Search bioRxiv⌕ Search

Biology subjects

Shukla, R.

Publications and source records attributed to Shukla, R..

At least 19 recordsLinked to original sources

Safe Redosable Low-Immunogenic In Vivo CAR-T Therapy for B Cell Malignancies and Solid Tumors

In vivo CAR-T cell therapy eliminates manufacturing complexities associated with ex vivo autologous approaches, but safety concerns have limited adoption. We developed viroVbot, a next-generation in vivo CAR-T platform, by combining computational immunogenicity prediction (CIMMEXTM) with envelope engineering. Screening 22,562 glycoprotein sequences, we identified 641 vesiculovirus homologs, from which we selected Piry virus glycoprotein (PIRYV) as the optimal candidate. PIRYV exhibited lower MHC-epitope density, reduced human seroprevalence, with decreased T cell activation compared to VSV-G. To enhance targeting specificity, we engineered receptor-binding-deficient PIRYV (ePIRYVRBD) displaying CD3/CD7 nanobodies for T cell-selective transduction. To maximize safety, we engineered CAR-TRAP producer cells to eliminate unwanted B cell transduction and incorporated machine learning-optimized T cell-specific promoters that restrict CAR activation exclusively to lymphocytes. Additional modifications suppressed hepatocyte expression and prevented phagocytic uptake. In humanized xenograft models, viroVbot3 generated potent BCMA/CD19 specific CAR-T responses against multiple myeloma and Claudin18.2-targeting gastric cancer, demonstrating sequential redosing with alternative envelopes. Critically, viroVbot3 exhibited minimal off-target organ biodistribution with CAR expression restricted to T lymphocytes. These findings establish viroVbot as a low-immunogenic platform for scalable in vivo CAR-T manufacturing with capability for sequential redosing across hematologic and solid tumors.

bioengineering↗

Loss of Glucose Transporter 1 in Mouse Uterine Cells Disrupts Trophoblast Differentiation and Promotes Gestational Diabetes

A successful pregnancy hinges on a finely coordinated dialogue between the maternal endometrium and the implanting embryo. Following embryo attachment to the uterine epithelium, underlying stromal cells undergo a transformation into decidual cells that promote a vascularized maternal-fetal interface and direct trophoblast lineage decisions through paracrine cues. However, the metabolic adaptations that enable decidual cells to support these energetically demanding processes remain poorly understood. Here, using a uterine-specific knockout mouse model, we identify Glucose Transporter 1 (Glut1) as a critical metabolic regulator linking endometrial glucose uptake to reproductive success. We demonstrate that stromal Glut1, induced by hypoxia-inducible factor 2 (Hif2), sustains a Hif2-Rab27b feed-forward circuit that drives vesicular trafficking during pregnancy through the glucose-sensing transcription factor MAX-like protein X (Mlx). Mice lacking endometrial Glut1 are severely subfertile despite normal embryo attachment. Glut1-deficient uteri exhibit impaired stromal extracellular vesicle secretion, defective decidual angiogenesis, and marked dysregulation of trophoblast differentiation, including expansion of trophoblast progenitors, accumulation of glycogen trophoblast cells, and altered placental lactogen production. These placental defects culminate in mid-gestation fetal loss and maternal gestational diabetes mellitus (GDM). Collectively, our findings establish endometrial Glut1 as a metabolic gatekeeper of maternal glucose homeostasis and placentation and introduce a genetically tractable mouse model of spontaneously developing GDM, a disorder affecting nearly one in seven pregnancies worldwide. SIGNIFICANCEThis study uncovers endometrial Glut1 as a previously unrecognized metabolic regulator of placentation, demonstrating that maternal stromal glucose uptake dictates trophoblast fate and maternal glycemic control, and providing the field with its first genetically defined mouse model of spontaneously arising gestational diabetes.

physiology↗

Polysome Profiling Method for Low-Input Human Postmortem Brain

Polysome profiling is a powerful technique used to analyze the association of mRNA with ribosomes, providing insights into the translational status of a cell. It relies on the separation of ribosome-bound mRNAs through sucrose density gradient centrifugation, where the number of ribosomes on an mRNA correlates with its sedimentation rate. While numerous studies have successfully applied this method to cell line and mouse tissue, application to the human postmortem brain remains scarce due to challenges related to sample quality and low concentration of recoverable material. To overcome these challenges, we: O_LIImplemented a protocol specifically optimized for low-concentration human post-mortem brain tissue. C_LIO_LIImplemented a gradient-maker-free method to manually prepare sucrose gradients with tunable sensitivity for low-input samples. C_LIO_LIAdapted the human brain tissue protocol for neuronal cell lines and mouse brain with minimal modification. C_LI

neuroscience↗

Molecular Characterization of the Progressive Landscape of Depression

Major Depressive Disorder (MDD) frequently follows a recurrent trajectory of episodes and remissions, often culminating in treatment-resistance. Molecular differences defining state-specific changes during episode and remission have been explored. However, progressive differences--defined here as cross-sectional linear trends across clinical stages from first to recurrent episodes or remissions, reflecting increasing illness burden over time--remain poorly understood, limiting sustained therapeutic outcomes. Here, we analyzed RNA-seq data from postmortem sgACC to identify progressive differences across MDD episodes or remission relative to state-specific differences, using an integrative assessment of molecular and cellular specificity, genetic-risk, disease-comorbidity and potential therapeutic targets. Differential expression analysis showed greater overlap between progressive and state-specific differences during remission than episode. Pathway enrichment highlighted disruptions in extracellular-matrix pathways shared by state-specific and progressive episodes, while metabolic and catalytic pathways were restored during remission. Cell-type-specific analyses showed that progressive changes were linked to superficial-layer intra-telencephalic neurons, whereas state-specific changes were enriched in pyramidal neuron subtypes and deeper layer SST-positive interneurons. Genome-wide association-informed enrichment analysis further linked these transcriptomic changes to genetic risk factors and symptom dimensions. Anhedonia was associated with both state-specific episode and progressive-remission signatures, suggesting that it is a persistent trait-like feature of MDD. Finally, an integrative pharmacological analysis revealed shared molecular mechanisms between pro-disease and therapeutic targets, highlighting pleiotropic effects of key pathways depending on disease state and dosage. Together, these findings provide a novel perspective on biological underpinnings of MDD progression over episodes or remissions and identify pharmacological targets that account for pathological and/or compensatory/therapeutic processes.

neuroscience↗

Robust scoring system to evaluate animal well-being in murine orthotopic breast cancer and ovarian cancer models

Orthotopic models are critical to the development of new cancer therapies, as they have the greatest potential to mimic human cancer progression. However, orthotopic models are often underutilized due to practical challenges. These challenges include the need for specialized surgeries and the presence of complicating symptoms, such as ascites fluid accumulation in ovarian cancer and liver disease models, as well as ulceration of breast tumors growing in the mammary fat pad. An adaptable, quantitative animal health assessment system that utilizes simple, non-invasive, visual measurements can allow researchers to use these models to their full potential while safeguarding humane endpoints. The goal of this work was to establish such health scoring systems for translationally-relevant ovarian (ID8 Defb29-Vegf-A) and breast cancer (triple-negative model 4T1) models. We developed a tractable health assessment system by monitoring a combination of activity and responsiveness, coat condition, respiratory function, changes in body weight, posture, gait, tumor size (where measurable), and extent of ulceration, and scoring each of these parameters using a simple numerical scale. The scores at which euthanasia or other interventions were required were estimated and then adjusted based on clinical assessment by a team of researchers and veterinarians. These semi-quantitative health scoring systems were applied to survival experiments, in which mice were euthanized at a predetermined score or upon meeting a superseding health criterion, to confirm their applicability and effectiveness in maintaining humane endpoints. The scoring systems presented are intended to build on previously-established generic tumor model scoring systems that do not accommodate for the particular phenotypes present in orthotopic breast and ovarian cancer models.

cancer biology↗

Cigarette smoke aggravates atherosclerosis by promoting the infiltration of inflammasome-primed neutrophils and disrupting macrophage function in lesions

BackgroundCigarette smoking (CS) is a major risk factor for cardiovascular disease (CVD) through chronic inflammation. While its pulmonary effects are well established, the mechanisms linking lung inflammation to vascular injury remain unclear. Because neutrophils are early responders to CS-induced inflammation, we hypothesized that they drive systemic myelopoiesis and vascular inflammation via alarmin release. MethodsWild-type (WT) mice were exposed to inhaled CS or orally administered cigarette smoke extract (CSE). Immune cell composition in lung, bronchoalveolar lavage fluid (BALF), blood, spleen, and bone marrow (BM) was assessed by flow cytometry. Hematopoietic stem and progenitor cell (HSPC) proliferation, reactive oxygen species (ROS) production, and S100A8/A9 release were quantified. Atherosclerosis progression was evaluated in Ldlr-/- mice fed a Western diet and treated with CSE. To define the role of neutrophil-derived S100A8/A9, bone marrow transplantation was performed using S100a9-/- or WT donors. ResultsCS exposure increased circulating monocytes and neutrophils through enhanced BM myelopoiesis and elevated ROS-dependent S100A8/A9 release. Oral CSE reproduced these effects, indicating direct activation of neutrophils independent of pulmonary inflammation or lipid changes. In Ldlr-/- mice, CSE accelerated atherosclerosis by promoting infiltration of inflammasome-primed neutrophils, increased IL-1{beta} release, and impaired macrophage efferocytosis. Hematopoietic S100a9 deletion normalized myelopoiesis and reduced vascular inflammation and plaque burden. ConclusionsIngested CS components directly activate neutrophils to release S100A8/A9, triggering myelopoiesis and vascular inflammation. These findings reveal that tobaccos cardiovascular toxicity extends beyond inhalation, implicating oral exposure as a driver of systemic inflammation and atherogenesis. Novelty and SignificanceO_ST_ABSWhat Is Known?C_ST_ABSO_LICigarette smoking (CS) is a major risk factor for atherosclerosis, driving systemic inflammation and innate immune activation. C_LIO_LINeutrophils and monocytes contribute to plaque progression, but the upstream mechanisms by which CS exacerbates their pathogenic roles remain incompletely understood. C_LIO_LIS100A8/A9 levels correlate with neutrophilia and cardiovascular risk in smokers, but their functional role in lesion biology is not fully defined. C_LI What New Information Does This Article Contribute?O_LIIdentifies S100A8/A9 as a key mediator linking CS exposure to enhanced medullary myelopoiesis, neutrophilia, and increased lesional infiltration of inflammasome-primed myeloid cells. C_LIO_LIDemonstrates that neutrophil-derived IL-1{beta} impairs macrophage efferocytosis by downregulating phagocytosis receptors, thereby promoting plaque vulnerability. C_LIO_LIReveals that CS drives atherosclerosis even in the absence of lipid perturbations or overt pulmonary injury, highlighting a novel oral exposure-vascular axis of disease propagation. C_LI

immunology↗

Tomato Omics Research: Mapping Bibliometric Footprints of Global Research Trends, Collaboration Networks, and Impact Trajectories

Tomato is a globally vital crop and model system for fleshy fruit development, with profound agricultural and economic significance. Omics-based tomato research has revolutionized understanding of fruit quality traits, disease resistance mechanisms, and stress tolerance pathways reflecting insights for breeding innovations to address food security challenges. This bibliometric analysis on tomato omics delivered crucial insights into the evolution and impact of tomato omics research over two decades. Examining 1,702 Scopus-indexed publications, we have shown a remarkable acceleration in research output after 2017, signifying the fields growing significance. Our findings revealed that Biochemistry, Genetics and Molecular Biology dominated the landscape with 1,054 publications, establishing the molecular foundation for tomato research. It identified key global research hubs, with the United States (450 publications) leading, followed by China (310) and Italy (171), while mapping eight distinct International collaboration networks that drive innovation. Through citation analysis, we have pinpointed transformative contributions in microRNA research and genome sequencing, with the fields most influential paper garnering 2,570 citations. Co-authorship network visualization exposed 25 research clusters among 8,103 authors, highlighting prolific contributors including Fernie A.R. (39 publications) and Lucini L. (26). The keyword co-occurrence mapping revealed critical research priorities centered on stress responses, fruit quality, and plant immunity, with "Frontiers in Plant Science" emerging as the fields premier publication venue (92 articles). Our analysis provided a roadmap of tomato omics research progression, offering strategic value for prioritization, collaboration development, and funding allocation to address pressing challenges in global food security and crop improvement.

plant biology↗

Proteomic characterisation of the early rheumatoid arthritis-cardiovascular disease multimorbid axis.

BackgroundInflammation contributes to the increased risk of cardiovascular disease (CVD) observed in people with rheumatoid arthritis (RA), with increased prevalence observed from time of diagnosis. Subclinical vascular and myocardial abnormalities can be detected with cardiovascular magnetic resonance (CMR) imaging in otherwise low risk individuals. Identifying associated circulating markers could enable diagnostics and implicate biological pathways of RA-CVD. The studys objective was to identify blood-based proteins associated with CMR measures of vascular and myocardial abnormality and associated inflammatory and/or cardio-metabolic pathways in a new-onset RA cohort. MethodsSerum samples (baseline/pre-treatment, N = 75 and year 1, N = 71) from CADERA (Coronary Artery Disease Evaluation in Rheumatoid Arthritis) participants, a subgroup of a randomised controlled trial, who underwent CMR, were used to measure 334 proteins across 4 pre-defined Olink panels (Inflammation, Cardiovascular-II, Cardiovascular-III, Cardiometabolic). Bayesian mixed effects regression analyses, unsupervised hierarchical clustering and protein network analyses were applied. Normalised protein expression from 334 Olink proteins were used as exposures in the regression analyses. CMR measures of vascular stiffness (aortic distensibility and stiffness index) and myocardial tissue characteristics (native T1, myocardial extracellular volume and late gadolinium enhancement) were each used as individual outcomes in regression analyses. Associations were considered significant at 95% threshold for credible intervals. An expanded physical protein-protein interaction (PPI) network created using the significant (seed) proteins was subjected to topological and enrichment analysis to identify enriched biological pathways. Results54/334 proteins were associated significantly with CMR measures at baseline (7 - vascular; 48 - myocardial tissue characteristics; Coagulation factor 11 with both). Two proteins, TNFSF13B (B-cell activating factor) and CRTAC1, were associated with CMR measures at baseline, were sensitive to change over time and co-varied with changes in CMR measure. Topological analysis of expanded PPI network revealed GRB2 as most connected (degree score=64; closeness score=118.83) and four key signalling pathways, including JAK-STAT and EGFR tyrosine kinase inhibitor resistance, emerged as significant. ConclusionsThis first proteomic study of treatment-naive early RA and subclinical cardiovascular pathology identifies proteins that could aid diagnostic test development and implicates signalling pathways in the RA-cardiovascular axis to inform on our understanding of the basis of RA-CVD.

systems biology↗

Comparative proteomics uncovers distinct biomarkers, protein networks and defense responses in tomato during beneficial and pathogenic microbial interactions

The molecular mechanisms underlying plant responses to beneficial and pathogenic microbial interactions has been uncovered in tomato at the proteomic level. Our study employed LC-MS- based proteomics to investigate differential protein regulation in tomato plants during interactions with beneficial bacteria (Bacillus subtilis BV7) versus pathogenic fungus (Alternaria solani). Comparative analysis revealed distinct protein signatures characterizing each interaction: 232 unique proteins in BV7-treated plants versus 96 in pathogen-infected plants, with 54 proteins shared between treatments. BV7 inoculation enhanced proteins involved in photosynthesis and primary metabolism, with PSI-K emerging as the top biomarker (score 2.53), while pathogen infection triggered focused defense responses with Cytochrome b559 (score 2.38) as the key biomarker. Metabolic pathway analysis demonstrated that BV7 uniquely enhanced vitamin metabolism (thiamine, riboflavin, folate) and energy production pathways, while pathogen infection activated defense-related phenylpropanoid biosynthesis. Analysis of defense enzymes showed pathogen infection induced highest activities of PAL (39.4{+/-}0.46 U h-1 g-1 fw), SOD (29.9{+/-}0.94 U mg-1 protein), POD (3.18{+/-}0.07 g g-1 fw min-1), APx (15.58{+/-}0.23 U mg-1 protein), and GPx (71.51{+/-}0.7 U mg-1 protein), while BV7 maintained moderate enzyme levels, suggesting balanced growth-defense responses. The shared proteins between treatments indicate a common molecular framework potentially contributing to induced systemic resistance. These findings provide novel insights into plant-microbe interactions at the molecular level, identifying specific protein biomarkers and metabolic pathways that could be targeted for enhancing crop productivity and disease resistance. The results have significant implications for developing biological control strategies and improving sustainable agricultural practices.

plant biology↗

MLC1 alteration in iPSCs give rise to disease-like cellular vacuolation phenotype in the astrocyte lineage

BackgroundMegalencephalic leukoencephalopathy with subcortical cysts (MLC), a rare and progressive neurodegenerative disorder involving the white matter, is not adequately recapitulated by current disease models. Somatic cell reprogramming, along with advancements in genome engineering, may allow the establishment of in-vitro human models of MLC for disease modeling and drug screening. In this study, we utilized cellular reprogramming and gene-editing techniques to develop induced pluripotent stem cell (iPSC) models of MLC to recapitulate the cellular context of the classical MLC-impacted nervous system. MethodsSomatic cell reprogramming of peripheral patient-derived blood mononuclear cells (PBMCs) was used to develop iPSC models of MLC. CRISPR-Cas9 system-based genome engineering was also utilized to create the MLC1 knockout model of the disease. Directed differentiation of iPSCs to neural stem cells (NSCs) and astrocytes was performed in a 2D cell culture format, followed by various cellular and molecular biology approaches, to characterize the disease model. ResultsMLC iPSCs established by somatic cell reprogramming and genome engineering were well characterized for pluripotency. iPSCs were subsequently differentiated to disease-relevant cell types: neural stem cells (NSCs) and astrocytes. RNA sequencing profiling of MLC NSCs revealed a set of differentially expressed genes related to neurological disorders and epilepsy, a common clinical finding within MLC disease. This gene set can serve as a target for drug screening for the development of a potential therapeutic for this disease. Upon differentiation to the more disease relevant cell type-astrocytes, MLC-characteristic vacuoles were clearly observed, which were distinctly absent from controls. This emergence recapitulated a distinguishing phenotypic marker of the disease. ConclusionThrough the creation and analyses of iPSC models of MLC, our work addresses a critical need for relevant cellular models of MLC for use in both disease modeling and drug screening assays. Further investigation can utilize MLC iPSC models, as well as generated transcriptomic data sets and analyses, to identify potential therapeutic interventions for this debilitating disease.

cell biology↗

Impact of Paraben on Uterine Collagen: An Integrated and Targeted Correlative Approach Using Second Harmonic Generation Microscopy, Nanoindentation, and Atomic Force Microscopy

This study investigates the structural and mechanical changes in uterine collagen following exposure to propylparaben (PP), using a combined methodology of Second Harmonic Generation (SHG) microscopy, Nanoindentation (NI), and Atomic Force Microscopy (AFM). SHG analysis identified significant disorganization in collagen fibril orientation in the circumferential layer and heterogeneous distribution of regions with elevated forward to backward ratios (F/B) across all uterine layers due to PP exposure. High F/B can indicate multiple potential fibril-level changes like thickened fibrils, higher crosslinking, fibril disorganization - changes not fully decipherable by SHG alone. Recognizing this limitation, the study employs NI and AFM to provide complementary mechanical and nanoscale insights. NI revealed increased indentation modulus in the exposed uteri, suggesting increased stiffness. Co-registration of the indentation response with SHG parameters uncovered that elevated F/B regions show enhanced mechanical stiffness, suggesting a fibrotic transformation following PP exposure. AFM was specifically performed on regions identified by SHG as having low or high F/B, providing the necessary nanoscale resolution to elucidate the structural changes in fibrils that are likely responsible for the observed alterations. This approach confirmed the presence of disordered and entangled collagen fibrils in the circumferential layer in all regions and an increase in fibril diameter in the high F/B regions in the exposed uteri. Together, these findings demonstrate significant alterations in collagen architecture due to PP exposure, revealing disruptions at both the fiber and fibril levels and highlighting the potential for broader applications of the multi-scale, multi-modal approach in collagenous tissue studies.

bioengineering↗

Long-term dietary exposure to a mixture of phthalates enhances estrogen and beta-catenin signaling pathways, leading to endometrial hyperplasia in mice

Phthalates, synthetic chemicals widely utilized as plasticizers and stabilizers in various consumer products, present a significant concern due to their persistent presence in daily human life. While past research predominantly focused on individual phthalates, real-life human exposure typically encompasses complex mixtures of these compounds. The cumulative effects of prolonged exposure to phthalate mixtures on uterine health remain poorly understood. To address this knowledge gap, we conducted studies utilizing adult female mice exposed to a phthalate mixture for 6 and 12 months through ad libitum chow consumption. We previously reported that continuous exposure to this phthalate mixture for 6 months led to uterine fibrosis. In this study, we show that the exposure, when continued beyond 6 months to 1 year, caused fibrotic uteri to display hyperplasia with a significant increase in gland to stroma ratio. Endometrial hyperplasia is commonly caused by unopposed estrogen action, which promotes increased expression of pro-inflammatory cytokines and chemokines and proliferation of the endometrial epithelial cells. Indeed, RNA sequencing analysis revealed a marked upregulation of several estrogen-regulated genes, Wnt ligands that are involved in oncogenic pathways, as well as chemokines, in phthalate-exposed uterine tissues. Consequently, the exposed uteri exhibited increased proliferation of endometrial epithelial cells, and a heightened inflammatory response indicated by extensive homing of macrophages. Further studies revealed a marked enhancement of the Wnt/{beta}-Catenin signaling pathway, potentially contributing to the development of endometrial hyperplasia. Collectively, this study underscores the significance of understanding the exposure to environmental factors in the pathogenesis of endometrial disorders.

physiology↗

Abnormal activation of the mineralocorticoid receptor in the aldosterone-sensitive distal nephron contributes to fructose-induced salt-sensitive hypertension

Fructose high-salt (FHS) diets increase blood pressure (BP) in an angiotensin II (Ang II)-dependent manner. Ang II stimulates aldosterone release, which, by acting on the mineralocorticoid receptor (MR), regulates Na+ reabsorption by the aldosterone-sensitive distal nephron (ASDN). The MR can be transactivated by glucocorticoids, including those locally produced by 11{beta}-HSD1. The epithelial sodium channel (ENaC) is a key transporter regulated by MRs. We hypothesized that fructose-induced salt-sensitive hypertension depends in part on abnormal activation of MRs in the ASDN with consequent increases in ENaC expression. We found that aldosterone-upregulated genes in mice ASDN, significantly overlapped with 74 genes upregulated by FHS in the rat kidney cortex (13/74; p[≤]1x10-8), and that these 74 genes are prominently expressed in rat ASDN cells. Additionally, the average z-score expression of mice-aldosterone-upregulated genes is highly correlated with FHS compared to glucose high-salt (GHS) in the rat kidney cortex (Pearson correlation; r=0.66; p[≤]0.005). There were no significant differences in plasma aldosterone concentrations between the FHS and GHS. However, 11{beta}-HSD1 transcripts were upregulated by FHS (log2FC=0.26, p[≤]0.02). FHS increased BP by 23{+/-}6 mmHg compared to GHS, and blocking MRs with eplerenone prevented this increase. Additionally, inhibiting ENaC with amiloride significantly reduced BP in FHS from 148{+/-}6 to 134{+/-}5 mmHg (p[≤]0.019). Compared to GHS, FHS increased total and cleaved ENaC protein by 89{+/-}14 % (p[≤]0.03) and 47{+/-}16 % (p[≤]0.01) respectively. FHS did not change {beta}- or {gamma}-subunit expression. These results suggest that fructose-induced salt-sensitive hypertension depends, in part, on abnormal Na+ retention by ENaC, resulting from the activation of MRs by glucocorticoids.

physiology↗

Bridging fungal resistance and plant growth through constitutive overexpression of Thchit42 gene in Pelargonium graveolens

Pelargonium graveolens essential oil possesses significant attributes, known for perfumery and aromatherapy. However, optimal yield and propagation are predominantly hindered by biotic stress. All biotechnological approaches have yet to prove effective in addressing fungal resistance. The current study developed transgenic geranium bridging molecular mechanism of fungal resistance and plant growth by introducing cassette 35S::Thchit42. Furthermore, 120 independently putative transformed explants were regenerated on kanamycin fortified medium. Primarily transgenic lines were demonstrated peak pathogenicity and antifungal activity against formidable Colletotrichum gloeosporioides and Fusarium oxysporum. Additionally, phenotypic analysis revealed [~]2fold increase in leaf size and [~]2.1fold enhanced oil content. To elucidate the molecular mechanisms for genotypic cause, De novo transcriptional profiles were analyzed to indicate that the auxin-regulated longifolia gene is accountable for augmentation in leaf size, and ZF RICESLEEPER attributes growth upregulation. Collectively, data provides valuable insights into unravelling the mechanism of Thchit42-mediated crosstalk between morphological and chemical alteration in transgenic plants. This knowledge might create novel opportunities to cultivate fungal-resistant geranium throughout all seasons to fulfil demand.

plant biology↗

AlzGenPred: A CatBoost based method using network features to classify the Alzheimers Disease associated genes from the high throughput sequencing data

Background and ObjectiveAD is a progressive neurodegenerative disorder characterized by memory loss. Due to the advancement in next-generation sequencing technologies, an enormous amount of AD-associated genomics data is available. However, the information about the involvement of these genes in AD association is still a research topic because all these algorithms are based on statistical techniques. Therefore, AlzGenPred is developed to identify the AD-associated genes from a large set of data. MethodsTo develop the AlzGenPred, we have compiled a benchmark dataset consisting of 1086 AD and non-AD genes and used them as positive and negative datasets. We have generated several features including the fused features and evaluated them through machine learning methods. Then hyperparameter tuning approach was also applied and the final model was selected. The proposed method was validated by using the AlzGene and transcriptomics datasets and proposed as a standalone tool. ResultsTotal 13504 features belonging to eight different encoding schemes of these sequences were generated and evaluated by using 16 ML algorithms. It reveals that network-based features can classify AD genes while sequence-based features are not able to classify them. Then we generated 24 different fused features (6020 D) using sequence-based features and fed them into a two-step lightGBM-based recursive feature selection method. It increased up to 5-7% accuracy. After that selected eight fused features with CKSAAP were used for the hyperparameter tuning. They showed <70% accuracy. Therefore, network-based features were used to generate the CatBoost-based ML method called AlzGenPred with 96.55% accuracy and 98.99% AUROC. The developed method is tested on the AlzGene dataset where it showed 96.43% accuracy. Then the model is validated using the transcriptomics dataset also. ConclusionThe validation of AlzGenPred using the AlzGene dataset and transcriptomics dataset obtained from Human, mouse, and ES-derived neural cells revealed that it can classify the omics data and can sort the AD-associated genes. These predicted genes can be directly used in the wet lab for further testing which will reduce labor cost and time expenses. The AlzGenPred is developed as a standalone package and is available for users at https://www.bioinfoindia.org/alzgenpred/ and https://github.com/shuklarohit815/AlzGenPred.

bioinformatics↗

Developmental pyrethroid exposure disrupts molecular pathways for circadian rhythms and synaptic plasticity in mouse brain.

Neurodevelopmental disorders (NDDs) are a category of pervasive disorders of the developing nervous system with few or no recognized biomarkers. A significant portion of the risk for NDDs, including attention deficit hyperactivity disorder (ADHD), is contributed by the environment, and exposure to pyrethroid pesticides during pregnancy has been identified as a potential risk factor for NDD in the unborn child. We recently showed that low-dose developmental exposure to the pyrethroid pesticide deltamethrin in mice causes male-biased changes to ADHD- and NDD-relevant behaviors as well as the striatal dopamine system. Here, we used an integrated multiomics approach to determine the broadest possible set of biological changes in the mouse brain caused by developmental pyrethroid exposure (DPE). Using a litter-based, split-sample design, we exposed mouse dams during pregnancy and lactation to deltamethrin (3 mg/kg or vehicle every 3 days) at a concentration well below the EPA-determined benchmark dose used for regulatory guidance. We raised male offspring to adulthood, euthanized them, and pulverized and divided whole brain samples for split-sample transcriptomics, kinomics and multiomics integration. Transcriptome analysis revealed alterations to multiple canonical clock genes, and kinome analysis revealed changes in the activity of multiple kinases involved in synaptic plasticity, including the mitogen-activated protein (MAP) kinase ERK. Multiomics integration revealed a dysregulated protein-protein interaction network containing primary clusters for MAP kinase cascades, regulation of apoptosis, and synaptic function. These results demonstrate that DPE causes a multi-modal biophenotype in the brain relevant to ADHD and identifies new potential mechanisms of action. NEW & NOTEWORTHYHere, we provide the first evidence that low-dose developmental exposure to the pyrethroid pesticide, deltamethrin, results in molecular disruptions in the adult mouse brain in pathways regulating circadian rhythms and neuronal growth (MAP kinase). This same exposure causes a neurodevelopmental disorder (NDD) relevant behavioral changes in adult mice, making these findings relevant to the prevention of NDDs.

neuroscience↗

A new antibiotic from an uncultured bacterium binds to an immutable target

Antimicrobial resistance is a leading mortality factor worldwide. Here we report the discovery of clovibactin, a new antibiotic, isolated from uncultured soil bacteria. Clovibactin efficiently kills drug-resistant bacterial pathogens without detectable resistance. Using biochemical assays, solid-state NMR, and atomic force microscopy, we dissect its mode of action. Clovibactin blocks cell wall synthesis by targeting pyrophosphate of multiple essential peptidoglycan precursors (C55PP, Lipid II, LipidWTA). Clovibactin uses an unusual hydrophobic interface to tightly wrap around pyrophosphate, but bypasses the variable structural elements of precursors, accounting for the lack of resistance. Selective and efficient target binding is achieved by the irreversible sequestration of precursors into supramolecular fibrils that only form on bacterial membranes that contain lipid-anchored pyrophosphate groups. Uncultured bacteria offer a rich reservoir of antibiotics with new mechanisms of action that could replenish the antimicrobial discovery pipeline.

microbiology↗

Chronic exposure of mice to phthalates enhances TGF beta signaling and promotes uterine fibrosis

Phthalates are synthetic chemicals widely used as plasticizers and stabilizers in various consumer products. Because of the extensive production and use of phthalates, humans are exposed to these chemicals daily. While most studies focus on a single phthalate, humans are exposed to a mixture of phthalates on a regular basis. The impact of continuous exposure to phthalate mixture on uterus is largely unknown. Thus, we conducted studies in which adult female mice were exposed for 6 months to 0.15 ppm and 1.5 ppm of a mixture of phthalates containing di(2-ethylhexyl) phthalate, di-iso-nonyl phthalate, benzyl butyl phthalate, di-n-butyl phthalate, diisobutyl phthalate, and diethyl phthalate via chow ad libitum. Our studies revealed that consumption of phthalate mixture at 0.15 ppm and 1.5 ppm for 6 months led to a significant increase in the thickness of the myometrial layer compared to control. Further investigation employing RNA-sequencing revealed an elevated transforming growth factor beta (TGF-{beta}) signaling in the uteri of mice fed with phthalate mixture. TGF-{beta} signaling is associated with the development of fibrosis, a consequence of excessive accumulation of extracellular matrix components, such as collagen fibers in a tissue. Consistent with this observation, we found a higher incidence of collagen deposition in uteri of mice exposed to phthalate mixture compared to unexposed controls. Second Harmonic Generation imaging showed disorganized collagen fibers and an increase in uterine stiffness upon exposure to phthalate mixture. Collectively, our results demonstrate that chronic exposure to phthalate mixture can have adverse effects on uterine homeostasis.

physiology↗