Search bioRxiv⌕ Search

Biology subjects

Mukherjee, S.

Publications and source records attributed to Mukherjee, S..

At least 109 records · Page 6Linked to original sources

A combined approach to extract rotational dynamics of globular proteins undergoing liquid-liquid phase separation

The formation of protein condensates (droplets) via liquid-liquid phase separation (LLPS) is a commonly observed phenomenon in vitro. Changing the environmental properties with cosolutes, molecular crowders, protein partners, temperature, pressure, etc. was shown to favour or disfavour the formation of protein droplets by fine-tuning the water-water, water-protein and protein-protein interactions. Therefore, these environmental properties and their spatiotemporal fine-tuning are likely to be important also in a cellular context at the existing protein expression levels. One of the key physicochemical properties of biomolecules impacted by molecular crowding is diffusion, which determines the viscoelastic behaviour of the condensates. Here we investigate the change in the rotational diffusion of {gamma}D-crystallin, undergoing LLPS in vitro in aqueous solutions in absence and presence of cosolutes. We studied its rotational dynamics using molecular dynamics simulations (MD), electron paramagnetic resonance (EPR) spectroscopy and fluorescence spectroscopy. MD simulations performed under dilute and crowded conditions show that the rotational diffusion of crystallin in water is retarded by one to two orders of magnitude in the condensed phase. To obtain the rotational dynamics in the dilute phase we used fluorescence anisotropy and to extract the retardation factor in the condensed phase we used spin-labeled {gamma}D-crystallin proteins as EPR viscosity nanoprobes. Aided by a viscosity nanoruler calibrated with solutions at increasing sucrose concentrations, we validate the rotational diffusion retardation predicted by MD simulations. This study underlines the predictive power of MD simulations and showcases the use of a sensitive EPR nanoprobe to extract the viscosity of biomolecular condensates.

biophysics↗

Enhancing NADPH to Restore Redox Homeostasis and Lysosomal Function in G6PD-Deficient Microglia

Microglia, the residential immune cells in the central nervous system (CNS) exhibited in multiple states from resting to activated, play a significant role in neurogenesis, myelination, synaptic transmission, immune surveillance, and neuroinflammation. The aggravated inflammatory response by microglia triggers the generation of superoxide, which often causes the degeneration of neurons, leading to the development of Parkinsons and Alzheimers. The oxidative stress is key to many neurological disorders, often regulated by many genes. The terminal neutralization of oxidative stress is mediated by NADPH and glutathione. The cytosolic NADPH level is majorly contributed by a key enzyme called glucose-6-phosphate dehydrogenase (G6PD). The deficiency of G6PD is associated with hemolytic anemia, diabetes, cardiovascular, autoimmune, and neurological disorders. Our recent study indicated that G6PD deficiency decreases cytosolic NADPH levels and alters redox homeostasis and lysosomal function in microglia. Therefore, replenishment of NADPH is crucial for targeting G6PD deficiency-mediated microglial dysfunctions. This research promotes alternate metabolic pathways by targeting the expression and activity of enzymes such as isocitrate dehydrogenase 1 (IDH1) and malic enzyme 1 (ME1), which are responsible for cytoplasmic NADPH production. Metabolites like citric and malic acid supplementation promote NADPH production and reduce microglial oxidative stress. Additionally, using another group of small-molecule metabolites, such as dieckol and resveratrol, enhances the expression of IDH1 and ME1 enzymes to resolve potential tissue heterogeneity. Finally, combining these metabolites supplementation increased NADPH production and restored redox homeostasis and lysosomal function in G6PD deficient microglia, indicating their further use as potential therapeutics against G6PD deficiency disorders. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=101 SRC="FIGDIR/small/607918v1_ufig1.gif" ALT="Figure 1"> View larger version (19K): org.highwire.dtl.DTLVardef@5e69f2org.highwire.dtl.DTLVardef@7d9015org.highwire.dtl.DTLVardef@17e5500org.highwire.dtl.DTLVardef@fe9bc5_HPS_FORMAT_FIGEXP M_FIG C_FIG

pharmacology and toxicology↗

Additive, substitutable, and antagonistic prey responses to feral and native predator combinations

In captive experiments of Negev Desert granivores, we investigated the ways in which combinations of feral mesocarnivores and native predators alter wild prey behavior. We hypothesized that feral mesocarnivores would have a greater impact on prey energy acquisition, reflected in foraging dynamics, than native predators. Allenbys gerbils (Gerbillus andersoni allenbyi) and greater Egyptian gerbils (Gerbillus pyramidum) were used as prey species, with feral dogs (Canis lupus familiaris), feral cats (Felis catus), barn owls (Tyto alba), and horned vipers (Cerastes gasperetti) as predators. Gerbil perceived risk was measured using optimal patch-use theory, with exposures to tethered predators occurring hourly throughout the night. Some nights, two predators were alternated every other hour. We found that human-commensal predators, particularly feral cats, induced stronger foraging than native predators, such as barn owls. Combined predators caused gerbils to decrease foraging only when a higher-risk predator was introduced, as indicated by higher giving-up densities (GUDs) for the dog and cat combination compared to the dog alone, and a nonsignificant increase compared to the cat alone. The impact of feral cats especially appears to outweigh that of native predators. This highlights the conservation challenges to arid environments where feral cats have become ubiquitous. HighlightsO_LIFeral predators, particularly cats and dogs, elicit stronger anti-predator responses in Negev Desert gerbils than native predators, significantly altering foraging behavior and habitat use. C_LIO_LIThe presence of feral predators in the Negev Desert leads to cumulative impacts on prey species, resulting in increased vigilance and reduced resource acquisition, which suggests a disruption of native predator-prey dynamics. C_LIO_LIThe studys findings emphasize the unique conservation challenges posed by human-commensal species in arid ecosystems, where limited refugia increases the predation risk from invasive and feral species. C_LIO_LIThis research demonstrates how predator-prey interactions in the arid communities tested are impacted by both additive predator effects between native predators, and between feral predators, but when combining feral predators with native ones, the effect is substitutable with feral predators disproportionately influencing prey behavior. C_LI Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=145 SRC="FIGDIR/small/612031v2_ufig1.gif" ALT="Figure 1"> View larger version (80K): org.highwire.dtl.DTLVardef@1d2b45eorg.highwire.dtl.DTLVardef@3f9490org.highwire.dtl.DTLVardef@32a733org.highwire.dtl.DTLVardef@17f2111_HPS_FORMAT_FIGEXP M_FIG C_FIG

animal behavior and cognition↗

The alternative polyadenylation regulator CFIm25 promotes macrophage differentiation and activates the NF-κβ pathway

Macrophages are required for our bodys development and tissue repair and protect against microbial attacks. We previously reported a crucial role for regulation of mRNA 3-end cleavage and polyadenylation (C/P) in monocyte to macrophage differentiation. The CFIm25 subunit of the C/P complex showed a striking increase upon differentiation of monocytes with Phorbol Myristate Acetate, suggesting that it promotes this process. To test this hypothesis, CFIm25 was overexpressed in two different monocytic cell lines, followed by differentiation. Both cell lines showed a significant increase in macrophage characteristics and an earlier slowing of the cell cycle. In contrast, depletion of CFIm25 hindered differentiation. Cell cycle slowing upon CFIm25 overexpression was consistent with a greater decrease in the proliferation markers PCNA and cyclin D1, coupled with increased 3UTR lengthening of cyclin D1 mRNA. Since choice of other poly(A) sites could be affected by manipulating CFIm25, we identified additional genes with altered use of poly(A) sites during differentiation and examined how this changed upon CFIm25 overexpression. The mRNAs of positive regulators of NF-{kappa}B signaling, TAB2 and TBL1XR1, and NFKB1, which encodes the NF-{kappa}B p50 precursor, underwent 3UTR shortening that was associated with increased protein expression compared to the control. Cells overexpressing CFIm25 also showed elevated levels of phosphorylated NF-{kappa}B-p65 and the NF-{kappa}B targets p21, Bcl-XL, ICAM1 and TNF- at an earlier time and greater resistance to NF-{kappa}B chemical inhibition. In conclusion, our study supports a model in which CFIm25 accelerates the monocyte to macrophage transition by promoting alternative polyadenylation events which lead to activation of the NF-{kappa}B pathway.

molecular biology↗

Biomechanical Evaluation of Temporomandibular Joint Implants Under Complete Mastication Cycle

To ensure the long-term success of temporomandibular joint (TMJ) implants, it is imperative to understand their biomechanical performances. This study aims to compare the biomechanical performance of two stock implants (narrow and standard) under unilateral and bilateral clenching during both osseointegrated and non-osseointegrated conditions. Finite element models of a human mandible were developed from QCT data, with the left TMJ being replaced by the implants. Six clenching tasks were simulated to evaluate stress and strain distributions in the mandible and implants. Ipsilateral clenching produced higher mandibular strains, while contralateral clenching generated larger implant stresses. Furthermore, intercuspal biting was found to have produced the highest strain (1750-1880 {micro}{varepsilon}) and stress ([~]17 MPa) in the mandible. Osseointegration reduced stresses (up to 0.14 MPa) and strains (up to 30 {micro}{varepsilon}) in mandible as well as stresses in mandibular components (up to 48 MPa) and screws (up to 71 MPa). However, during non-osseointegrated conditions, stresses in cortical bone were higher for standard TMJ implant as compared to narrow implant. This suggests possible preference of narrow implant over standard ones.

bioengineering↗

Transmembrane channel-like 4 and 5 proteins at microvillar tips are potential ion channels and lipid scramblases

Microvilli--membrane bound actin protrusions on the surface of epithelial cells--are sites of critical processes including absorption, secretion, and adhesion. Increasing evidence suggests microvilli are mechanosensitive, but underlying molecules and mechanisms remain unknown. Here, we localize transmembrane channel-like proteins 4 and 5 (TMC4 and 5) and calcium and integrin binding protein 3 (CIB3) to microvillar tips in intestinal epithelial cells, near glycocalyx insertion sites. We find that TMC5 colocalizes with CIB3 in cultured cells and that a TMC5 fragment forms a complex with CIB3 in vitro. Homology and AlphaFold2 models reveal a putative ion permeation pathway in TMC4 and 5, and molecular dynamics simulations predict both proteins can conduct ions and perform lipid scrambling. These findings raise the possibility that TMC4 and 5 interact with CIB3 at microvillar tips to form a mechanosensitive complex, akin to TMC1 and 2, and CIB2 and 3, within the mechanotransduction channel complex at the tips of inner ear stereocilia.

cell biology↗

Social and environmental predictors of gut microbiome age in wild baboons

Mammalian gut microbiomes are highly dynamic communities that shape and are shaped by host aging, including age-related changes to host immunity, metabolism, and behavior. As such, gut microbial composition may provide valuable information on host biological age. Here we test this idea by creating a microbiome-based age predictor using 13,563 gut microbial profiles from 479 wild baboons collected over 14 years. The resulting "microbiome clock" predicts host chronological age. Deviations from the clocks predictions are linked to some demographic and socio-environmental factors that predict baboon health and survival: animals who appear old-for-age tend to be male, sampled in the dry season (for females), and have high social status (both sexes). However, an individuals "microbiome age" does not predict the attainment of developmental milestones or lifespan. Hence, in our host population, gut microbiome age largely reflects current, as opposed to past, social and environmental conditions, and does not predict the pace of host development or host mortality risk. We add to a growing understanding of how age is reflected in different host phenotypes and what forces modify biological age in primates.

evolutionary biology↗

Substrate stiffness regulates neuronal maturation via Piezo1-mediated TTR activity

During brain development, neurons extend axons to connect to their target cells while initiating a maturation process during which neurons start expressing voltage-gated ion channels, form synapses, express synaptic transmitters and receptors, and start communicating via action potentials. Little is known about external factors regulating this process. Here, we identified environmental mechanics as an important regulator of neuronal maturation, and a molecular pathway linking tissue stiffness to this process. Using patch clamp electrophysiology, calcium imaging and immunofluorescence, we found that neurons cultured on stiffer substrates showed a delay in voltage-gated ion channel activity, spontaneous and evoked action potentials, and synapse formation. RNA sequencing and CRISPR/Cas9 knockdown revealed that the mechanosensitive ion channel Piezo1 supresses transthyretin (TTR) expression on stiffer substrates, slowing down synapse formation and consequently electrical maturation. In agreement, the stiffness of developing Xenopus laevis brain negatively correlated with local synapse densities, and stiffening of brain tissue resulted in a significant delay of synaptic activity in vivo. Our data indicate that environmental stiffness represents a fundamental regulator of neuronal maturation, which is important for the development of normal circuitry in the brain, and potentially for neurodevelopmental disorders. Furthermore, the mechanical regulation of TTR downstream of Piezo1 may be found in many other biological systems.

developmental biology↗

Heterogeneous Slowdown of Dynamics in the Condensate of an Intrinsically Disordered Protein

The high concentration of proteins and other biological macromolecules inside biomolecular condensates leads to dense and confined environments, which can affect the dynamic ensembles and the time-scales of the conformational transitions. Here we use atomistic molecular dynamics (MD) simulations of the intrinsically disordered low complexity domain (LCD) of the human fused in sarcoma (FUS) RNA-binding protein to study how self-crowding inside a condensate affects the dynamic motions of the protein. We found a heterogeneous retardation of the protein dynamics in the condensate with respect to the dilute phase, with large-amplitude motions being strongly slowed by up to two orders of magnitude, whereas small-scale motions, such as local backbone fluctuations and side-chain rotations, are less affected. The results support the notion of a liquid-like character of the condensates and show that different protein motions respond differently to the environment.

biophysics↗

Chemical inactivation of two non-enveloped viruses follows distinct molecular pathways

Non-enveloped viruses, which lack a lipid envelope, typically display higher resistance to disinfectants, soaps and sanitizers compared to enveloped viruses. The capsids of these viruses are highly stable and symmetric protein shells that resist inactivation by commonly employed virucidal agents. This group of viruses include highly transmissible human pathogens such as Rotavirus, Poliovirus, Foot and Mouth Disease Virus, Norovirus and Adenovirus; thus, devising appropriate strategies for chemical disinfection is essential. We tested a mild combination of a denaturant, alcohol, and organic acid on two representative non-enveloped viruses - Human Adenovirus 5 (HAdV5) and Feline Calicivirus (FCV)- and evaluated the molecular pathway of capsid neutralization using biophysical methods. The transition temperatures signifying conformational shifts in the capsid were established in the presence and absence of chemical treatment using Differential Scanning Calorimetry (DSC), while the corresponding morphological alterations were visualized and correlated using Transmission Electron Microscopy (TEM). We found that while chemical treatment of purified HAdV5 particles resulted in increased thermal instability, followed by large scale particle aggregation; similar treatment of FCV particles resulted in complete collapse of the capsids. The distinct effects of the chemical treatment on the morphology of HAdV5 and FCV suggests that non-enveloped viruses with icosahedral geometry can follow different molecular pathways to inactivation. Further, while individual components of the chemical formulation caused significant damage to the capsids, a synergistic action of the whole formulation was evident against both non-enveloped viruses tested. Molecular level understanding of inactivation pathways may result in the design and development of effective mass-market formulations for rapid neutralization of non-enveloped viruses. HighlightsO_LIformulation consisting of 3.2% citric acid, 1% urea in 70% ethanol, pH4 effectively inactivates HAdV5 and FCV. C_LIO_LIinactivation pathways with complete formulation, are different for the two viruses. C_LIO_LIeffect of whole formulation is more effective compared to individual components. C_LI

microbiology↗

A rewiring of the earliest immune events leading to T-cell mediated disease following intestinal infection in a PINK1KO mouse model of Parkinsons disease

Parkinsons disease (PD) is characterized by a protracted period of non-motor symptoms, including gastrointestinal (GI) dysfunction, which can precede the development of the cardinal motor deficits by decades. This long prodrome of disease is highly suggestive of immune cell involvement in the initiation of disease, but currently the field lacks robust model systems to study such mechanisms. It has been hypothesized that pathology may be first initiated in the periphery due to environmental triggers, such as pathogens that enter the GI tract. We further speculate that the impact of such pathogens on the immune system could be exacerbated in genetically predisposed individuals. Our group has developed a GI-targeted pathogen-induced PD mouse model system in PINK1 KO mice with Gram-negative bacterial infections and found that T cells are a major player in driving PD-like motor symptoms at late stages following infection. Herein, we now map the initiating immune events at the site of infection at the earliest stages with the goal of shedding light on the earliest mechanisms triggering immune-mediated pathological processes relevant to PD. Using unbiased single cell sequencing, we demonstrate that myeloid cells are the earliest dysregulated immune cell type in PINK1 KO infected mice at 1-week post-infection, followed by a dysregulated T cell response shortly after, at 2 weeks post-infection. We find that these myeloid cells have an enhanced proinflammatory profile, are more mature, and develop enhanced capacity for antigen presentation. Using unbiased prediction analysis, our data suggest that cytotoxic T cells and myeloid cells are particularly poised for interacting with each other, and we identify possible direct cell-cell interaction pathways that might be implicated. Taken together, deciphering the earliest immune mechanisms in the periphery underpinning PD autoimmunity will be instrumental in the development of effective therapeutic targeting strategies before irrevocable neuronal damage ensues.

immunology↗

Membrane binding properties of the cytoskeletal protein bactofilin

Bactofilins are a widespread family of cytoskeletal proteins with important roles in bacterial morpho-genesis, chromosome organization and motility. They polymerize in a nucleotide-independent manner, forming non-polar filaments that are typically associated with the cytoplasmic membrane. Membrane binding was suggested to be mediated by a short N-terminal peptide, but the underlying mechanism and the conservation of this interaction determinant among bacteria remain unclear. Here, we use the bacto-filin homolog BacA of the stalked bacterium Caulobacter crescentus as a model to analyze the membrane-binding behavior of bactofilins. Based on site-directed mutagenesis of the N-terminal region, we identify the full membrane-targeting sequence of BacA (MFSKQAKS) and pinpoint amino acid residues that are critical for its function in vivo and in vitro. Molecular dynamics simulations then provide detailed insight into the molecular mechanism underlying the membrane affinity of this peptide. Collectively, these analyses reveal a delicate interplay between the water exclusion of hydrophobic N-terminal residues, the arrangement of the peptide within the membrane and the electrostatic attraction between positively charged groups in the peptide and negative charges in the phospholipid molecules. A comprehensive bio-informatic analysis shows that the composition and properties of the membrane-targeting sequence of BacA are conserved in numerous bactofilin homologs from diverse bacterial phyla. Importantly, our findings reveal cooperative effects between the membrane-binding and polymerization activities of BacA. Moreover, they demonstrate that both of these activities critically contribute to the recruitment of the BacA client protein PbpC, a membrane-bound cell wall synthase that uses a conserved peptide in its N-terminal cytoplasmic tail to interact with BacA assemblies. Finally, we show that PbpC can functionally replace the endogenous membrane-targeting sequence of BacA when provided at elevated levels in trans, indicating that client proteins can make a significant contribution to the membrane association of bacto-filin polymers. Together, these results unravel the mechanistic underpinnings of membrane binding by bactofilin homologs, thereby illuminating a previously obscure but important aspect in the biology of this cytoskeletal protein family.

microbiology↗

Hierarchical Bayesian inference to model continuous phenotypical progression in Alzheimer's Disease

Throughout an organisms life, a multitude of complex and interdependent biological systems transition through biophysical processes that serve as indicators of the underlying biological states. Inferring these latent, unobserved states is a goal of modern biology and neuroscience. However, in many experimental setups, we can at best obtain discrete snapshots of the system at different times and for different individuals. This challenge is particularly relevant in the study of Alzheimers Disease (AD) progression, where we observe the aggregation of pathology in brain donors, but the underlying disease state is unknown. This paper proposes a biophysically motivated Bayesian framework (B-BIND: Biophysical Bayesian Inference for Neurode-generative Dynamics), where the disease state is modeled and continuously inferred from observed quantifications of multiple AD pathological proteins. Inspired by biophysical models, we describe pathological burden as an exponential process. The progression of AD is modeled by assigning a latent score, termed pseudotime, to each pathological state, creating a pseudotemporal order of donors based on their pathological burden. We study the theoretical properties of the model using linearization to reveal convergence and identifiability properties. We provide Markov chain Monte Carlo estimation algorithms, illustrating the effectiveness of our approach with multiple simulation studies across various data conditions. Applying this methodology to data from the Seattle Alzheimers Disease Brain Cell Atlas, we infer the pseudotime ordering of donors. Finally, we analyze the information within each pathological feature to refine the model, focusing on the most informative pathologies. This framework lays the groundwork for continuous pseudotime modeling in the analysis of neurodegenerative diseases.

neuroscience↗

Legionella uses host Rab GTPases and BAP31 to create a unique ER niche

Upon entry into host cells, the facultative intracellular bacterium Legionella pneumophila (L.p.) uses its type IV secretion system, Dot/Icm, to secrete ~330 bacterial effector proteins into the host cell. Some of these effectors hijack endoplasmic reticulum (ER)-derived vesicles to form the Legionella-containing vacuole (LCV). Despite extensive investigation over decades, the fundamental question persists: Is the LCV membrane distinct from or contiguous with the host ER network? Here, we employ advanced photobleaching techniques, revealing a temporal acquisition of both smooth and rough ER (sER and rER) markers on the LCV. In the early stages of infection, the sER intimately associates with the LCV. Remarkably, as the infection progresses, the LCV evolves into a distinct niche comprising an rER membrane that is independent of the host ER network. We discover that the L.p. effector LidA binds to and recruits two host proteins of the Rab superfamily, Rab10, and Rab4, that play significant roles in acquiring sER and rER membranes, respectively. Additionally, we identify the pivotal role of a host ER-resident protein, BAP31, in orchestrating the transition from sER to rER. While previously recognized for shuttling between sER and rER, we demonstrate BAP31s role as a Rab effector, mediating communication between these ER sub-compartments. Furthermore, using genomic deletion strains, we uncover a novel L.p. effector, Lpg1152, essential for recruiting BAP31 to the LCV and facilitating its transition from sER to rER. Depletion of BAP31 or infection with an isogenic L.p. strain lacking Lpg1152 results in a growth defect. Collectively, our findings illuminate the intricate interplay between molecular players from both host and pathogen, elucidating how L.p. orchestrates the transformation of its residing vacuole membrane from a host-associated sER to a distinct rER membrane that is not contiguous with the host ER network.

cell biology↗

Playback-aided surveys and acoustic monitoring in the detection of the Endangered Forest Owlet Athene blewitti

Long-term monitoring of populations of rare, endangered species is often challenging. Both the availability of baseline historical datasets and appropriate methods for long-term monitoring are often limited. Anthropogenic climate change and landscape change can impact species distributions significantly, sometimes resulting in a distributional shift of species and, in some cases, driving species to extinction. The Forest Owlet is an endangered bird that was considered extinct but was rediscovered after 113 years in 1997. Since its rediscovery, followed by the description of its calls, there have been regular sightings of the species from newer locations, leading to its down-listing in the IUCN Red List from Critically Endangered to Endangered. One area of interest is the Dang region in Gujarat, India, where there have been no historical records despite previous ornithological studies, but there are several recent records. Through field surveys, we repurpose data from the last three decades (1990, 2000, and 2019) to explore if this bird currently occurs in previous study sites where it was not recorded. The period has seen the rise of acoustic data, and we assess if new survey techniques using playback of its call could increase its detection. Additionally, we examined any changes in landscape and climate in this region across the same period. We also developed an acoustic detection framework for detecting the Forest Owlet from co-occurring sympatric owlets using Automated Recording Units (ARU) and sound-analysis software. We assessed appropriate detection distances from vocalizing birds on the field to design a spacing grid for future surveys of the species. We could locate the Forest Owlet from the resurveys at locations where previous studies three decades ago had not. We also find a significant change in the landscape - loss of native forests and increased agriculture, along with a significant change in climatic variables - mean maximum temperature and mean rainfall. Although the detection of the Forest Owlet is higher when accompanied by playback of its call, there is considerable variation across the landscape. Our acoustic detector comparison led us to a detection strategy for long-term monitoring - different approaches for songs and calls, and an effective detection distance of 300m in its habitat. Although the species responds to climate and habitat change, our study cannot determine the cause of the increased reports of this endangered species. All possibilities remain; the increase in the recent records of the species could be from variable detection or changes in climate and land use. However, we do find increased detections with newer survey techniques with bioacoustics, and we recommend they be used with care for future baseline studies that are urgently required.

ecology↗

Chloroquine attenuates hypoxia-mediated autophagy to curb thrombosis- an ex vivo and in vivo study

BackgroundHypoxia can trigger the activation of blood platelets, leading to thrombosis. If not addressed clinically, it can cause severe complications and fatal consequences as well. The current treatment regime for thrombosis is often palliative and includes long-term administration of anticoagulants, which has the risk of over-bleeding in injury and other secondary effects as well. This demands a deeper understanding of the process and exploration of an alternative therapeutic avenue. Interestingly, recent studies demonstrate that platelets though atypical and enucleated, possess components of autophagy machinery. This cellular homeostatic process though well-studied in non-platelet cells, is under-explored in platelets. MethodsIn this study, we report an activation of autophagy in rat-derived platelets cultured under physiologically relevant hypoxic condition (10% O2) ex vivo. Furthermore, autophagy was triggered in vivo when rats were exposed to hypobaric hypoxic conditions. Subsequently, restriction or surgical ligation of the inferior vena cava (IVC) was performed to induce thrombus formation. Post confirming the impact of autophagy induction on platelet functioning, it was inhibited, and then platelet activation and aggregation status were evaluated using light transmission aggregometry, flow cytometry, immunofluorescence and immunoblotting. ResultsHerein, we show that autophagy inhibition with the potent autophagy inhibitor-CQ, a repurposed FDA-approved drug, can significantly reduce platelet activation, both in ex vivo and in vivo settings. CQ withdrawal reversed the phenomenon indicating a dynamic effect. Thereafter, in flow restriction or surgical ligation model, interestingly, CQ-pre-treated rats showed reduced clotting ability. Importantly, CQ at the stipulated dose was found to be non-toxic to the tissues, as analyzed through histological staining. ConclusionThus, we propose that the repurpose of the FDA approved drug CQ can attenuate hypoxia-induced thrombosis through inhibition of autophagy and can be explored as an effective therapeutic alternative. HighlightsO_LIExposure of ex-vivo cultured platelets to physiologically relevant hypoxic condition (O2 concentration) can induce autophagy causing them to get activated and eventually aggregate. C_LIO_LIFDA approved drug chloroquine (CQ) is able to inhibit autophagy in anucleate cellular fragments, platelets, similar to nucleated cells and curb platelet functioning under hypoxic condition in both ex-vivo and in-vivo model. C_LIO_LIFlow restriction model mimicking deep vein thrombosis, emphasizes on the effect of CQ on impeding thrombus formation when used at a non-toxic dosage. C_LI

physiology↗

Comparative analysis of serological assays and sero-surveillance for SARS-CoV-2 exposure in US cattle

Coronavirus disease-2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) continues to pose a significant threat to public health globally. Notably, SARS-CoV-2 demonstrates a unique capacity to infect various non-human animal species, documented in captive and free-living animals. However, experimental studies revealed low susceptibility of domestic cattle (Bos taurus) to ancestral B.1 lineage SARS-CoV-2 infection, with limited viral replication and seroconversion. Despite the emergence of viral variants with potentially altered host tropism, recent experimental findings indicate greater permissiveness of cattle to SARS-CoV-2 Delta variant infection compared to other variants, though with limited seroconversion and no clear evidence of transmission. While some studies detected SARS-CoV-2 antibodies in cattle in Italy and Germany, there is no evidence of natural SARS-CoV-2 infection in cattle from the United States or elsewhere. Since serological tests have inherent problems of false positives and negatives, we conducted a comprehensive assessment of multiple serological assays on over 600 cattle serum samples, including pre-pandemic and pandemic cattle sera. We found that SARS-CoV-2 pseudovirus neutralization assays with a luciferase reporter system can produce false positive results, and care must be taken to interpret serological diagnosis using these assays. We found no serological evidence of natural SARS-CoV-2 infection or transmission among cattle in the USA. Hence, it is critical to develop more reliable serological assays tailored to accurately detect SARS-CoV-2 antibodies in cattle populations and rigorously evaluate diagnostic tools. This study underscores the importance of robust evaluation when employing serological assays for SARS-CoV-2 detection in cattle populations.

microbiology↗

Genome-wide association study elucidates the genetic architecture of manganese tolerance in Brassica napus

Brassica napus (canola) is a significant contributor to the worlds oil production and is cultivated across continents, yet acidic soils with Al3+ and Mn2+ toxicities limit its production. The genetic determinants underlying acidic soil tolerance in canola are unknown and require to be uncovered for canola breeding and production. Here, through comprehensive phenotyping, whole genome resequencing, and genome-wide association analysis, we identified three QTLs for tolerance to Mn2+ toxicity on chromosomes A09, C03, and C09. Allelism tests between four tolerance sources confirmed that at least one locus on A09 controls Mn2+ tolerance in B. napus. Integrated analysis of genomic and expression QTL and Mn2+ tolerance data reveals that BnMTP8.A09, in conjunction with BnMATE.C03, BnMTP8.C04 and BnMTP8.C08, play a central role in conferring Mn2+ tolerance in B. napus. Gene expression analysis revealed a high correlation (R2 = 0.74) between Mn2+ tolerance and the BnMTP8.A09 expression. Yeast complementation assays show that BnMTP8.A09 can complement manganese-hypersensitive yeast mutant strain PMR1{Delta} and restore Mn2+ tolerance to wild-type levels. Inductively coupled plasma mass spectrometry revealed that Mn2+ tolerant accessions accumulate less Mn in the shoots compared to Mn2+ sensitives, suggesting that the BnMTP8.A09 transporter likely sequesters Mn2+ into the tonoplast. Taken together, our research unveils the genetic architecture of Mn2+ tolerance and identifies BnMTP8.A09 as a major gene imparting tolerance to Mn2+ toxicity in B. napus.

plant biology↗