Patterns (N Y). 2023 Mar 10;4(3):100705. doi: 10.1016/j.patter.2023.100705. eCollection 2023 Mar 10.

ABSTRACT

The dynamics of cellular mechanisms can be investigated through the analysis of networks. One of the simplest but most popular modeling strategies involves logic-based models. However, these models still face exponential growth in simulation complexity compared with a linear increase in nodes. We transfer this modeling approach to quantum computing and use the upcoming technique in the field to simulate the resulting networks. Leveraging logic modeling in quantum computing has many benefits, including complexity reduction and quantum algorithms for systems biology tasks. To showcase the applicability of our approach to systems biology tasks, we implemented a model of mammalian cortical development. Here, we applied a quantum algorithm to estimate the tendency of the model to reach particular stable conditions and further revert dynamics. Results from two actual quantum processing units and a noisy simulator are presented, and current technical challenges are discussed.

PMID:36960443 | PMC:PMC10028428 | DOI:10.1016/j.patter.2023.100705

Sci Rep. 2023 Mar 23;13(1):4734. doi: 10.1038/s41598-023-31962-5.

ABSTRACT

70-kDa Heat Shock Proteins (HSPA/HSP70) are chaperones playing a central role in the proteostasis control mechanisms. Their basal expression can be highly elevated as an adaptive response to environmental and pathophysiological stress conditions. HSPA2, one of poorly characterised chaperones of the HSPA/HSP70 family, has recently emerged as epithelial cells differentiation-related factor. It is also commonly expressed in cancer cells, where its functional significance remains unclear. Previously, we have found that proteotoxic stress provokes a decrease in HSPA2 levels in cancer cells. In the present study we found that proteasome inhibition-related loss of HSPA2 from cancer cells neither is related to a block in the gene transcription nor does it relate to increased autophagy-mediated disposals of the protein. Proteotoxic stress stimulated extracellular release of HSPA2 in extracellular vesicles (EVs). Interestingly, EVs containing HSPA2 are also released by non-stressed cancer and normal cells. In human urinary EVs levels of HSPA2 were correlated with the levels of TSG101, one of the main EVs markers. We conclude that HSPA2 may constitute basic components of EVs. Nevertheless, its specific role in EVs and cell-to-cell communication requires further investigation.

PMID:36959387 | DOI:10.1038/s41598-023-31962-5

Nat Nanotechnol. 2023 Mar 23. doi: 10.1038/s41565-023-01365-8. Online ahead of print.

NO ABSTRACT

PMID:36959302 | DOI:10.1038/s41565-023-01365-8

Nat Commun. 2023 Mar 23;14(1):1610. doi: 10.1038/s41467-023-37328-9.

ABSTRACT

As a key component of the standard of care for glioblastoma, radiotherapy induces several immune resistance mechanisms, such as upregulation of CD47 and PD-L1. Here, leveraging these radiotherapy-elicited processes, we generate a bridging-lipid nanoparticle (B-LNP) that engages tumor-associated myeloid cells (TAMCs) to glioblastoma cells via anti-CD47/PD-L1 dual ligation. We show that the engager B-LNPs block CD47 and PD-L1 and promote TAMC phagocytic activity. To enhance subsequent T cell recruitment and antitumor responses after tumor engulfment, the B-LNP was encapsulated with diABZI, a non-nucleotidyl agonist for stimulator of interferon genes. In vivo treatment with diABZI-loaded B-LNPs induced a transcriptomic and metabolic switch in TAMCs, turning these immunosuppressive cells into antitumor effectors, which induced T cell infiltration and activation in brain tumors. In preclinical murine models, B-LNP/diABZI administration synergized with radiotherapy to promote brain tumor regression and induce immunological memory against glioma. In summary, our study describes a nanotechnology-based approach that hijacks irradiation-triggered immune checkpoint molecules to boost potent and long-lasting antitumor immunity against glioblastoma.

PMID:36959214 | DOI:10.1038/s41467-023-37328-9

Proteomes. 2023 Mar 23;11(2):11. doi: 10.3390/proteomes11020011.

ABSTRACT

Although numerous studies support a dose-effect relationship between Endocrine disruptors (EDs) and the progression and malignancy of tumors, the impact of a chronic exposure to non-lethal concentrations of EDs in cancer remains unknown. More specifically, a number of studies have reported the impact of Aldrin on a variety of cancer types, including prostate cancer. In previous studies, we demonstrated the induction of the malignant phenotype in DU145 prostate cancer (PCa) cells after a chronic exposure to Aldrin (an ED). Proteins are pivotal in the regulation and control of a variety of cellular processes. However, the mechanisms responsible for the impact of ED on PCa and the role of proteins in this process are not yet well understood. Here, two complementary computational approaches have been employed to investigate the molecular processes underlying the acquisition of malignancy in prostate cancer. First, the metabolic reprogramming associated with the chronic exposure to Aldrin in DU145 cells was studied by integrating transcriptomics and metabolomics via constraint-based metabolic modeling. Second, gene set enrichment analysis was applied to determine (i) altered regulatory pathways and (ii) the correlation between changes in the transcriptomic profile of Aldrin-exposed cells and tumor progression in various types of cancer. Experimental validation confirmed predictions revealing a disruption in metabolic and regulatory pathways. This alteration results in the modification of protein levels crucial in regulating triacylglyceride/cholesterol, linked to the malignant phenotype observed in Aldrin-exposed cells.

PMID:37092452 | DOI:10.3390/proteomes11020011

J Appl Microbiol. 2023 Mar 23:lxad059. doi: 10.1093/jambio/lxad059. Online ahead of print.

ABSTRACT

Engineering of the bacterial genome plays a key role in systems biology and synthetic biology. Genetic engineering of the bacterial genome involves the design and synthesis of large DNA molecules. However, functional studies of the designed and synthesized large DNA molecules are lagging. Methods for the transformation of large DNA molecules of bacterial chromosome size into bacterial cells through a single operation have not yet been established. Two major methods can be used for transferring large DNA molecules of bacterial chromosome size into bacterial cells: transformation mediated by liposomes or by microinjection. In both methods, cell wall (peptidoglycan layer)-deficient cells (L-form, protoplast, or spheroplast) should be used as the bacterial host cells. We succeeded in transferring a heterologous bacterial genome into an enlarged bacterial protoplast using a micromanipulator. This method for transferring large DNA molecules into bacterial cells through a single operation will contribute to both fundamental and applied research in microbial genome science.

PMID:36958863 | DOI:10.1093/jambio/lxad059

Vascul Pharmacol. 2023 Mar 21:107167. doi: 10.1016/j.vph.2023.107167. Online ahead of print.

ABSTRACT

BACKGROUND: Calcification, a key feature of advanced human atherosclerosis, is positively associated with vascular disease burden and adverse events. We showed that macrocalcification can be a stabilizing factor for carotid plaque molecular biology, due to inverse association with immune processes. Mast cells (MCs) are important contributors to plaque instability, but their relationship with macrocalcification is unexplored. With a hypothesis that MC activation negatively associates with carotid plaque macrocalcification, we aimed to investigate the link between MCs and carotid plaque vulnerability, and study MC role in plaque calcification via smooth muscle cells (SMCs).

METHODS: Pre-operative computed tomography angiographies of patients (n = 40) undergoing surgery for carotid stenosis were used to characterize plaque morphology. Plaque microarrays (n = 40 and n = 126) were used for bioinformatic deconvolution of immune cell populations. Tissue microarrays (n = 103) were used to histologically validate the contribution of activated and resting MCs in plaques.

RESULTS: Activated MCs and their typical markers were negatively correlated with macrocalcification. The ratio of activated vs. resting MCs was increased in low-calcified plaques from symptomatic patients. There was no modulating effect of medication on MC ratios. In vitro experiments showed that SMC calcification attenuated MC activation, while both active and resting MCs stimulated SMC calcification and induced dedifferentiation towards a pro-inflammatory-, osteochondrocyte-like phenotype, without modulating their migro-proliferative function.

CONCLUSIONS: Integrative analyses from human plaques showed that MC activation is inversely associated with macrocalcification and positively with parameters of plaque vulnerability. Mechanistically, MCs induce SMC osteogenic reprograming, while matrix calcification in turn attenuates MC activation, offering new therapeutic avenues for exploration.

PMID:36958707 | DOI:10.1016/j.vph.2023.107167

J Invest Dermatol. 2023 Mar 21:S0022-202X(23)01838-9. doi: 10.1016/j.jid.2023.03.1653. Online ahead of print.

NO ABSTRACT

PMID:36958602 | DOI:10.1016/j.jid.2023.03.1653

J Biomed Inform. 2023 Mar 21:104345. doi: 10.1016/j.jbi.2023.104345. Online ahead of print.

ABSTRACT

Stroke is the second largest cause of mortality in the world. Genome-wide association studies (GWAS) have identified some genetic variants associated with stroke risk, but their putative functional causal genes are unknown. Hence, we aimed to identify putative functional causal gene biomarkers of stroke risk. We used a summary-based Mendelian randomisation (SMR) approach to identify the pleiotropic associations of genetically regulated traits (i.e., gene expression and DNA methylation) with stroke risk. Using SMR approach, we integrated cis-expression quantitative loci (cis-eQTLs) and cis-methylation quantitative loci (cis-mQTLs) data with GWAS summary statistics of stroke. We also utilised heterogeneity in dependent instruments (HEIDI) test to distinguish pleiotropy from linkage from the observed associations identified through SMR analysis. Our integrative SMR analyses and HEIDI test revealed 45 candidate biomarker genes (FDR < 0.05; PHEIDI>0.01) that were pleiotropically or potentially causally associated with stroke risk. Of those candidate biomarker genes, 10 genes (HTRA1, PMF1, FBN2, C9orf84, COL4A1, BAG4, NEK6, SH2B3, SH3PXD2A, ACAD10) were differentially expressed in genome-wide blood transcriptomics data from stroke and healthy individuals (FDR<0.05). Functional enrichment analysis of the identified candidate biomarker genes revealed gene ontologies and pathways involved in stroke, including "cell aging", "metal ion binding" and "oxidative damage". Based on the evidence of genetically regulated expression of genes through SMR and directly measured expression of genes in blood, our integrative analysis suggests ten genes as blood biomarkers of stroke risk. Furthermore, our study provides a better understanding of the influence of DNA methylation on the expression of genes linked to stroke risk.

PMID:36958462 | DOI:10.1016/j.jbi.2023.104345

Mol Metab. 2023 Mar 21:101711. doi: 10.1016/j.molmet.2023.101711. Online ahead of print.

ABSTRACT

Heart diseases are the leading cause of deaths worldwide. Metabolic interventions via ketogenic diets (KDs) have been used for decades to treat epilepsy, and more recently, also diabetes and obesity, as common comorbidities of heart diseases. However, recent reports linked KDs, based on long-chain triglycerides (LCTs), to cardiac fibrosis and a reduction of heart function in rodents. As intervention using medium-chain triglycerides (MCTs) was recently shown to be beneficial in murine cardiac reperfusion injury, the question arises as to what extent the fatty acid (FA)-composition in a KD alters molecular markers of FA-oxidation (FAO) and modulates cardiac fibrotic outcome. Here, we show that eight weeks of feeding an LCT-KD as well as an LCT/MCT mix (8:1 ketogenic ratio) induces cardiac fibrosis in male C57/BL6NRJ mice. Despite the increased amount of collagen fibers, cardiac tissue was immunologically indistinguishable between groups. MCT supplementation resulted in i) profound changes in plasma metabolome, ii) reduced hydroxymethylglutaryl-CoA synthase upregulation, and mitofusin 2 downregulation, iii) abrogation of LCT-induced mitochondrial enlargement, and iv) enhanced FAO profile. Contrary to literature, mitochondrial biogenesis was unaffected by KDs. We propose that the tissue remodeling, which we observed, is caused by the accumulation of 4-hydroxy-2-nonenal protein adducts, despite an inconspicuous nuclear factor (erythroid-derived 2)-like 2 pathway. We conclude that in spite of the generally favorable effects of MCTs, they cannot inhibit 4-hydroxy-2-nonenal adduct formation and fibrotic tissue formation in this setting. Furthermore, we support the burgeoning concern about the effect of KDs on the cardiac safety profile.

PMID:36958422 | DOI:10.1016/j.molmet.2023.101711

Redox Biol. 2023 Feb 23;62:102639. doi: 10.1016/j.redox.2023.102639. Online ahead of print.

ABSTRACT

Despite a strong rationale for why cancer cells are susceptible to redox-targeting drugs, such drugs often face tumor resistance or dose-limiting toxicity in preclinical and clinical studies. An important reason is the lack of specific biomarkers to better select susceptible cancer entities and stratify patients. Using a large panel of lung cancer cell lines, we identified a set of "antioxidant-capacity" biomarkers (ACB), which were tightly repressed, partly by STAT3 and STAT5A/B in sensitive cells, rendering them susceptible to multiple redox-targeting and ferroptosis-inducing drugs. Contrary to expectation, constitutively low ACB expression was not associated with an increased steady state level of reactive oxygen species (ROS) but a high level of nitric oxide, which is required to sustain high replication rates. Using ACBs, we identified cancer entities with a high percentage of patients with favorable ACB expression pattern, making it likely that more responders to ROS-inducing drugs could be stratified for clinical trials.

PMID:36958250 | DOI:10.1016/j.redox.2023.102639

PLoS Comput Biol. 2023 Mar 23;19(3):e1010903. doi: 10.1371/journal.pcbi.1010903. eCollection 2023 Mar.

ABSTRACT

COVID-19 is one of the deadliest respiratory diseases, and its emergence caught the pharmaceutical industry off guard. While vaccines have been rapidly developed, treatment options for infected people remain scarce, and COVID-19 poses a substantial global threat. This study presents a novel workflow to predict robust druggable targets against emerging RNA viruses using metabolic networks and information of the viral structure and its genome sequence. For this purpose, we implemented pymCADRE and PREDICATE to create tissue-specific metabolic models, construct viral biomass functions and predict host-based antiviral targets from more than one genome. We observed that pymCADRE reduces the computational time of flux variability analysis for internal optimizations. We applied these tools to create a new metabolic network of primary bronchial epithelial cells infected with SARS-CoV-2 and identified enzymatic reactions with inhibitory effects. The most promising reported targets were from the purine metabolism, while targeting the pyrimidine and carbohydrate metabolisms seemed to be promising approaches to enhance viral inhibition. Finally, we computationally tested the robustness of our targets in all known variants of concern, verifying our targets' inhibitory effects. Since laboratory tests are time-consuming and involve complex readouts to track processes, our workflow focuses on metabolic fluxes within infected cells and is applicable for rapid hypothesis-driven identification of potentially exploitable antivirals concerning various viruses and host cell types.

PMID:36952396 | DOI:10.1371/journal.pcbi.1010903

Cell Rep. 2023 Mar 22;42(4):112300. doi: 10.1016/j.celrep.2023.112300. Online ahead of print.

ABSTRACT

Mechanical allodynia (MA) represents one prevalent symptom of chronic pain. Previously we and others have identified spinal and brain circuits that transmit or modulate the initial establishment of MA. However, brain-derived descending pathways that control the laterality and duration of MA are still poorly understood. Here we report that the contralateral brain-to-spinal circuits, from Oprm1 neurons in the lateral parabrachial nucleus (lPBNOprm1), via Pdyn neurons in the dorsal medial regions of hypothalamus (dmHPdyn), to the spinal dorsal horn (SDH), act to prevent nerve injury from inducing contralateral MA and reduce the duration of bilateral MA induced by capsaicin. Ablating/silencing dmH-projecting lPBNOprm1 neurons or SDH-projecting dmHPdyn neurons, deleting Dyn peptide from dmH, or blocking spinal κ-opioid receptors all led to long-lasting bilateral MA. Conversely, activation of dmHPdyn neurons or their axonal terminals in SDH can suppress sustained bilateral MA induced by lPBN lesion.

PMID:36952340 | DOI:10.1016/j.celrep.2023.112300

Theor Appl Genet. 2023 Mar 23;136(4):71. doi: 10.1007/s00122-023-04243-y.

ABSTRACT

Quantitative disease resistance (QDR) controls the association of the light leaf spot pathogen with Brassica napus; four QDR loci that were in linkage disequilibrium and eight gene expression markers were identified. Quantitative disease resistance (QDR) can provide durable control of pathogens in crops in contrast to resistance (R) gene-mediated resistance which can break down due to pathogen evolution. QDR is therefore a desirable trait in crop improvement, but little is known about the causative genes, and so it is difficult to incorporate into breeding programmes. Light leaf spot, caused by Pyrenopeziza brassicae, is an important disease of oilseed rape (canola, Brassica napus). To identify new QDR gene loci, we used a high-throughput screening pathosystem with P. brassicae on 195 lines of B. napus combined with an association transcriptomics platform. We show that all resistance against P. brassicae was associated with QDR and not R gene-mediated. We used genome-wide association analysis with an improved B. napus population structure to reveal four gene loci significantly (P = 0.0001) associated with QDR in regions showing linkage disequilibrium. On chromosome A09, enhanced resistance was associated with heterozygosity for a cytochrome P450 gene co-localising with a previously described locus for seed glucosinolate content. In addition, eight significant gene expression markers with a false discovery rate of 0.001 were associated with QDR against P. brassicae. For seven of these, expression was positively correlated with resistance, whereas for one, a HXXXD-type acyl-transferase, negative correlation indicated a potential susceptibility gene. The study identifies novel QDR loci for susceptibility and resistance, including novel cryptic QDR genes associated with heterozygosity, that will inform future crop improvement.

PMID:36952022 | DOI:10.1007/s00122-023-04243-y

J Med Virol. 2023 Mar 23. doi: 10.1002/jmv.28698. Online ahead of print.

ABSTRACT

OBJECTIVE: To evaluate the genetic relationship between hypertension and COVID-19 and explore the molecular pathways linking hypertension to COVID-19.

METHODS: We performed genetic correlation and Mendelian randomization (MR) analyses to assess potential associations between hypertension and hospitalized COVID-19. We compared genome-wide association signals to reveal shared genetic variation between hypertension and hospitalized COVID-19. Moreover, hypertension-driven molecular pathways were constructed based on large-scale literature data to understand the influence of hypertension on COVID-19 at the molecular level.

RESULTS: Hypertension has a positive genetic correlation with COVID-19 (rg = 0.19). The MR analyses indicate that genetic liability to hypertension confers a causal effect on hospitalized COVID-19 (OR: 1.05, CI: 1.00-1.09, P = 0.030). Hypertension and hospitalized COVID-19 have three overlapping loci and share eight protein-coding risk genes, including ABO, CSF2, FUT2, IZUMO1, MAMSTR, NPNT, RASIP1, and WNT3. Molecular pathway analysis suggests that hypertension may promote the development of COVID-19 through the induction of inflammatory pathways.

CONCLUSION: Our study suggests that genetically determined hypertension may increase the risk for severe COVID-19. The shared genetic variation and the connecting molecular pathways may underline causal links between hypertension and COVID-19. This article is protected by copyright. All rights reserved.

PMID:36951353 | DOI:10.1002/jmv.28698

J Biomed Mater Res A. 2023 Mar 23. doi: 10.1002/jbm.a.37529. Online ahead of print.

ABSTRACT

The field of biomaterials science is highly active, with a steadily increasing number of publications and new journals being founded. This article brings together contributions from the editors of six leading journals in the area of biomaterials science and engineering. Each contributor highlights specific advances, topics, and trends that have emerged through the publications in their respective journal in the calendar year 2022. It presents a global perspective on a wide range of material types, functionalities, and applications. The highlighted topics include a diversity of biomaterials; from proteins, polysaccharides, and lipids to ceramics, metals, advanced composites, and a variety of new forms of these materials. Important advances in dynamically functional materials are presented, including a range of fabrication techniques such as bioassembly, 3D bioprinting and microgel formation. Similarly, several applications are highlighted in drug and gene delivery, biological sensing, cell guidance, immunoengineering, electroconductivity, wound healing, infection resistance, tissue engineering, and treatment of cancer. The goal of this paper is to provide the reader with both a broad view of recent biomaterials research, as well as expert commentary on some of the key advances that will shape the future of biomaterials science and engineering.

PMID:36951261 | DOI:10.1002/jbm.a.37529

Cell Genom. 2023 Feb 2;3(3):100262. doi: 10.1016/j.xgen.2023.100262. eCollection 2023 Mar 8.

ABSTRACT

Precision oncology promises accurate prediction of disease trajectories by utilizing molecular features of tumors. We present a systematic analysis of the prognostic potential of diverse molecular features across large cancer cohorts. We find that the mRNA expression of biologically coherent sets of genes (modules) is substantially more predictive of patient survival than single-locus genomic and transcriptomic aberrations. Extending our analysis beyond existing curated gene modules, we find a large novel class of highly prognostic DNA/RNA cis-regulatory modules associated with dynamic gene expression within cancers. Remarkably, in more than 82% of cancers, modules substantially improve survival stratification compared with conventional clinical factors and prominent genomic aberrations. The prognostic potential of cancer modules generalizes to external cohorts better than conventionally used single-gene features. Finally, a machine-learning framework demonstrates the combined predictive power of multiple modules, yielding prognostic models that perform substantially better than existing histopathological and clinical factors in common use.

PMID:36950380 | PMC:PMC10025453 | DOI:10.1016/j.xgen.2023.100262

Comput Struct Biotechnol J. 2023 Mar 2;21:1995-2008. doi: 10.1016/j.csbj.2023.02.051. eCollection 2023.

ABSTRACT

The vital cellular functions in Gram-positive bacteria are controlled by signaling molecules known as quorum sensing peptides (QSPs), considered promising therapeutic interventions for bacterial infections. In the bacterial system QSPs bind to membrane-coupled receptors, which then auto-phosphorylate and activate intracellular response regulators. These response regulators induce target gene expression in bacteria. One of the most reliable trends in drug discovery research for virulence-associated molecular targets is the use of peptide drugs or new functionalities. In this perspective, computational methods act as auxiliary aids for biologists, where methodologies based on machine learning and in silico analysis are developed as suitable tools for target peptide identification. Therefore, the development of quick and reliable computational resources to identify or predict these QSPs along with their receptors and inhibitors is receiving considerable attention. The databases such as Quorumpeps and Quorum Sensing of Human Gut Microbes (QSHGM) provide a detailed overview of the structures and functions of QSPs. The tools and algorithms such as QSPpred, QSPred-FL, iQSP, EnsembleQS and PEPred-Suite have been used for the generic prediction of QSPs and feature representation. The availability of compiled key resources for utilizing peptide features based on amino acid composition, positional preferences, and motifs as well as structural and physicochemical properties, including biofilm inhibitory peptides, can aid in elucidating the QSP and membrane receptor interactions in infectious Gram-positive pathogens. Herein, we present a comprehensive survey of diverse computational approaches that are suitable for detecting QSPs and QS interference molecules. This review highlights the utility of these methods for developing potential biomarkers against infectious Gram-positive pathogens.

PMID:36950221 | PMC:PMC10025024 | DOI:10.1016/j.csbj.2023.02.051

iScience. 2023 Mar 2;26(4):106319. doi: 10.1016/j.isci.2023.106319. eCollection 2023 Apr 21.

ABSTRACT

Cuproptosis is a novel form of cell death driven by a copper-dependent proteotoxic stress response whose comprehensive landscape in tumors remains unclear. Here, we comprehensively characterized cuproptosis-related genes (CRGs) across 33 cancers using multi-omic data from The Cancer Genome Atlas (TCGA), showing complicated and diverse results in different cancers. We also explored the relationships between CRGs and cancer metabolic patterns, pathway activity, and tumor microenvironment (TME), suggesting that they played critical roles in tumor progression and TME cell infiltration. We further established the cuproptosis potential index (CPI) to reveal the functional roles of cuproptosis, and characterized multi-omic molecular features associated with cuproptosis. In clinical applications, we performed a combined analysis of the sensitivity of CRGs and CPI to drug response and immunotherapy. This study provides a rich resource for understanding cuproptosis, offering a broad molecular perspective for future functional and therapeutic studies of multiple cancer pathways mediated by cuproptosis.

PMID:36950125 | PMC:PMC10025971 | DOI:10.1016/j.isci.2023.106319

iScience. 2023 Feb 28;26(4):106295. doi: 10.1016/j.isci.2023.106295. eCollection 2023 Apr 21.

ABSTRACT

Sea urchins can detect light and move in relation to luminous stimuli despite lacking eyes. They presumably detect light through photoreceptor cells distributed on their body surface. However, there is currently no mechanistic explanation of how these animals can process light to detect visual stimuli and produce oriented movement. Here, we present a model of decentralized vision in echinoderms that includes all known processing stages, from photoreceptor cells to radial nerve neurons to neurons contained in the oral nerve ring encircling the mouth of the animals. In the model, light stimuli captured by photoreceptor cells produce neural activity in the radial nerve neurons. In turn, neural activity in the radial nerves is integrated in the oral nerve ring to produce a profile of neural activity reaching spatially across several ambulacra. This neural activity is readout to produce a model of movement. The model captures previously published data on the behavior of sea urchin Diadema africanum probed with a variety of physical stimuli. The specific pattern of neural connections used in the model makes testable predictions on the properties of single neurons and aggregate neural behavior in Diadema africanum and other echinoderms, offering a potential understanding of the mechanism of visual orientation in these animals.

PMID:36950121 | PMC:PMC10025101 | DOI:10.1016/j.isci.2023.106295