Polyamine biosynthesis and eIF5A hypusination are modulated by the DNA tumor virus KSHV and promote KSHV viral infection.

Polyamines are critical metabolites involved in various cellular processes and often dysregulated in cancers. Kaposi's sarcoma-associated Herpesvirus (KSHV), a defined human oncogenic virus, leads to profound alterations of host metabolic landscape to favor development of KSHV-associated malignancies. In our studies, we identified that polyamine biosynthesis and eIF5A hypusination are dynamically regulated by KSHV infection through modulation of key enzymes (ODC1 and DHPS) of these pathways. During KSHV latency, ODC1 and DHPS are upregulated along with increase of hypusinated eIF5A (hyp-eIF5A), while hyp-eIF5A is further induced along with reduction of ODC1 and intracellular polyamines during KSHV lytic reactivation. In return these metabolic pathways are required for both KSHV lytic reactivation and de novo infection. Further analysis unraveled that synthesis of critical KSHV latent and lytic proteins (LANA, RTA) depends on hypusinated-eIF5A. We also demonstrated that KSHV infection can be efficiently and specifically suppressed by inhibitors targeting these pathways. Collectively, our results illustrated that the dynamic and profound interaction of a DNA tumor virus (KSHV) with host polyamine biosynthesis and eIF5A hypusination pathways promote viral propagation, thus defining new therapeutic targets to treat KSHV-associated malignancies.

Tissue nanotransfection causes tumor regression by its effect on nanovesicle cargo that alters microenvironmental macrophage state.

Extracellular vesicles (EVs) are nanovesicles released by all eukaryotic cells. This work reports the first nanoscale fluorescent visualization of tumor-originating vesicles bearing an angiogenic microRNA (miR)-126 cargo. In a validated experimental model of lethal murine vascular neoplasm, tumor-originating EV delivered its miR-126 cargo to tumor-associated macrophages (TAMs). Such delivery resulted in an angiogenic (LYVE+) change of state in TAM that supported tumor formation. Study of the trafficking of tumor-originating fluorescently tagged EV revealed colocalization with TAM demonstrating uptake by these cells. Ex vivo treatment of macrophages with tumor-derived EVs led to gain of tumorigenicity in these isolated cells. Single-cell RNA sequencing of macrophages revealed that EV-borne miR-126 characterized the angiogenic change of state. Unique gene expression signatures of specific macrophage clusters responsive to miR-126-enriched tumor-derived EVs were revealed. Topical tissue nanotransfection (TNT) delivery of an oligonucleotide comprising an anti-miR against miR-126 resulted in significant knockdown of miR-126 in the tumor tissue. miR-126 knockdown resulted in complete involution of the tumor and improved survival rate of tumor-affected mice. This work identifies a novel tumorigenic mechanism that relies on tumorigenic state change of TAM caused by tumor-originating EV-borne angiomiR. This disease process can be effectively targeted by topical TNT of superficial tumors.

FACT subunit SUPT16H associates with BRD4 and contributes to silencing of interferon signaling.

FACT (FAcilitates Chromatin Transcription) is a heterodimeric protein complex composed of SUPT16H and SSRP1, and a histone chaperone participating in chromatin remodeling during gene transcription. FACT complex is profoundly regulated, and contributes to both gene activation and suppression. Here we reported that SUPT16H, a subunit of FACT, is acetylated in both epithelial and natural killer (NK) cells. The histone acetyltransferase TIP60 contributes to the acetylation of SUPT16H middle domain (MD) at lysine 674 (K674). Such acetylation of SUPT16H is recognized by bromodomain protein BRD4, which promotes protein stability of SUPT16H in both epithelial and NK cells. We further demonstrated that SUPT16H-BRD4 associates with histone modification enzymes (HDAC1, EZH2), and further regulates their activation status and/or promoter association as well as affects the relevant histone marks (H3ac, H3K9me3 and H3K27me3). BRD4 is known to profoundly regulate interferon (IFN) signaling, while such function of SUPT16H has never been explored. Surprisingly, our results revealed that SUPT16H genetic knockdown via RNAi or pharmacological inhibition by using its inhibitor, curaxin 137 (CBL0137), results in the induction of IFNs and interferon-stimulated genes (ISGs). Through this mechanism, depletion or inhibition of SUPT16H is shown to efficiently inhibit infection of multiple viruses, including Zika, influenza, and SARS-CoV-2. Furthermore, we demonstrated that depletion or inhibition of SUPT16H also causes the remarkable activation of IFN signaling in NK cells, which promotes the NK-mediated killing of virus-infected cells in a co-culture system using human primary NK cells. Overall, our studies unraveled the previously un-appreciated role of FACT complex in coordinating with BRD4 and regulating IFN signaling in both epithelial and NK cells, and also proposed the novel application of the FACT inhibitor CBL0137 to treat viral infections.

Inhibition of polo-like kinase 1 (PLK1) facilitates reactivation of gamma-herpesviruses and their elimination.

Both Kaposi's sarcoma-associated herpesvirus (KSHV) and Epstein-Barr virus (EBV) establish the persistent, life-long infection primarily at the latent status, and associate with certain types of tumors, such as B cell lymphomas, especially in immuno-compromised individuals including people living with HIV (PLWH). Lytic reactivation of these viruses can be employed to kill tumor cells harboring latently infected viral episomes through the viral cytopathic effects and the subsequent antiviral immune responses. In this study, we identified that polo-like kinase 1 (PLK1) is induced by KSHV de novo infection as well as lytic switch from KSHV latency. We further demonstrated that PLK1 depletion or inhibition facilitates KSHV reactivation and promotes cell death of KSHV-infected lymphoma cells. Mechanistically, PLK1 regulates Myc that is critical to both maintenance of KSHV latency and support of cell survival, and preferentially affects the level of H3K27me3 inactive mark both globally and at certain loci of KSHV viral episomes. Furthremore, we recognized that PLK1 inhibition synergizes with STAT3 inhibition to efficiently induce KSHV reactivation. We also confirmed that PLK1 depletion or inhibition yields the similar effect on EBV lytic reactivation and cell death of EBV-infected lymphoma cells. Lastly, we noticed that PLK1 in B cells is elevated in the context of HIV infection and caused by HIV Nef protein to favor KSHV/EBV latency.

Quantum Communications Feasibility Tests over a UK-Ireland 224 km Undersea Link.

The future quantum internet will leverage existing communication infrastructures, including deployed optical fibre networks, to enable novel applications that outperform current information technology. In this scenario, we perform a feasibility study of quantum communications over an industrial 224 km submarine optical fibre link deployed between Southport in the United Kingdom (UK) and Portrane in the Republic of Ireland (IE). With a characterisation of phase drift, polarisation stability and the arrival time of entangled photons, we demonstrate the suitability of the link to enable international UK-IE quantum communications for the first time.

Nucleolar protein NOP2/NSUN1 suppresses HIV-1 transcription and promotes viral latency by competing with Tat for TAR binding and methylation.

Recent efforts have been paid to identify previously unrecognized HIV-1 latency-promoting genes (LPGs) that can potentially be targeted for eradication of HIV-1 latent reservoirs. From our earlier orthologous RNAi screens of host factors regulating HIV-1 replication, we identified that the nucleolar protein NOP2/NSUN1, a m5C RNA methyltransferase (MTase), is an HIV-1 restriction factor. Loss- and gain-of-function analyses confirmed that NOP2 restricts HIV-1 replication. Depletion of NOP2 promotes the reactivation of latently infected HIV-1 proviruses in multiple cell lines as well as primary CD4+ T cells, alone or in combination with latency-reversing agents (LRAs). Mechanistically, NOP2 associates with HIV-1 5' LTR, interacts with HIV-1 TAR RNA by competing with HIV-1 Tat protein, as well as contributes to TAR m5C methylation. RNA MTase catalytic domain (MTD) of NOP2 mediates its competition with Tat and binding with TAR. Overall, these findings verified that NOP2 suppresses HIV-1 transcription and promotes viral latency.

Profiling of immune related genes silenced in EBV-positive gastric carcinoma identified novel restriction factors of human gammaherpesviruses.

EBV-associated gastric cancer (EBVaGC) is characterized by high frequency of DNA methylation. In this study, we investigated how epigenetic alteration of host genome contributes to pathogenesis of EBVaGC through the analysis of transcriptomic and epigenomic datasets from NIH TCGA (The Cancer Genome Atlas) consortium. We identified that immune related genes (IRGs) is a group of host genes preferentially silenced in EBV-positive gastric cancers through DNA hypermethylation. Further functional characterizations of selected IRGs reveal their novel antiviral activity against not only EBV but also KSHV. In particular, we showed that metallothionein-1 (MT1) and homeobox A (HOXA) gene clusters are down-regulated via EBV-driven DNA hypermethylation. Several MT1 isoforms suppress EBV lytic replication and release of progeny virions as well as KSHV lytic reactivation, suggesting functional redundancy of these genes. In addition, single HOXA10 isoform exerts antiviral activity against both EBV and KSHV. We also confirmed the antiviral effect of other dysregulated IRGs, such as IRAK2 and MAL, in scenario of EBV and KSHV lytic reactivation. Collectively, our results demonstrated that epigenetic silencing of IRGs is a viral strategy to escape immune surveillance and promote viral propagation, which is overall beneficial to viral oncogenesis of human gamma-herpesviruses (EBV and KSHV), considering that these IRGs possess antiviral activities against these oncoviruses.

Cinema:Bandit: a visualization application for beamline science demonstrated on XFEL shock physics experiments.

A new visualization tool, Cinema:Bandit, and its demonstration with a continuous workflow for analyzing shock physics experiments and visually exploring the data in real time at X-ray light sources is presented. Cinema:Bandit is an open-source, web-based visualization application in which the experimenter may explore an aggregated dataset to inform real-time beamline decisions and enable post hoc data analysis. The tool integrates with experimental workflows that process raw detector data into a simple database format, and it allows visualization of disparate data types, including experimental parameters, line graphs, and images. Use of parallel coordinates accommodates the irregular sampling of experimental parameters and allows for display and filtering of both experimental inputs and measurements. The tool is demonstrated on a dataset of shock-compressed titanium collected at the Matter in Extreme Conditions hutch at the Linac Coherent Light Source.

Multivariate information processing characterizes fitness of a cascaded gene-transcription machinery.

We report that a genetic two-step activation cascade processes diverse flavors of information, e.g., synergy, redundancy, and unique information. Our computations measuring reduction in Shannon entropies and reduction in variances produce differently behaving absolute magnitudes of these informational flavors. We find that similarity can be brought in if these terms are evaluated in fractions with respect to corresponding total information. Each of the input signal and final gene-product is found to generate common or redundant information fractions (mostly) to predict each other, whereas they also complement one another to harness synergistic information fraction, predicting the intermediate biochemical species. For an optimally growing signal to maintain fixed steady-state abundance of activated downstream gene-products, the interaction information fractions for this cascade module shift from net-redundancy to information-independence.

Multivariate Pointwise Information-Driven Data Sampling and Visualization.

With increasing computing capabilities of modern supercomputers, the size of the data generated from the scientific simulations is growing rapidly. As a result, application scientists need effective data summarization techniques that can reduce large-scale multivariate spatiotemporal data sets while preserving the important data properties so that the reduced data can answer domain-specific queries involving multiple variables with sufficient accuracy. While analyzing complex scientific events, domain experts often analyze and visualize two or more variables together to obtain a better understanding of the characteristics of the data features. Therefore, data summarization techniques are required to analyze multi-variable relationships in detail and then perform data reduction such that the important features involving multiple variables are preserved in the reduced data. To achieve this, in this work, we propose a data sub-sampling algorithm for performing statistical data summarization that leverages pointwise information theoretic measures to quantify the statistical association of data points considering multiple variables and generates a sub-sampled data that preserves the statistical association among multi-variables. Using such reduced sampled data, we show that multivariate feature query and analysis can be done effectively. The efficacy of the proposed multivariate association driven sampling algorithm is presented by applying it on several scientific data sets.

Energy-efficient switching of nanomagnets for computing: straintronics and other methodologies.

The need for increasingly powerful computing hardware has spawned many ideas stipulating, primarily, the replacement of traditional transistors with alternate 'switches' that dissipate miniscule amounts of energy when they switch and provide additional functionality that are beneficial for information processing. An interesting idea that has emerged recently is the notion of using two-phase (piezoelectric/magnetostrictive) multiferroic nanomagnets with bistable (or multi-stable) magnetization states to encode digital information (bits), and switching the magnetization between these states with small voltages (that strain the nanomagnets) to carry out digital information processing. The switching delay is ∼1 ns and the energy dissipated in the switching operation can be few to tens of aJ, which is comparable to, or smaller than, the energy dissipated in switching a modern-day transistor. Unlike a transistor, a nanomagnet is 'non-volatile', so a nanomagnetic processing unit can store the result of a computation locally without refresh cycles, thereby allowing it to double as both logic and memory. These dual-role elements promise new, robust, energy-efficient, high-speed computing and signal processing architectures (usually non-Boolean and often non-von-Neumann) that can be more powerful, architecturally superior (fewer circuit elements needed to implement a given function) and sometimes faster than their traditional transistor-based counterparts. This topical review covers the important advances in computing and information processing with nanomagnets, with emphasis on strain-switched multiferroic nanomagnets acting as non-volatile and energy-efficient switches-a field known as 'straintronics'. It also outlines key challenges in straintronics.

Interplay of synergy and redundancy in diamond motif.

The formalism of partial information decomposition provides a number of independent components which altogether constitute the total information provided by the source variable(s) about the target variable(s). These non-overlapping terms are recognized as unique information, synergistic information, and redundant information. The metric of net synergy conceived as the difference between synergistic and redundant information is capable of detecting effective synergy, effective redundancy, and information independence among stochastic variables. The net synergy can be quantified using appropriate combinations of different Shannon mutual information terms. The utilization of the net synergy in network motifs with the nodes representing different biochemical species, involved in information sharing, uncovers rich store for exciting results. In the current study, we use this formalism to obtain a comprehensive understanding of the relative information processing mechanism in a diamond motif and two of its sub-motifs, namely, bifurcation and integration motif embedded within the diamond motif. The emerging patterns of effective synergy and effective redundancy and their contribution toward ensuring high fidelity information transmission are duly compared in the sub-motifs. Investigation on the metric of net synergy in independent bifurcation and integration motifs are also executed. In all of these computations, the crucial roles played by various systemic time scales, activation coefficients, and signal integration mechanisms at the output of the network topologies are especially emphasized. Following this plan of action, we become confident that the origin of effective synergy and effective redundancy can be architecturally justified by decomposing a diamond motif into bifurcation and integration motif. According to our conjecture, the presence of a common source of fluctuations creates effective redundancy. Our calculations reveal that effective redundancy empowers signal fidelity. Moreover, to achieve this, input signaling species avoids strong interaction with downstream intermediates. This strategy is capable of making the diamond motif noise-tolerant. Apart from the topological features, our study also puts forward the active contribution of additive and multiplicative signal integration mechanisms to nurture effective redundancy and effective synergy.

Experimental Demonstration of Complete 180° Reversal of Magnetization in Isolated Co Nanomagnets on a PMN-PT Substrate with Voltage Generated Strain.

Rotating the magnetization of a shape anisotropic magnetostrictive nanomagnet with voltage-generated stress/strain dissipates much less energy than most other magnetization rotation schemes, but its application to writing bits in nonvolatile magnetic memory has been hindered by the fundamental inability of stress/strain to rotate magnetization by full 180°. Normally, stress/strain can rotate the magnetization of a shape anisotropic elliptical nanomagnet by only up to 90°, resulting in incomplete magnetization reversal. Recently, we predicted that applying uniaxial stress sequentially along two different axes that are not collinear with the major or minor axis of the elliptical nanomagnet will rotate the magnetization by full 180°. Here, we demonstrate this complete 180° rotation in elliptical Co nanomagnets (fabricated on a piezoelectric substrate) at room temperature. The two stresses are generated by sequentially applying voltages to two pairs of shorted electrodes placed on the substrate such that the line joining the centers of the electrodes in one pair intersects the major axis of a nanomagnet at ∼ +30° and the line joining the centers of the electrodes in the other pair intersects at ∼ -30°. A finite element analysis has been performed to determine the stress distribution underneath the nanomagnets when one or both pairs of electrodes are activated, and this has been approximately incorporated into a micromagnetic simulation of magnetization dynamics to confirm that the generated stress can produce the observed magnetization rotations. This result portends an extremely energy-efficient nonvolatile "straintronic" memory technology predicated on writing bits in nanomagnets with electrically generated stress.

Information Guided Exploration of Scalar Values and Isocontours in Ensemble Datasets.

Uncertainty of scalar values in an ensemble dataset is often represented by the collection of their corresponding isocontours. Various techniques such as contour-boxplot, contour variability plot, glyphs and probabilistic marching-cubes have been proposed to analyze and visualize ensemble isocontours. All these techniques assume that a scalar value of interest is already known to the user. Not much work has been done in guiding users to select the scalar values for such uncertainty analysis. Moreover, analyzing and visualizing a large collection of ensemble isocontours for a selected scalar value has its own challenges. Interpreting the visualizations of such large collections of isocontours is also a difficult task. In this work, we propose a new information-theoretic approach towards addressing these issues. Using specific information measures that estimate the predictability and surprise of specific scalar values, we evaluate the overall uncertainty associated with all the scalar values in an ensemble system. This helps the scientist to understand the effects of uncertainty on different data features. To understand in finer details the contribution of individual members towards the uncertainty of the ensemble isocontours of a selected scalar value, we propose a conditional entropy based algorithm to quantify the individual contributions. This can help simplify analysis and visualization for systems with more members by identifying the members contributing the most towards overall uncertainty. We demonstrate the efficacy of our method by applying it on real-world datasets from material sciences, weather forecasting and ocean simulation experiments.

Multidrug Resistance-associated Protein-1 (MRP-1)-dependent Glutathione Disulfide (GSSG) Efflux as a Critical Survival Factor for Oxidant-enriched Tumorigenic Endothelial Cells.

Endothelial cell tumors are the most common soft tissue tumors in infants. Tumor-forming endothelial (EOMA) cells are able to escape cell death fate despite excessive nuclear oxidant burden. Our previous work recognized perinuclear Nox-4 as a key contributor to EOMA growth. The objective of this work was to characterize the mechanisms by which EOMA cells evade oxidant toxicity and thrive. In EOMA cells, compared with in the cytosol, the nuclear GSSG/GSH ratio was 5-fold higher. Compared to the ratio observed in healthy murine aortic endothelial (MAE) cells, GSSG/GSH was over twice as high in EOMA cells. Multidrug resistance-associated protein-1 (MRP-1), an active GSSG efflux mechanism, showed 2-fold increased activity in EOMA compared with MAE cells. Hyperactive YB-1 and Ape/Ref-1 were responsible for high MRP-1 expression in EOMA. Proximity ligand assay demonstrated MRP-1 and YB-1 binding. Such binding enabled the nuclear targeting of MRP-1 in EOMA in a leptomycin-B-sensitive manner. MRP-1 inhibition as well as knockdown trapped nuclear GSSG, causing cell death of EOMA. Disulfide loading of cells by inhibition of GSSG reductase (bischoloronitrosourea) or thioredoxin reductase (auranofin) was effective in causing EOMA death as well. In sum, EOMA cells survive a heavy oxidant burden by rapid efflux of GSSG, which is lethal if trapped within the cell. A hyperactive MRP-1 system for GSSG efflux acts as a critical survival factor for these cells, making it a potential target for EOMA therapeutics.

Endothelial cell tumor growth is Ape/ref-1 dependent.

Tumor-forming endothelial cells have highly elevated levels of Nox-4 that release H2O2 into the nucleus, which is generally not compatible with cell survival. We sought to identify compensatory mechanisms that enable tumor-forming endothelial cells to survive and proliferate under these conditions. Ape-1/ref-1 (Apex-1) is a multifunctional protein that promotes DNA binding of redox-sensitive transcription factors, such as AP-1, and repairs oxidative DNA damage. A validated mouse endothelial cell (EOMA) tumor model was used to demonstrate that Nox-4-derived H2O2 causes DNA oxidation that induces Apex-1 expression. Apex-1 functions as a chaperone to keep transcription factors in a reduced state. In EOMA cells Apex-1 enables AP-1 binding to the monocyte chemoattractant protein-1 (mcp-1) promoter and expression of that protein is required for endothelial cell tumor formation. Intraperitoneal injection of the small molecule inhibitor E3330, which specifically targets Apex-1 redox-sensitive functions, resulted in a 50% decrease in tumor volume compared with mice injected with vehicle control (n = 6 per group), indicating that endothelial cell tumor proliferation is dependent on Apex-1 expression. These are the first reported results to establish Nox-4 induction of Apex-1 as a mechanism promoting endothelial cell tumor formation.

Dicer knockdown inhibits endothelial cell tumor growth via microRNA 21a-3p targeting of Nox-4.

MicroRNAs (miR) are emerging as biomarkers and potential therapeutic targets in tumor management. Endothelial cell tumors are the most common soft tissue tumors in infants, yet little is known about the significance of miR in regulating their growth. A validated mouse endothelial cell (EOMA) tumor model was used to demonstrate that post-transcriptional gene silencing of dicer, the enzyme that converts pre-miR to mature miR, can prevent tumor formation in vivo. Tumors were formed in eight of eight mice injected with EOMA cells transfected with control shRNA but formed in only four of ten mice injected with EOMA cells transfected with dicer shRNA. Tumors that formed in the dicer shRNA group were significantly smaller than tumors in the control group. This response to dicer knockdown was mediated by up-regulated miR 21a-3p activity targeting the nox-4 3'-UTR. EOMA cells were transfected with miR 21a-3p mimic and luciferase reporter plasmids containing either intact nox-4 3'-UTR or with mutation of the proposed 3'-UTR miR21a-3p binding sites. Mean luciferase activity was decreased by 85% in the intact compared with the site mutated vectors (p < 0.01). Attenuated Nox-4 activity resulted in decreased cellular hydrogen peroxide production and decreased production of oxidant-inducible monocyte chemoattractant protein-1, which we have previously shown to be critically required for endothelial cell tumor formation. These findings provide the first evidence establishing the significance of dicer and microRNA in promoting endothelial cell tumor growth in vivo.

The straintronic spin-neuron.

In artificial neural networks, neurons are usually implemented with highly dissipative CMOS-based operational amplifiers. A more energy-efficient implementation is a 'spin-neuron' realized with a magneto-tunneling junction (MTJ) that is switched with a spin-polarized current (representing weighted sum of input currents) that either delivers a spin transfer torque or induces domain wall motion in the soft layer of the MTJ to mimic neuron firing. Here, we propose and analyze a different type of spin-neuron in which the soft layer of the MTJ is switched with mechanical strain generated by a voltage (representing weighted sum of input voltages) and term it straintronic spin-neuron. It dissipates orders of magnitude less energy in threshold operations than the traditional current-driven spin neuron at 0 K temperature and may even be faster. We have also studied the room-temperature firing behaviors of both types of spin neurons and find that thermal noise degrades the performance of both types, but the current-driven type is degraded much more than the straintronic type if both are optimized for maximum energy-efficiency. On the other hand, if both are designed to have the same level of thermal degradation, then the current-driven version will dissipate orders of magnitude more energy than the straintronic version. Thus, the straintronic spin-neuron is superior to current-driven spin neurons.

Environmental bisphenol A disrupts methylation of steroidogenic genes in the ovary of Paradise threadfin Polynemus paradiseus via abnormal DNA methylation: Implications for human exposure and health risk assessment.

Bisphenol A, endocrine-disrupting chemicals (EDCs) impacting disease development via epigenetic modifications, is crucial in transcriptional regulation. However, ecotoxicology's limited exploration of epigenetics prompted our study's objective: examining the extended exposure of riverine Bisphenol A (BPA), a potent EDC, on DNA methylation during female paradise threadfin (Polynemus paradiseus) reproductive maturation. Assessing BPA contamination in riverine water, we collected fish samples from two locations with distinct contamination levels. In the highly contaminated region (Hc), we observed elevated DNA methylation in aromatase (7.5-fold), 20ß-HSD (3-fold), and FSHR (2-fold) genes. Hormone receptor investigation highlighted an escalating connection between transcriptional hyper-methylation and contamination levels. Additionally, our study revealed a positive correlation between oocyte growth and global DNA methylation, suggesting BPA's potential to modify DNA methylation in female paradise threadfins. This effect likely occurs through changes in hormone receptor expression, persisting throughout oocyte maturation. Notably, our research, the first of its kind in estuarine areas, confirmed BPA contamination in paradise threadfins, raising concerns about potential health risks for humans.

Cr-Detector: A simple chemosensing system for onsite Cr (VI) detection in water.

Due to the increase in urbanization and industrialization, the load of toxicants in the environment is alarming. The most common toxicants, including heavy metals and metalloids such as hexavalent Chromium, have severe pathophysiological impacts on humans and other aquatic biotas. Therefore, developing a portable rapid detection device for such toxicants in the aquatic environment is necessary. This work portrays the development of a field-portable image analysis device coupled with 3,3',5,5'-tetramethylbenzidine (TMB) as a sensing probe for chromium (VI) detection in the aquatic ecosystem. Sensor parameters, such as reagent concentration, reaction time, etc., were optimized for the sensor development and validation using a commercial UV-Vis spectrophotometer. The chemoreceptor integrated with a uniform illumination imaging system (UIIS) revealed the system's applicability toward Cr(VI) detection. The calibration curve using the R-value of image parameters allows Cr(VI) detection in the linear range of 25 to 600 ppb, which covers the prescribed permissible limit by various regulatory authorities. Furthermore, the adjusted R2 = 0.992 of the linear fit and correlation coefficients of 0.99018 against the spectrophotometric method signifies the suitability of the developed system. This TMB-coupled field-portable sensing system is the first-ever reported image analysis-based technology for detecting a wide range of Cr(VI) in aquatic ecosystems to our knowledge.