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Das, S.

Publications and source records attributed to Das, S..

At least 55 records · Page 3Linked to original sources

Implementing considered elements of standardisation for Time Kill Curve experiments across multiple sites: A European collaboration perspective

SynopsisO_ST_ABSBackgroundC_ST_ABSThe main advantages of Time Kill Curves (TKCs) in antimicrobial drug development are the ability to track bacterial kill and regrowth over time and with varying drug concentrations. Whilst there are guideline documents in place, such as M26-A in CLSI, there remains scope for individual laboratory differences in practice. Here we evaluated several factors which potentially influenced data generated in TKCs. MethodsFirstly, E. coli ATCC 25922 was used to determine optimum sampling volume, culture vessel volume, CFU enumeration variance factors and static versus agitated cultures in a single laboratory. Secondly, a ring test comprising of TKCs was performed by six laboratories focusing on: standardised inoculum, static culture and two culture vessel sizes 10 mL and 200 {micro}L. Data analysis was performed to determine consistency within centres and between them. ResultsConsistently accurate inocula could be achieved by use of: larger sampling volumes between 100 {micro}L > 20 mL; larger culture vessels volumes (10 mL > 100 {micro}L) and higher inocula (10 8 > 1.5x10 5 CFU). Culture agitation during the TKC experiment resulted in reduced killing compared to static cultures. Reproducibility of TKCs was best between centres when they were performed in 10 mL culture vessels. There was more variability per site when performing TKC in 96 well trays. ConclusionsTechnical factors such as preparation of inocula, agitation, vessel size and enumeration of cultures are important variables in performing TKCs that need to be standardised in drug development programmes involving multiple laboratory centres.

microbiology↗

Multi-platform reassessment of human mitochondrial DNA methylation reveals signals consistent with technical artifacts

The existence and functional relevance of mitochondrial DNA methylation remain controversial. Here, we systematically profiled cytosine methylation and hydroxymethylation across human brain and blood tissues spanning healthy and malignant states using orthogonal sequencing approaches that avoid chemical conversion during library preparation. While nuclear DNA exhibited canonical methylation patterns, mitochondrial DNA consistently showed negligible signal, indistinguishable from background technical noise. By mapping cytosine-guanine sites between mitochondrial DNA and nuclear-embedded mitochondrial sequences, we demonstrate the potential of these nuclear counterparts to confound not only cytosine methylation but also hydroxymethylation measurements, corroborating and extending prior findings implicating nuclear contamination as a potential source of apparent mitochondrial epigenetic signals. Additional technical factors that inflate apparent mtDNA methylation signals were identified, including sequence context biases, flow cell chemistries, and coverage-dependent discrepancies between the heavy and light strands. Collectively, these results provide convergent evidence against the presence of biologically meaningful cytosine methylation or hydroxymethylation in mitochondrial DNA. These findings caution against interpreting apparent mtDNA methylation signals in human adult tissues as meaningful without rigorous orthogonal validation and comprehensive consideration of technical and analytical confounding factors.

bioinformatics↗

Tube to Tumour: an integrative epigenomic analysis of DNA methylation in high-grade serous ovarian cancer and precursor serous tubal intraepithelial carcinoma

Serous tubal intraepithelial carcinoma (STIC) is a known precursor of high-grade serous ovarian cancer (HGSOC). Yet, molecular events driving progression from STIC to HGSOC remain poorly defined. Aberrant DNA methylation is a hallmark of cancer, yet its role in early HGSOC remains unclear. We performed a comprehensive meta-analysis of publicly available Illumina Infinium DNA methylation EPIC array datasets assessing 255 samples comprising STIC, HGSOC, and histologically normal fallopian tube tissues. We mapped DNA methylation alterations during early tumorigenesis, identified conserved methylation patterns across STIC and HGSOC, and assessed RNA-sequencing data to define transcriptional consequences within genomic and epigenomic landscapes. STIC and HGSOC exhibited widespread DNA hypomethylation relative to normal tissue, accompanied by focal hypermethylation in CpG islands and 5' regulatory regions. DNA Hypomethylation intensifies during progression from STIC to HGSOC, particularly in cis-regulatory enhancer domains and intergenic regions. We identified 11,660 CpG sites and 447 genomic regions with conserved DNA methylation patterns across STIC and HGSOC. Within these, 70 genes showed coordinated DNA methylation and expression changes, including TRIM15, NKAPL, and RIPPLY3. These findings reveal that epigenetic remodelling occurs in STIC lesions, prior to malignant transformation. DNA methylation alterations at regulatory regions may drive invasion and offer novel avenues for early detection and targeted intervention.

Cancer Biology↗

Is there a need to implement standardisation into in vitro antimicrobial evaluation systems? A European collaboration perspective

SynopsisO_ST_ABSBackgroundC_ST_ABSTime kill curve (TKC) assessments are an essential step in the study of an antimicrobials pharmacodynamic characteristics. Surprisingly TKCs have not be formally standardised, therefore there remain concerns that different testing centres/methodologies may produce different results. Six centres participating in Gram-negative-Antibiotics NOW (GNA-NOW) consortium measured a series of TKCs with meropenem against E. coli to establish: Same-day (SD) vs different-day (DD) replication per centre (intra-site), and centre to centre (inter-site) correlations. MethodsMeropenem was tested against three strains of E. coli (ATCC 25922; ESBL producer C1.55; OXA-48 producer C1.62). An inoculum of 1.5x106 CFU was specified with meropenem concentrations of x0, x1 to x16 MIC; and sampling assessment of bacterial density was determined at 0-24h. Experiments were performed in triplicate, aerobically at 37{degrees}C. Centre-specific methodology was collected. Meropenem, media, bacterial strains, were shipped from one central laboratory to participating laboratories. ANOVA and Friedman tests were used to assess SD, DD and between centre replications. ResultsAssessment of the methodologies between centres revealed many differences, including bacterial inoculum, meropenem preparation, volume of TKC vessel, vessel materials, agitation vs static cultures and sampling volumes. Intra-centre SD and DD analysis for all strains were generally associated with P>0.05 suggesting consistency. Inter-centre SD and DD comparisons resulted in P<0.05, indicating variable total bacterial load measurement between centres. ConclusionsTKC methodologies varied between different centres, and while intra-centre comparison of SD and DD were generally consistent, inter-centre comparisons were not. Standardisation of TKC methodologies is required.

microbiology↗

Comparison of a Novel Real-World Speech in Noise Auditory Attention Task to Standard Clinical Audiological Metrics

Pure tone audiometry (PTA) remains the clinical standard for evaluating hearing ability, yet individuals with similar audiometric profiles often exhibit substantial variability in their capacity to understand speech in everyday listening environments. Growing evidence suggests this variance is related to contributions from cognitive ability and auditory processing that standard threshold measures do not capture. To investigate how PTA, cognitive factors, and demographics such as age jointly predict real-world speech perception, 116 veteran adults 20-70 years old spanning a range of normal to moderate sensorineural hearing losses completed a spatial auditory attention task. Target color words were embedded within naturalistic short-story narratives presented under two conditions: a mono-talker speech-in-quiet (SIQ) condition and a dual-talker speech-in-noise (SIN) condition with a spatially separated competing narrative. Behavioral performance was quantified via color word hit accuracy, reaction time, and comprehension question accuracy. Participants also completed pure tone audiometry, the Montreal Cognitive Assessment (MoCA), and the Speech, Spatial and Qualities of Hearing Scale (SSQ12). Mixed-effects regression models were used to evaluate the contributions of PTA, age, cognitive ability, and self-reported hearing difficulty (SSQ12) to task performance across conditions. Results demonstrate a complex interplay between age, PTA, MoCA, and/or listening condition (SIQ vs. SIN) in predicting identification accuracy, reaction time, and comprehension. Age and condition significantly predicted hit accuracy and reaction time, with older participants showing improved accuracy in quiet but declining accuracy and slower responses in noise. PTA did not emerge as a significant main effect predictor but interacted with cognitive ability and condition to modulate performance, in some cases exhibiting a paradoxical inverse relationship with accuracy dependent on MoCA score. MoCA scores significantly predicted comprehension across conditions, and SIN hit accuracy was positively correlated with SSQ12 scores, validating the task against participants real-world listening experiences. These findings highlight the importance of incorporating cognitive screening and ecologically valid speech perception tasks into audiological assessment to better identify individuals at risk for functional hearing impairment in complex listening environments.

neuroscience↗

Spike antibodies targeting GRP78 predispose to cardiovascular complications compared to Dengue

One major aftermath of COVID-19 pandemic is cardiovascular consequences. SARS-CoV-2 binds to ACE2 and downregulates vasodilation. Dengue favors hypotension by weakening endothelial glycocalyx leading to plasma leakage. C1q levels, immune complexes (ICs), and proteomic profiles in serum samples from 52 COVID-19 and 19 pre-pandemic Dengue cases were studied. Unlike Dengue, COVID-19 serums showed elevated coagulation proteins promoting vaso-occlusion and peripheral artery diseases. The stress-induced chaperone and atherosclerosis marker, GRP78 (gene/ protein) was found upregulated upon SARS-CoV-2 spike expression in cardiac/ lung cell lines. Elevated GRP78 levels were also observed in serum samples from COVID-19-diagnosed individuals and subjects with myocardial infarction (MI) in post COVID-era. Surprisingly, spike antibodies (Abs) showed cross-binding to GRP78 and possibly contributed to the observed higher-level ICs in COVID-19 serums (cardiovascular embolism?). Co-localization studies showed that spike Abs (analogous to pro-atherosclerotic GRP78 auto-Abs) could directly bind to upregulated cellular GRP78 (type II hypersensitivity?). Both pathways could worsen vascular injury and atherosclerosis, leading to cardiac complications in COVID-19 cases with narrowed vessels.

microbiology↗

Influenza virus Non Structural protein 1 (NS1) Chaperones Nucleoprotein (NP) Oligomerization to Coordinate Ribonucleoprotein Assembly and Genome Replication

Influenza virus nucleoprotein (NP) co-transcriptionally enwraps viral genomic/antigenomic RNAs to assemble viral ribonucleoprotein complexes (RNPs), while the non-structural protein-1 (NS1) is classically recognized as an antagonist of host antiviral responses. Although NP-NS1 interaction has long been reported, the molecular basis of this protein-protein interaction and its relevance in the virus life cycle remain elusive. Here, we define the NP-NS1 interaction interface and uncover a noncanonical role of NS1 in regulating RNP assembly and viral genome replication. Using integrated biochemical, biophysical, and structural analyses, we demonstrate that the RNA-binding domain (RBD) of NS1 directly engages the NP tail-loop, conferring high affinity for monomeric NP. Functional assays reveal that a cytoplasm-restricted NS1 variant acts as an NP-specific chaperone by stabilizing monomeric NP through sequestration of its intrinsically flexible tail-loop and by scaffolding NP-NP interactions. During influenza virus infection, phosphorylation at the homotypic interface restricts NP in a replication-competent monomeric state. Cytoplasmic NS1 recruits these phosphorylated monomeric NPs into assembling RNPs, thereby facilitating viral genome replication and virus propagation. Collectively, our findings establish NS1 as a selective cytoplasmic chaperone of NP and reveal a novel regulatory axis governing influenza virus RNP biogenesis and replication.

molecular biology↗

Manipulation of rhizosphere microbiome by Microbacterium sp. GB16_1_BI to promote plant growth.

Plant growth promoting microbes enhance developmental progression of the host by influencing its nutrient availability or by deploying secondary metabolites responsible for manipulating the hormonal crosstalk. Microbacterium bengalense sp. nov. GB16_1_BI (Accession number: SRX9280401), a newly identified ammonium releasing Actinomycetota, could enhance plant growth by manipulating rhizosphere bacteria. Amplicon sequencing of the 16S rRNA V3-V4 region from the rhizosphere of the black rice (Chakhao Poireiton) showed that GB16_1_BI could inhibit most bacteria. However, GB16_1_BI inoculation encouraged the growth of rare bacteria specific to waterlogged rice rhizosphere. Analysis of the OTUs using PICRUSt2 (Phylogenetic investigation of communities by reconstruction of unobserved states) showed increased abundance in the marker genes for nitrogen cycling (nifH, nrfA and nrt) but not for nifD or nifK which was also reflected in the ANOSIM analysis in the OTUs of the N-fixing bacteria. Marker genes for methane metabolism (comA, comB, cofG and cofH) were also more abundant in the inoculated plants than the control; however, ANOSIM studies did not support this observation in the OTUs of methane cycling bacteria. Both Methylosinus and Methylocystis, the two most abundant methanotrophic OTUs, are also known to be nitrogen fixers. Hence, GB16_1_BI could influence plant growth predominantly by manipulating nitrogen cycling microbes. The genome sequence as well as untargeted metabolome analyses of GB16_1_BI showed abundance of secondary metabolites with probable antimicrobial activity. GB16_1_BI could utilize varied carbohydrates and amino acid as energy source and form persister-like cells may help it to survive in the soil in absence of the host plant.

microbiology↗

Histone quality control by prokaryotic ClpP/ClpR regulates the eukaryotic mitotic cell cycle in malaria parasites

In Plasmodium falciparum, DNA replication and asynchronous nuclei formation precede cytokinesis during intraerythrocytic schizogony. Inhibition of fatty acids (FAs) import and impaired membrane biogenesis led to the arrest of mitosis through the inhibition of DNA replication and nuclei formation. On the iRBC surface, parasite ribosomal protein P2 (PfP2) complex mediated FAs import and membrane biogenesis, seemingly prior events before the commitment for DNA replication and nuclei formation. The inhibition of FAs import led to the degradation of histones by the evolutionarily conserved bacterial serine protease ClpP/ClpR in the parasite nucleus. Noncanonical arginine hyperphosphorylation by a novel arginine kinase in the nucleus was subjected for proteostasis and marks histones for degradation by ClpP/ClpR machinery. Inhibition of de novo FAs biosynthesis by an anti-cancer drug, Cerulenin and C75, in HEK293T and HCT116 carcinoma mammalian cells showed histone degradation. Lipid (L) induced histone proteostasis by ClpP/ClpR, seemingly an indispensable L-checkpoint before mitotic commitment.

cell biology↗

An optimized workflow for spatial transcriptomics across early development in Xenopus

How gene expression patterns change spatially as the embryo transitions from simple to complex structures remains a major developmental biology question. Recently developed imaging-based spatial transcriptomics (ST) enable mapping expression of multiple gene at a single-cell resolution. Although Xenopus is a key model in embryology there is no established ST pipeline, and commercially available techniques face many challenges (sample preparation, probe design, cell segmentation). Furthermore, the highly diverse cell shapes and sizes across developmental stages and between different tissues represent major hurdles to accurately defining cells. Here, we describe an optimized workflow for ST in blastula-to-tailbud-stage frog embryos using Merscope, commercial MERFISH (Multiplexed Error-Robust Fluorescence In Situ Hybridization) originally designed for standard mammalian tissues. With stringent quality control and tailored computational pipelines, we optimize this technology for robust, semi-quantitative profiling of spatial transcriptomic landscapes in non-mammalian embryos. Reliable tissue preservation and cell-segmentation enable high-resolution mapping of gene expression during the development of a complex multi-tissue organization. This versatile strategy applies broadly to various dynamic systems, from embryos of various model organisms to complex and heterogeneous organs in mammals. Summary statementThis Single-cell Spatial Transcriptomics pipeline and reference atlas in Xenopus - a model organism in embryology - overcome technical challenges and resolve dynamic changes in patterning during development.

developmental biology↗

PFAS triggers a SpoT-associated metabolic switch that promotes persister-like phenotype in Salmonella Typhi

Per- and polyfluoroalkyl substances (PFAS) are new pollutants in the environment whose effects on bacterias physiology is not well understood. In this study, we show that exposure to PFAS causes membrane depolarization in Salmonella enterica serovar Typhi. This works as a metabolic uncoupler that breaks down proton motive force without immediately killing the cells. This disturbance results in a significant elevation of intracellular NADH and NAD levels while preserving redox equilibrium, signifying an augmented metabolic flux. At the same time, we see that {beta}-oxidation pathways are turned on, which suggests that the cells are shifting toward breaking down fats to make up for the lack of energy. Even though there are more reducing equivalents, ATP levels go down, which is what happens when respiration is uncoupled. This puts the cells in a state of "pseudo-starvation." This metabolic stress triggers the SpoT-dependent stringent response, leading to the accumulation of (p)ppGpp. Genetic analysis employing {Delta}relA and {Delta}relA{Delta}spoT mutants confirm that SpoT is necessary for this adaptive response. Functionally, PFAS-treated populations show an enhanced proportion of persister-like cells, which connects exposure to environmental pollutant in the environment to antibiotic tolerance. Our findings reveal a previously unidentified mechanism by which PFAS alters bacterial metabolism and stress responses, facilitating persistence through membrane depolarization, metabolic reconfiguration, and stringent response activation. This study underscores the potential influence of environmental pollutants on bacterial survival mechanisms and antibiotic resistance.

microbiology↗

Herbivory-induced alterations in cytosolic proteins of pigeon pea (Cajanus cajan) leaves

Insect herbivory triggers cytosolic proteome reprogramming by activating defense pathways and modulating key metabolic processes. We found that simulated herbivory in pigeon pea (Cajanus cajan) induced reactive oxygen species (ROS) production and molecular alterations within 12 hours (h) of post treatment. We compared the leaf proteome profiles of two cultivated genotypes, ICPL 332 (moderately resistant) and ICPL 87 (susceptible), using two-dimensional polyacrylamide gel electrophoresis (2D-PAGE) coupled with mass spectrometry (MS). More than 220 protein spots were detected in ICPL 332 and over 200 in ICPL 87. Comparative analysis revealed 75 differentially accumulated proteins (DAPs), of which 40 were consistently reproducible across biological replicates. These included 11 unique to ICPL 87, 9 unique to ICPL 332, and 10 common to both genotypes. Among the shared DAPs, ICPL 332 showed five upregulated and five downregulated, whereas ICPL 87 exhibited only two upregulated and eight downregulated. Functional categorization grouped DAPs into primary metabolism, stress response, and growth and development. Proteins related to primary metabolism were largely downregulated in both genotypes, while stress-associated proteins exhibited substantial downregulation in ICPL 87 compared to ICPL 332. Overall, the results demonstrate proteomic adjustments underlying defense responses in pigeon pea genotypes.

plant biology↗

Vascular tree structure-based perfusion phantom fabrication using modified Hele-Shaw Cell technique

Tissue phantoms that mimic microvasculature and perfusion are essential for modelling vascular function, guiding interventions, and calibrating imaging systems, which require faithful replication of vascular geometry and flow. Conventional fabrication strategies, including wire-based molding, lithographic micromachining, and additive manufacturing, offer useful capabilities but remain constrained by predefined designs, rectangular channel cross-sections, limited scalability, and high production costs. Reliance on predefined digital vascular models restricts design flexibility and limits the ability to capture the natural variability and complexity of real vascular systems. Here, we present a lithography-free, fractal-generating approach based on a modified Lifted Hele-Shaw Cell (LHSC) technique, in which vascular networks emerge spontaneously via interfacial fluid instabilities. Unlike pre-designed methods, these structures are governed by fluid properties and flow conditions, enabling adaptive, physiologically relevant geometries with smooth Gaussian cross-sections and natural diameter tapering. We demonstrate four phantom designs: a planar vascular tree, an anatomically guided cerebral network, a retinal vascular model, and a conformable curved substrate phantom. Validation using Laser Speckle Contrast Imaging confirms structural fidelity and physiologically relevant flow consistent with Murrays law. This platform uniquely integrates realistic vascular architecture with emergent, fractal driven formation, highlighting its potential as a reproducible and biologically relevant alternative to conventional vascular phantom fabrication. Furthermore, the availability of such realistic in vitro vascular models can reduce reliance on animal experiments and contribute towards more ethical and sustainable preclinical research.

bioengineering↗

An integrated RNA-centric imaging and omics approach reveals distinct properties and composition of neuronal RNA granules

RNA granules are essential regulators of post-transcriptional gene expression, enabling mRNA transport, localization, and local translation in neurons. The localized transcriptome is diverse; however, how different mRNAs are organized into granules for efficient localization and translation remains unknown. Here, we combine real-time endogenous single RNA imaging with protein and RNA proximity labeling to investigate two distinct endogenous neuronal mRNA granule populations, Actb and Arc, in stimulated primary hippocampal neurons. Using orthogonal RNA labeling systems in a dual knock-in mouse model, we show that Actb and Arc mRNAs are packaged into spatially segregated granules with distinct trafficking dynamics, localization kinetics, and responses to synaptic stimulation. Actb granules displayed rapid and sustained localization, whereas Arc granules showed delayed, transient recruitment, consistent with their respective roles in structural and activity-dependent plasticity. Proximity labeling reveals that these granules are distinct in their mRNA composition, despite sharing core RNA-binding proteins, suggesting that shared cis-regulatory elements within mRNA 3UTR regions drive selective co-packaging of mRNAs into unique granules. Together, these findings demonstrate that neuronal mRNAs are differentially sorted into molecularly and functionally distinct granules, providing a framework for understanding how precise spatio-temporal control of mRNA localization and translation is achieved across complex neuronal arbors.

neuroscience↗

Rewiring Oncogenic Transcriptional Complexes with Domain-ALTeration Chimeras (DALTACs) in Prostate Cancer

Transcriptional addiction to the androgen receptor (AR) underlies metastatic castration-resistant prostate cancer (mCRPC), where AR maintains oncogenic programs through domain-specific interactions with the acetyltransferases p300/CBP. Here, we describe a distinct therapeutic modality, Domain-ALTerAtion Chimeras (DALTACs), that rewire endogenous protein complexes by enforcing non-native domain-domain interactions. Our first-in-class AR-p300/CBP DALTAC-1 induces synthetic proximity between the AR ligand-binding domain and p300/CBP-bromodomain, misconfiguring their native interface and locking the complex in a non-productive state. DALTAC-1 triggers a super-inhibitory effect, suppressing AR-driven transcription and proliferation more potently than combined AR and p300/CBP inhibition. Mechanistically, DALTAC-1 reprograms p300/CBP substrate engagement, abolishing the histone mark H2B N-terminal acetylation (H2BNTac) while inducing neomorphic acetylation of AR and coactivators, ultimately collapsing the AR neo-enhanceosome. Chromatin profiling revealed redistribution of AR and p300/CBP toward palindromic AREs, accompanied by disruption of cofactor and transcriptional machinery recruitment at oncogenic AR/ERG neo-enhancers. DALTAC-1 exhibits exquisite lineage selectivity, displaying potent activity in AR-p300/CBP dual-dependent cells while sparing AR-negative cells. In multiple in vivo models, DALTAC-1 induces deep and durable tumor regressions. Together, these findings establish DALTACs as a broadly applicable strategy to rewire disease-defining complexes through domain-topology alteration, expanding induced-proximity therapeutics, while DALTAC-1's precise lineage-selectivity supports its translational potential in AR-driven prostate cancer.

cancer biology↗

The association of extracellular vesicle (EV)-cargo miR-330-3p with postoperative delirium and a potential mechanism of tau phosphorylation and neuron toxicity

BackgroundPostoperative delirium (POD) is a frequent and severe neurocognitive complication following cardiac surgery, associated with poor long-term outcomes. The underlying mechanisms are unclear, and objective biomarkers are urgently needed. MethodsWe used pre- and post-operative plasma samples from 59 patients undergoing cardiac surgery in three separate studies with rigorous delirium assessment using the Confusion Assessment Method in a case-control design. Small extracellular vesicles (sEVs) were isolated from plasma, and their miRNA cargo was profiled using RNA sequencing. Target miRNAs were validated by qRT-PCR, and digital PCR (dPCR). The functional impact of the lead candidate miRNA was investigated in vitro by assessing tau phosphorylation and cell viability in HT22 neuronal cell line. ResultsThere were no differences in sEV morphology or numbers between patients with and without POD. While three candidate miRNAs were initially validated by qRT-PCR, subsequent dPCR analysis confirmed that only the perioperative change in plasma sEV-cargo miR-330-3p expression was significantly greater in patients who developed POD (n = 20) compared with those who did not (n = 20) (5.22 copies/L plasma; 95% Confidence Interval (CI), 1.187 to 9.256; p = 0.0139). Receiver operating characteristic curve analysis for this change yielded an area under the curve of 0.745 (95% CI, 0.589 to 0.901). In vitro overexpression of miR-330-3p in a neuronal cell line significantly increased the phosphorylation of tau at Ser199 (p < 0.0001) and Ser396 (p < 0.001) and reduced cell viability (p < 0.001). ConclusionsOur findings suggest that sEV-bound miR-330-3p increases in patients with POD after cardiac surgery. In vitro results suggest a potential pathogenic role for miR-330-3p, linking a systemic signal to tau-related neuronal injury. Clinical PerspectiveO_ST_ABSWhat Is New?C_ST_ABSO_LIThis study identifies a specific perioperative increase in small extracellular vesicle (sEV)-cargo miR-330-3p in patients with postoperative delirium (POD) following cardiac surgery. C_LIO_LIWe provide the first evidence that miR-330-3p directly induces tau hyperphosphorylation and reduces neuronal viability in vitro, establishing a potential mechanistic link between systemic sEV signaling and neurodegeneration. C_LI What Are the Clinical Implications?O_LIThe measurement of perioperative change in miR-330-3p could serve as an objective biological marker to assist in the early identification and risk stratification of patients at high risk for POD. C_LIO_LIThe identified miR-330-3p/tau pathway represents a potential new therapeutic target; future interventions aimed at inhibiting this specific miRNA might help prevent or mitigate POD-related neuronal injury. C_LIO_LIThese findings emphasize the importance of monitoring dynamic sEV-cargo changes to better understand and manage perioperative neurocognitive disorders. C_LI

molecular biology↗

The CLAMP-Linked Invasion Protein (CLIP) plays an essential role in Plasmodium berghei zoites

Apicomplexan parasites such as Toxoplasma and Plasmodium spp. rely on the sequential secretion of parasite apical organelles, called micronemes and rhoptries, to invade host cells. The claudin-like apicomplexan microneme protein (CLAMP) is a conserved protein that plays an essential role during host cell invasion in Toxoplasma and Plasmodium zoites. Previous studies have shown that CLAMP is essential in Plasmodium merozoites for erythrocyte invasion and also in sporozoites for the invasion of the mosquito vector salivary glands and of mammalian host hepatocytes. In Toxoplasma gondii tachyzoites, CLAMP forms a complex with two other microneme proteins, the Secreted Protein with an Altered Thrombospondin Repeat (SPATR) and the CLAMP-Linked Invasion Protein (CLIP). Both SPATR and CLIP are also expressed in Plasmodium sporozoites, and downregulation of SPATR impacts sporozoite infectivity in P. berghei. In contrast, the role of CLIP in sporozoites remains unknown. To study the function of CLIP, we used a CRISPR-assisted conditional genome editing strategy based on the dimerisable Cre recombinase in the rodent malaria model parasite P. berghei. Deletion of clip in P. berghei blood stages impaired parasite growth and prevented erythrocyte invasion by merozoites. Upon deletion of clip gene in P. berghei transmission stages, sporozoite development in mosquitoes was not affected, but invasion of the mosquito salivary glands was dramatically reduced. In addition, CLIP-deficient sporozoites were impaired in cell traversal and productive invasion of mammalian hepatocytes, associated with a defect in gliding motility, recapitulating the phenotype of CLAMP-deficient parasites. Collectively, our data demonstrate that CLIP plays an essential role in host cell invasion by P. berghei merozoites and sporozoites, and support a conserved role of the CLAMP-CLIP-SPATR complex in invasive stages of apicomplexan parasites.

microbiology↗

SUN2 mediates epigenetic remodeling to drive mechanotransduction during skin fibrosis

Fibrosis involves sustained changes in fibroblast gene expression, leading to excessive extracellular matrix (ECM) deposition and progressive tissue stiffening. Although matrix stiffness is a potent regulator of cell fate and transcription, it is not clear how nuclear mechanosensing contributes to fibrosis. Here, we define a central role for SUN2, a component of linker of nucleoskeleton and cytoskeleton (LINC) complexes, as a mediator of stiffness-dependent nuclear and chromatin responses during skin fibrosis. SUN2 transcripts are upregulated in dermal fibroblasts of patients with systemic sclerosis and Sun2 protein is elevated in fibrotic mouse skin. Nuclear size, A-type lamins and Sun2 are elevated in dermal fibroblasts plated on stiff substrates. Loss of Sun2 protects against bleomycin-induced skin fibrosis in vivo and abolishes stiffness-induced changes in nuclear size and fibrotic gene expression in vitro. Mechanistically, we identify three Sun2-dependent mechanosensitive chromatin states and show that mechanical induction of the histone methyltransferase Ezh2 requires Sun2. These findings define SUN2 as a nuclear mechanosensor that couples matrix stiffness to chromatin regulation and transcriptional programs that drive fibrosis, identifying it as a potential therapeutic target pathway in fibrotic disease.

cell biology↗