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Biology subjects

Warden, A.

Publications and source records attributed to Warden, A..

4 recordsLinked to original sources

EMMAi: fast enzyme-allocation constraints in GEMs for improved biomass prediction across carbon sources

Genome-scale metabolic models (GEMs) predict emergent phenotypes by modeling the metabolic networks encoded in genomes. While GEMs have significantly advanced systems biology, metabolic engineering, biomedicine, and environmental science, they require extensive time and resources for manual curation, which can limit their utility in rapidly evolving research landscapes. Recent findings suggest that manually curated reactions can sometimes reduce prediction accuracy, indicating that integrating additional biologically grounded constraints may better capture emergent phenotypes. One promising approach is the incorporation of enzyme allocation constraints, which has been shown to enhance the predictive accuracy in metabolic models. Enzymatically constrained GEMs (ecGEMs) rely on enzyme turnover rates (kcat) and protein molecular weights (MWs) to account for intracellular resource limitations by introducing an enzyme pool variable and assigning costs to reactions, thereby simulating enzymatic resource constraints. Tools such as GECKO, AutoPACMEN, and ECMpy provide computational pipelines for ecGEM generation. However, these pipelines are often limited by their reliance on experimentally measured kcat values or deep learning-predicted values, such as those generated by DLKcat, which face challenges in predicting kinetics for enzymes dissimilar to their training data. Additionally, these methods frequently require extensive manual curation of kcat values based on empirical data, a time-intensive process that hampers scalability and applicability to non-model organisms. To address these limitations, we introduce EMMAi (Enzyme-constrained Metabolic Models with AI), a pipeline that fully automates the incorporation of enzyme constraints into GEMs. Unlike existing pipelines, EMMAi exclusively utilizes kcat values predicted by UniKP, an AI framework with improved accuracy over DLKcat, particularly for enzymes not present in training datasets. UniKP achieves a 13% improvement in correlation for unseen enzymes, enabling EMMAi to deliver ecGEMs with enhanced prediction accuracy without manual curation requirements. We evaluated EMMAi by applying it to three GEMs: two manually curated models, iJO1366 (Escherichia coli str. K-12 substr. MG1655) and iMO1056 (Pseudomonas aeruginosa PAO1), and one draft GEM constructed and gap-filled using CarveMe. EMMAi-generated ecGEMs showed an average Pearson Correlation Coefficient (PCC) improvement of 0.27 for manually curated GEMs when compared to predicted and experimentally measured growth rates and Biolog readings. Notably, for the draft GEM of Pseudomonas aeruginosa PAO1, the PCC improved dramatically from -0.3 to 0.6. EMMAi demonstrates that automating the integration of enzyme allocation constraints using AI-predicted kinetic parameters significantly enhances the prediction accuracy of GEMs, even in the absence of manual curation. These results underscore EMMAis potential as a scalable, efficient, and accurate tool for advancing GEM-based research in systems biology, metabolic engineering, and beyond.

systems biology↗

Caveolar Compartmentalization is Required for Stable Rhythmicity of Sinus Nodal Cells and is Disrupted in Heart Failure

BackgroundHeart rhythm relies on complex interactions between electrogenic membrane proteins and intracellular Ca2+ signaling in sinoatrial node (SAN) myocytes; however, mechanisms underlying the functional organization of proteins involved in SAN pacemaking and its structural foundation remain elusive. Caveolae are nanoscale, plasma membrane pits that compartmentalize various ion channels and transporters, including those involved in SAN pacemaking, via binding with the caveolin-3 scaffolding protein, but the precise role of caveolae in cardiac pacemaker function is unknown. Our objective was to determine the role of caveolae in SAN pacemaking and dysfunction (SND). MethodsBiochemical co-purification, in vivo electrocardiogram monitoring, ex vivo optical mapping, in vitro confocal Ca2+ imaging, and immunofluorescent and electron microscopy analyses were performed in wild type, cardiac-specific caveolin-3 knockout, and 8-weeks post-myocardial infarction heart failure (HF) mice. SAN tissue samples from donor human hearts were used for biochemical studies. We utilized a novel 3-dimensional single SAN cell mathematical model to determine the functional outcomes of protein nanodomain-specific localization and redistribution in SAN pacemaking. ResultsIn both mouse and human SANs, caveolae compartmentalized HCN4, Cav1.2, Cav1.3, Cav3.1 and NCX1 proteins within discrete pacemaker signalosomes via direct association with caveolin-3. This compartmentalization positioned electrogenic sarcolemmal proteins near the subsarcolemmal sarcoplasmic reticulum (SR) membrane and ensured fast and robust activation of NCX1 by subsarcolemmal local SR Ca2+ release events (LCRs), which diffuse across [~]15-nm subsarcolemmal cleft. Disruption of caveolae led to the development of SND via suppression of pacemaker automaticity through a 50% decrease of the L-type Ca2+ current, a negative shift of the HCN current (If) activation curve, and a 40% reduction of Na+/Ca2+-exchanger function, along with [~]2.3-times widening of the sarcolemma-SR distance. These changes significantly decreased the SAN depolarizing force, both during diastolic depolarization and upstroke phase, leading to bradycardia, sinus pauses, recurrent development of SAN quiescence, and significant increase in heart rate lability. Computational modeling, supported by biochemical studies, identified NCX1 redistribution to extra-caveolar membrane as the primary mechanism of SAN pauses and quiescence due to the impaired ability of NCX1 to be effectively activated by LCRs and trigger action potentials. HF remodeling mirrored caveolae disruption leading to NCX1-LCR uncoupling and SND. ConclusionsSAN pacemaking is driven by complex protein interactions within a nanoscale caveolar pacemaker signalosome. Disruption of caveolae leads to SND, potentially demonstrating a new dimension of SAN remodeling and providing a newly recognized target for therapy.

physiology↗

Transcriptome analysis of alcohol dependence and stress interactions in the nucleus of the solitary tract

Stress exposure contributes to the development of drug and alcohol use disorders. In animal models, stress exacerbates escalations in alcohol consumption in alcohol-dependent animals. The nucleus of the solitary tract (NTS) is a critical brainstem region for integrating and relaying peripheral signals to regulate stress responses. To define the molecular adaptions within this brain region that may contribute to stress-induced alcohol drinking, we exposed animals to chronic intermittent bouts of ethanol vapor (CIE), forced swim stress (FSS), or both (CIE + FSS) and then transcriptionally profiled the NTS at three different timepoints after the last vapor exposure (0-hr, 72-hr, and 186-hr). We identified interferon (IFN) signaling as a critical gene network correlated with alcohol consumption levels. Using a likelihood ratio test, we identified genes that were differentially expressed across time and between groups. Clustering analysis of these genes to identify unique expression patterns identified a subset of genes that fail to normalize in the CIE + FSS group, but not the others. These genes were enriched for cell-to-cell interaction and cellular movement pointing to long-term structural and functional changes in this brain region caused by the unique interaction of alcohol dependence and stress. Specific genes of interest identified in this group include Aqp4, Il16, Reln, Grm4, Gabrd, and Gabra6. We also compared gene expression changes in the NTS to the PFC and found a significant overlap of genes between the two brain regions. Overlapping NTS/PFC genes in the CIE + FSS group were enriched for type I IFN signaling. Finally, we tested the hypothesis that activation of type I IFN signaling increases alcohol consumption based on the three lines of evidence identifying type I IFN signaling as critical for escalations in alcohol intake. Mice treated with recombinant IFN{beta} showed significantly elevated levels of alcohol intake in a two-bottle choice procedure compared to saline-treated controls. Overall, these results define the transcriptomic changes across time in the NTS that may be critical to the development of stress-induced increases in alcohol consumption and alcohol dependence.

molecular biology↗

Toll-like receptor 3 activation increases voluntary alcohol intake in C57BL/6J male mice

Many genes differentially expressed in brain tissue from human alcoholics and animals that have consumed large amounts of alcohol are components of the innate immune toll-like receptor (TLR) pathway. TLRs initiate inflammatory responses via two branches: (1) MyD88-dependent or (2) TRIF-dependent. All TLRs signal through MyD88 except TLR3. Prior work demonstrated a direct role for MyD88-dependent signaling in regulation of alcohol consumption. However, the role of TLR3 as a potential regulator of excessive alcohol drinking has not previously been investigated. To test the possibility TLR3 activation regulates alcohol consumption, we injected mice with the TLR3 agonist polyinosinic:polycytidylic acid (poly(I:C)) and tested alcohol consumption in an every-other-day two-bottle choice test. Poly(I:C) produced a persistent increase in alcohol intake that developed over several days. Repeated poly(I:C) and ethanol exposure altered innate immune transcript abundance; increased levels of TRIF-dependent pathway components correlated with increased alcohol consumption. Administration of poly(I:C) before exposure to alcohol did not alter alcohol intake, suggesting that poly(I:C) and ethanol must be present together to change drinking behavior. To determine which branch of TLR signaling mediates poly(I:C)-induced changes in drinking behavior, we tested either mice lacking MyD88 or mice administered a TLR3/dsRNA complex inhibitor. MyD88 null mutants showed poly(I:C)-induced increases in alcohol intake. In contrast, mice pretreated with a TLR3/dsRNA complex inhibitor reduced their alcohol intake, suggesting poly(I:C)-induced escalations in alcohol intake function are, at least partially, dependent on TLR3. Together, these results strongly suggest that TLR3-dependent signaling drives excessive alcohol drinking behavior.\n\nHighlightsO_LIActivation of TLR3 via poly(I:C) increased alcohol intake.\nC_LIO_LIPoly(I:C) and ethanol must be present together to change drinking behavior.\nC_LIO_LIIncreased alcohol intake due to poly(I:C) is independent of MYD88.\nC_LIO_LIIncreased alcohol intake due to poly(I:C) is dependent on TLR3.\nC_LI

neuroscience↗