nature of biological processes such as cell differentiation, immune responses, and cancer progression. In this work, we propose the use of quantitative phase imaging for morphological assessment due to its label-free nature. For analysis, we repurposed the genomic analysis toolbox to perform trajectory inference analysis purely based on morphology information. We applied the developed framework to study the progression of leukemia and breast cancer metastasis. Our approach revealed a clear pattern of morphological evolution tied to the diseases advancement, highlighting the efficacy of our method in identifying functionally significant shape changes where conventional techniques falter. This advancement offers a fresh perspective on analyzing cellular morphology and holds significant potential for the broader research community, enabling a deeper understanding of complex biological dynamics.

bioinformatics↗

GNOM-Dependent Endosomal Recycling Sets the Timing of Founder Cell Specification

1.Lateral root growth occurs from primed xylem pole pericycle cells that can be specified as founder cells, but how these cells acquire the pluripotency state to initiate a root organogenesis program is not fully understood. Here, we find that the EMS 204 mutant is unable to specify founder cells due to a point mutation affecting the C-terminal HDS3 domain of the GNOM protein. We used genetics and cell biology to study the trafficking machinery of xylem pole pericycle cells, cells in which GNOM is primarily associated with recycling endosomes. We found that the lack of the HDS3 domain negatively affects the stability of the GNOM protein within the cells of the xylem pole pericycle and, subsequently, the integrity of the trafficking machinery of these cells. We determined that GNOM is responsible for the recycling of AUX1 toward the plasma membrane at the xylem pole pericycle and impairment of this recycling results in premature accumulation of AUX1 in the vacuole. In this work, we describe a cell type-specific cellular mechanism and the role of a particular domain during lateral root development.

plant biology↗

Quantification of microenvironmental metabolites in murine cancer models reveals determinants of tumor nutrient availability

Cancer cell metabolism is heavily influenced by microenvironmental factors, including nutrient availability. Therefore, knowledge of microenvironmental nutrient levels is essential to understand tumor metabolism. To measure the extracellular nutrient levels available to tumors, we developed a quantitative metabolomics method to measure the absolute concentrations of >118 metabolites in plasma and tumor interstitial fluid, the extracellular fluid that perfuses tumors. Comparison of nutrient levels in tumor interstitial fluid and plasma revealed that the nutrients available to tumors differ from those present in circulation. Further, by comparing interstitial fluid nutrient levels between autochthonous and transplant models of murine pancreatic and lung adenocarcinoma, we found that tumor type, anatomical location and animal diet affect local nutrient availability. These data provide a comprehensive characterization of the nutrients present in the tumor microenvironment of widely used models of lung and pancreatic cancer and identify factors that influence metabolite levels in tumors.\n\nImpact StatementNutrient availability is an important tumor microenvironmental factor that impacts cancer cell biology; we developed methods to measure nutrients available to tumor cells and characterized factors that influence tumor nutrient availability.

cancer biology↗

The Plasmodium falciparum apicoplast cysteine desulfurase provides sulfur for both iron sulfur cluster assembly and tRNA modification

Iron sulfur clusters (FeS) are ancient and ubiquitous protein cofactors that play fundamental roles in many aspects of cell biology. These cofactors cannot be scavenged or trafficked within a cell and thus must be synthesized in any subcellular compartment where they are required. We examined the FeS synthesis proteins found in the relict plastid organelle, called the apicoplast, of the human malaria parasite Plasmodium falciparum. Using a chemical bypass method, we deleted four of the FeS pathway proteins involved in sulfur acquisition and cluster assembly and demonstrated that they are all essential for parasite survival. However, the effect that these deletions had on the apicoplast organelle differed. Deletion of the cysteine desulfurase SufS led to disruption of the apicoplast organelle and loss of the organellar genome, whereas the other deletions did not affect organelle maintenance. Ultimately, we discovered that the requirement of SufS for organelle maintenance is not driven by its role in FeS biosynthesis, but rather, by its function in generating sulfur for use by MnmA, a tRNA modifying enzyme that we localized to the apicoplast. By complementing the activity of the parasite MnmA and SufS with a bacterial MnmA and its cognate cysteine desulfurase, we showed that the parasite SufS provides sulfur for both FeS biosynthesis and tRNA modification in the apicoplast. The dual role of parasite SufS is likely to be found in other plastid-containing organisms and highlights the central role of this enzyme in plastid biology.

microbiology↗

Unsupervised weights selection for optimal transport based dataset integration

A formulation of the dataset integration problem describes the task of aligning two or more empirical distributions sampled from sources of the same kind, so that records of similar object end up close to one another. We propose a variant of the optimal transport (OT)- and Gromov-Wasserstein (GW)-based dataset integration algorithm introduced in SCOT [Demetci et al., 2020]. We formulate a constrained quadratic program to adjust sample weights before OT or GW so that weighted point density is close to be uniform over the point cloud, for a given kernel. We test this method with one synthetic and two real-life datasets from single-cell biology. Weights adjustment allows distributions with similar effective supports but different local densities to be reliably integrated, which is not always the case with the original method. This approach is entirely unsupervised, scales well to thousands of samples and does not depend on dimensionality of the ambient space, which makes it efficient for the analysis of single-cell datasets in biology. We provide an open-source implementation of this method in a Python package, woti.

bioinformatics↗

Intracellular pH differentially regulates transcription of metabolic and signaling pathways in normal epithelial cells

Intracellular pH (pHi) dynamics regulate normal cell function, and dysregulated pHi dynamics is an emerging hallmark of cancer (constitutively increased pHi) and neurodegeneration (constitutively decreased pHi). However, the molecular mechanisms by which pHi dynamics regulate cell biology are poorly understood. Here, we discovered that altering pHi in normal human breast epithelial cells triggers global transcriptional changes. We identified 176 genes differentially regulated by pHi, with pHi-dependent genes clustering in signaling and glycolytic pathways. Using various normal epithelial cell models, we showed pH-dependent Notch1 expression, with increased protein abundance at high pHi. This resulted in pH-dependent downstream signaling, with increased Notch1 signaling at high pHi. We also found that high pHi increased the expression of glycolytic enzymes and regulators of pyruvate fate, including lactate dehydrogenase and pyruvate dehydrogenase kinase. These transcriptional changes were sufficient to alter lactate production, with high pHi shifting these normal epithelial cells toward a glycolytic metabolism and increasing lactate production. Thus, pHi dynamics transcriptionally regulate signaling and metabolic pathways in normal epithelial cells. Our data reveal new molecular regulators of pHi-dependent biology and a role for increased pHi in driving the acquisition of cancer-associated signaling and metabolic changes in normal human epithelial cells.

biochemistry↗

Biomimetic, smart and multivalent ligands for G-quadruplex isolation and bioorthogonal imaging

G-quadruplexes (G4s) continue to gather wide attention in the field of chemical biology as their prevalence in the human genome and transcriptome strongly suggests that they may play key regulatory roles in cell biology. G4-specific, cell-permeable small molecules (G4-ligands) innovately permit the interrogation of cellular circuitries in order to assess to what extent G4s influence cell fate and functions. Here, we report on multivalent, biomimetic G4-ligands referred to as TASQs that enable both the isolation and visualization of G4s in human cells. Two biotinylated TASQs, BioTASQ and BioCyTASQ, are indeed efficient molecular tools to fish out G4s of mixtures of nucleic acids through simple affinity capture protocols and to image G4s in cells via a biotin/avidin pretargeted imaging system first applied here to G4s, found to be a reliable alternative to in situ click chemistry. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=109 SRC="FIGDIR/small/422878v1_ufig1.gif" ALT="Figure 1"> View larger version (42K): org.highwire.dtl.DTLVardef@2db02dorg.highwire.dtl.DTLVardef@1897e59org.highwire.dtl.DTLVardef@1c63716org.highwire.dtl.DTLVardef@4a8a5d_HPS_FORMAT_FIGEXP M_FIG C_FIG

biophysics↗

Tissue-resident, extravascular CD64-Ly6C- population forms a critical barrier for inflammation in the synovium

Monocytes are one of the most abundant immune cells infiltrating the inflamed organs. However, the majority of studies on monocytes focus on circulating cells, rather than those in the tissue. Here, we identify and characterize an intravascular (i.v.) and extravascular (e.v.) synovial population (Syn Ly6C- cells) which lack cell surface markers of classical monocytes (Ly6C and CD62) or tissue macrophages (CD64 and Tim4), are transcriptionally distinct and conserved in RA patients. e.v. Syn Ly6C- cells are independent of NR4A1 and CCR2, long-lived and embryonically derived while the i.v. Syn Ly6C- cells are dependent on NR4A1, short lived and derived from circulating NCM. e.v. Syn Ly6C- cells undergo increased proliferation and reverse diapedesis dependent on LFA1 in response to arthrogenic stimuli and are required for the development of RA-like disease. These findings uncover a new facet of mononuclear cell biology and are imperative to understanding tissue-resident myeloid cell function in RA.

immunology↗

Single-cell RNA transcriptome analysis reveals CXCL16/CXCR6 as maintenance factors for CNS tissue resident T cells that drive synapse elimination during viral recovery

BackgroundEmerging RNA viruses that target the central nervous system (CNS) lead to cognitive sequelae in survivors. Studies in humans and mice infected with West Nile virus (WNV), a re-emerging RNA virus associated with learning and memory deficits, revealed microglial-mediated synapse elimination within the hippocampus. Moreover, CNS resident memory T (TRM) cells activate microglia, limiting synapse recovery and inducing spatial learning defects in WNV-recovered mice. The signals involved in T cell-microglia interactions are unknown. MethodsHere, we examined the murine WNV-recovered forebrain using single-cell RNA sequencing to identify putative ligand-receptor pairs involved in intercellular communication between T cells and microglia. Clustering and differential gene analyses were followed by protein validation, genetic and antibody-based approaches utilizing an established murine model of WNV recovery in which microglia and complement promote ongoing hippocampal synaptic loss. ResultsProfiling of host transcriptome at 25 days post-infection revealed a shift in forebrain homeostatic microglia to activated subpopulations with transcriptional signatures that have previously been observed in studies of neurodegenerative diseases. Importantly, CXCL16/CXCR6, a chemokine signaling pathway involved in TRM cell biology, was identified as critically regulating CXCR6 expressing CD8+ TRM cell numbers within the WNV-recovered forebrain. We demonstrate that CXCL16 is highly expressed by all myeloid cells, and its unique receptor, CXCR6, is highly expressed on all CD8+ T cells. Using genetic and pharmacological approaches, we demonstrate that CXCL16/CXCR6 is required not only for the maintenance of WNV-specific, CD8 TRM cells in the post-infectious CNS, but also contributes to their expression of TRM cell markers. Moreover, CXCR6+CD8+ T cells are required for glial activation and ongoing synapse elimination. ConclusionsWe provide a comprehensive assessment of the role of CXCL16/CXCR6 as an interaction link between microglia and CD8+ T cells that maintains forebrain TRM cells, microglial and astrocyte activation, and ongoing synapse elimination in virally recovered animals. We also show that therapeutic targeting of CXCL16 during recovery may reduce CNS CD8+ TRM cells.

immunology↗

Deep Learning Enabled Label-free Cell Force Computation in Deformable Fibrous Environments

Cells move within tissues by pulling on and reshaping their fibrous surroundings. Measuring the associated forces has been a fundamental challenge in cell biology. Here, we develop deep-learning-enabled live-cell fiber-force microscopy (DLFM), which computes forces produced by living cells in real time as they interact with tissue-like fiber networks. DLFM combines basic phase microscopy with novel deep learning to simultaneously track cell movement and fiber deformation without disruptive fluorescent labels or chemical modifications. This allowed us to measure forces in real-time situations that were previously impossible to study, revealing an intricate mechanical landscape: cells generate ten-fold changes in force as they change shape during migration, create force-dipoles during cell-cell interactions, and dramatically alter their force patterns during stem cell differentiation. Through integrated experiments and mathematical modeling, we discovered that cells in fibrous environments form force-generating adhesions throughout their body, strikingly different from the edge-only adhesions seen in traditional petri dish experiments. Results clarify cytoskeletal pathways by which cells adapt force-generating machinery to navigate the fibrous architecture of tissues.

biophysics↗

Patch2MAP combines patch-clamp electrophysiology with super-resolution structural and protein imaging in identified single neurons without genetic modification

Recent developments in super-resolution microscopy have revolutionized the study of cell biology. However, dense tissues require exogenous protein expression for single cell morphological contrast. In the nervous system, many cell types and species of interest - particularly human - are not amenable to genetic modification and/or exhibit intricate anatomical specializations which make cellular delineation challenging. Here, we present a method for full morphological labeling of individual neurons from any species or cell type for subsequent cell-resolved protein analysis without genetic modification. Our method, which combines patch-clamp electrophysiology with epitope-preserving magnified analysis of proteome (eMAP), further allows for correlation of physiological properties with subcellular protein expression. We applied Patch2MAP to individual spiny synapses in human cortical pyramidal neurons and demonstrated that electrophysiological AMPA-to-NMDA receptor ratios correspond tightly to respective protein expression levels. Patch2MAP thus permits combined subcellular functional, anatomical, and proteomic analyses of any cell, opening new avenues for direct molecular investigation of the human brain in health and disease.

neuroscience↗

CASPULE: A computational tool to study sticker spacer polymer condensates

Phase separated condensates are recognized as a ubiquitous mechanism of spatial organization in cell biology. Biophysical modeling of condensates provides critical insights into the dynamics and functions of these subcellular structures that are difficult to extract via experiments. Here we present an efficient computational pipeline, CASPULE (Condensate Analysis of Sticker Spacer Polymers Using the LAMMPS Engine), to simulate and analyze the biological condensates made of sticker-spacer polymers. CASPULE implements a unique force field that combines traditional Langevin dynamics with a "detailed-balance proof" protocol for single-valent bond formation between stickers. This framework allows us to study the nontrivial biophysics that emerge from singlevalent sticker interactions, coupled with the effect of separating the energetic contributions of stickers and spacers. We provide detailed documentation on how to setup the simulation environment, perform simulations and analyze the results. Through case studies, we highlight the utility and efficacy of our pipeline. Importantly, we provide statistical parameters to characterize the cluster size distribution often observed in biological systems. We envision this tool to be broadly useful in decoding the interplay of kinetics and thermodynamics underlying the formation and function of biological condensates. Code and documentation: https://caspule.github.io/caspule/ Author SummaryLiving cells contain droplet-like compartments called biomolecular condensates that organize important molecules and reactions without a surrounding membrane. Understanding how these condensates form and behave helps us learn more about healthy cellular function and diseases. Condensate forming biopolymers (proteins and nucleic acids) often contain a sticker spacer architecture that gives rise to interesting emergent properties when they assemble into a condensate. Here we report an easy-to-use computational pipeline, called CASPULE, that allows us to simulate and analyze the condensation of polymer chains. Unlike previous tools, CASPULE models both the physical motion of these molecules and specific bonding interactions between sticker segments. This user-friendly tool will enable researchers to explore the governing principles underlying the formation and function of biomolecular condensates.

biophysics↗