Search bioRxiv⌕ Search

Biology subjects

Pal, D.

Publications and source records attributed to Pal, D..

At least 19 recordsLinked to original sources

Environment-Aware DNA Language Model for Stress-Responsive Genomic Prioritization in Maize

Abiotic stresses such as heat and drought severely reduce maize productivity, yet identifying genomic regions that confer stress resilience remains a challenge. Inspired by advances in Large Language Models (LLMs), Genomic Foundation Models (GFMs) have recently emerged as a promising approach for capturing regulatory patterns through large-scale pre-training on DNA sequences. However, their application to plant stress-response analysis remains unexplored. This study presents an environment-aware DNA-LLM that adapts AgroNT, a transformer-based GFM pre-trained on diverse plant genomes, by incorporating stress-specific prompt tokens. Through parameter-efficient fine-tuning, the model learns stress-conditioned sequence representations that form distinct clusters in the embedding space across environmental contexts. By combining stress-induced shifts in these sequence representations relative to control conditions with transformer attention patterns, we prioritized putative heat- and drought-responsive genomic regions associated with grain yield in the Genomes-to-Fields (G2F) panel. Prioritized regions were supported by spatiotemporal differential gene-expression evidence and overlap with stress-associated quantitative trait loci. They were further characterized through transcription-factor family analysis and regulatory motif enrichment. Attention-guided analysis additionally identified stress-associated motifs enriched within model-emphasized sequence regions. Overall, the prioritized loci were proximal to genes involved in transcriptional regulation, signaling, and metabolic pathways relevant to abiotic-stress adaptation, demonstrating the potential of stress-conditioned transformer-based sequence modeling for environment-aware genome-to-phenome analysis.

genomics↗

Psilocybin lengthens hippocampal sharp wave ripples

Psilocybin is a psychedelic which has been shown to induce neural plasticity through activation of intracellular serotonergic 5-HT2A receptors. It also produces brain-wide changes in structural and functional connectivity and holds promise as a therapeutic compound for treating anxiety and depression. Despite links between psilocybin-induced plasticity, the psychedelic experience, and reduction in depressive symptoms, little is known about the effects of psilocybin on the function of the highly plastic hippocampus, a region crucial for memory whose dysfunction is linked to neural disorders such as depression and anxiety. In this study, we investigated the acute and lasting effects of psilocybin on rodent sharp-wave ripples (SWRs), transient high frequency oscillations observable in the hippocampal local field potential which are linked to memory consolidation. We found that a 10 mg/kg dose of psilocybin robustly decreased the peak SWR frequency and increased the duration of SWRs immediately following administration compared to control sessions the day before and after. Psilocybin also perturbed sleep architecture, resulting in a pronounced reduction in non-rapid eye movement (NREM) sleep which lasted for hours. Therefore, psilocybin could impact memory processing by modulating hippocampal SWRs.

neuroscience↗

Comprehensive classification of HCN1 variants linked to neurodevelopmental disorders with and without epilepsy

Hyperpolarization-activated cyclic nucleotide-gated 1 channels (HCN1) mediate the Ih cationic current and play a central role in regulating neuronal excitability and synaptic integration. HCN1 is predominantly expressed in the neocortex and hippocampus. Pathogenic variants in HCN1 have been increasingly identified in individuals presenting with a broad spectrum of epileptic disorders, ranging from severe developmental and epileptic encephalopathy (DEE) to milder epilepsies. Here, we used patch-clamp electrophysiology in combination with confocal imaging in HEK293 cells to functionally characterize 43 HCN1 variants found in patients presenting with neurodevelopmental disorders, with or without epilepsy. Based on their biophysical properties, we defined four functional classes: (I) low or no current, (II) hyperpolarizing (i.e. left) shift in voltage dependence, (III) depolarizing (i.e. right) shift in voltage dependence, and (IV) generation of an instantaneous current. Integration of this functional classification with detailed clinical data from a cohort of 49 patients revealed a striking genotype-phenotype correlation. Loss-of-function variants were strongly enriched among individuals without epilepsy or with milder generalized phenotypes, whereas gain-of-function and mixed variants were predominantly associated with epilepsy, including all cases of DEE. Notably, non-epileptic cases clustered within a subgroup of loss-of-function variants affecting the selectivity filter. We further show that allosteric modulators, including the peptides NB6 and TRIP8bnano and the small molecule J&J12e, normalize the functional properties of mutant HCN1 channels in three classes. These findings establish a clinically relevant framework for interpreting HCN1 gain- and loss-of-function variants suggesting that the direction of channel dysfunction is a major determinant of epilepsy risk and severity.

pathology↗

BRD4 represses developmental and neuronal genes through interactions with polycomb complexes

BRD4 is best known as a transcriptional co-activator, yet heterozygous loss-of-function variants cause craniofacial and neurodevelopmental abnormalities through unclear mechanisms. Using human embryonic stem cells and neural organoids as an in vitro model of human embryonic brain development, we show that BRD4 represses polycomb-regulated developmental and neuronal genes. BRD4 co-occupies bivalent promoters with PRC1.6 and directly interacts with PCGF6 and RING1B through its C-terminal domain. H3K23ac contributes to BRD4 recruitment through BD2, linking acetylated chromatin recognition to polycomb-associated repression. Acute BRD4 depletion alters PRC1.6 occupancy, reduces ubiquitination of H2AK119 and rapidly increases developmental gene transcription. In neural organoids, BRD4 BD2 mutations alter neuronal cell composition and increase expression and chromatin accessibility associated with neuronal transcription-factor programmes. These findings establish BRD4 as a context-dependent chromatin regulator that prevents premature activation of developmental genes and provide mechanistic insight into BRD4-associated neurodevelopmental disorders.

molecular biology↗

Intravenous Administration of Serotonergic Psychedelics Produce Short-lasting Changes in Sleep-Wake Behavior and High Gamma Functional Connectivity in Rats

Background and PurposeGiven the increase in recreational psychedelic use and ongoing efforts to explore psychedelics as therapeutic agents for mental health disorders, there is an urgent need to understand the effect of psychedelics such as psilocybin and N,N-dimethyltryptamine (DMT) on sleep-wake states, which share a bidirectional relationship with mental health. Here, we investigated the effects of intravenous psilocybin and DMT on sleep-wake states and EEG spectral power and functional connectivity in rats. Experimental ApproachSprague Dawley rats (n=25, 13 male) were surgically instrumented to record high-density EEG (27 electrodes) and EMG during 12-h light and 12-h dark cycle after intravenous psilocybin (2.5 mg/kg, 10 mg/kg), DMT (3.75 mg/kg, 7.5 mg/kg) or 0.9% saline. The EEG/EMG data were scored in 4-second epochs into wake, slow-wave sleep (SWS), and rapid eye movement (REM) sleep. EEG spectral power and corticocortical coherence, a surrogate for functional connectivity, were computed in 12-second epochs. Key ResultsPsilocybin and DMT delayed the onset of SWS and REM sleep, and caused a short-lasting increase in wakefulness and decrease in SWS. Psilocybin also produced a 1) decrease in REM sleep, 2) decrease in theta power and coherence and increase in high gamma power and coherence during wake and SWS, and 3) increase in high gamma coherence during REM sleep. DMT increased gamma coherence only during wakefulness. Conclusions and ImplicationsSerotonergic psychedelics have minimal effects on sleep-wake states. The enhanced high gamma functional connectivity suggests that the psychedelic-induced changes in EEG/neural dynamics can occur independent of the arousal states.

neuroscience↗

Nuclear Fetuin-A Drives Adipocyte Senescence via HIF-1 α During Obesity

Fetuin-A (FetA), a liver derived glycoprotein, has emerged from genome-wide association studies and epidemiological surveillance as a serum biomarker linked to obesity-driven type 2 diabetes mellitus (T2D), primarily due to its contribution to adipose tissue dysfunction. Here, we uncovered an eccentric role of nuclear FetA in visceral white adipocytes of obese T2D conditions. Hypoxia-inducible factor-1 (HIF-1) facilitates the nuclear translocation of FetA via direct interaction, a process that promotes the emergence of a senescence-associated secretory phenotype (SASP). While nuclear co-localization of FetA and HIF-1 strongly promotes adipocyte senescence, silencing FetA alone is sufficient to prevent senescence, even in conditions of HIF-1 overexpression or lipid-rich hypoxic stress. Although nuclear FetA does not directly bind to DNA, it enhances HIF-1 transcriptional activity, potentiating the activation of senescence markers such as {beta}-galactosidase and p53. Selective knockdown of FetA in obese mice notably reduced adipocyte senescence in visceral white adipose tissue (vWAT) and improved fasting glycemic control. Collectively, our findings reveal a previously unrecognized nuclear function for FetA in orchestrating adipocyte senescence in obesity, establishing nuclear FetA as a potential therapeutic target for obesity related metabolic diseases.

cell biology↗

Transient chromatin decompaction by histone deacetylation inhibition preferentially radiosensitizes cancerous breast epithelial cells at lower radiation doses

Radiation therapy plays a prominent role in breast cancer treatment, but the high doses of radiation damage both healthy and cancerous cells. Therefore, additional research is needed into combination therapies that could preferentially radiosensitize cancer cells compared to surrounding healthy tissue without causing deleterious side effects. Histone deacetylase inhibitor drugs (HDACis) have been tested as radiosensitizers in both basic research and clinical trials, but the long exposure time typically used in these treatments and the lack of matched healthy cell controls often leave aspects of their mechanism of action unclear. Here, we show that transient (2 hour) trichostatin A (TSA) treatment of cancerous and non-tumorigenic breast epithelial cell lines increases immediate DNA damage and decreases long term cell viability in both cell types at high radiation doses. Transient TSA treatment also causes an increase in DNA damage signals after 5 Gy in other cancer and healthy cell types: A375 melanoma cells and BJ5-ta fibroblasts. This suggests that chromatin decompaction acts to increase cellular vulnerability to initial DNA damage from high doses of radiation DNA damage in a cell type independent manner that does not rely on changes to DNA repair pathways caused by longer TSA treatment. However, responses to lower doses of radiation and long term survival are more cell type specific: only MCF7 cells experience an effect of TSA on DNA damage after 1 Gy radiation while MCF10a cells experience somewhat more evident cell viability effects of combined TSA and radiation treatment long term. Scope statementThis manuscript covers several topics that are core to the mission of Frontiers in Cell and Developmental Biology, including cancer cell biology as compared to non-cancerous cell function, cell death vs. survival, and epigenetics and chromosome structure. While some of the implications of this work touch on cancer therapeutics, the study itself focuses on the basics of the interplay between genome architecture and DNA damage and cellular survival / response. We noted several recent articles on related topics in this journal, including the effects of combination treatments on cancer cells (doi 10.3389/fcell.2025.1636288), radiotherapy effects on cells (doi 10.3389/fcell.2025.1568634), and DNA damage (doi 10.3389/fcell.2025.1575483). Our work is well suited for a Brief Research Report as it provides key but focused data on comparisons of radiosensitivity in response to transient chromatin decompaction in cancer vs. healthy cells.

cancer biology↗

Genetic Expectations in Inheritance: A Probabilistic Algebraic Framework

This study introduces a formal framework for modeling inheritance patterns based on an algebraic representation of genotype distributions. The approach defines genotypes as probability measures rather than discrete states, enabling the computation of genetic expectations, a probabilistic analogue that captures the expected distribution of offspring genotypes under Mendelian inheritance rules. This formulation permits constant-time simulation of multi-locus inheritance processes and provides a means of incorporating uncertainty and partial information in genotype data. A series of eleven illustrative examples is presented, encompassing both Mendelian and selected non-Mendelian mechanisms, including polygenic inheritance, uniparental disomy, and haplodiploidy. While the current framework does not model recombination, linkage, or phenotypic traits, it is designed to accommodate extensions to some complex chromosomal structures, such as those encountered in polysomic inheritance. The model reproduces classical inheritance outcomes and is intended as a computational and theoretical tool for genetic analysis in both research and pedagogical settings. Future development will focus on increasing biological scope and integrating empirical data sources. HighlightsO_LIGenotypes modeled as probability distributions over allelic states. C_LIO_LIGenetic expectations summarize an individuals contribution to off-spring. C_LIO_LIExpectations are mating-independent, enabling modular inheritance logic. C_LIO_LIFramework supports constant-time, multi-locus inheritance simulation. C_LI

genetics↗

A549 tumorigenic and BEAS-2B non-tumorigenic cell line derived small extracellular vesicles show distinct proteomic, N-glycoproteomic and chondroitin/dermatan sulfate profiles

Extracellular vesicles (EVs) are critical mediators of intercellular communication and hold promise as biomarkers and therapeutic targets in cancer, but their molecular alterations remain poorly understood. Protein glycosylation is a frequent post-translational modification; however, most EV studies focus only on proteomics, while mapping glycosylation changes of proteins are still underrepresented. To address this shortcoming, we analyzed the proteomic, N-glycoproteomic, and chondroitin/dermatan sulfate (CS/DS) glycosaminoglycan (GAG) profiles of small EVs (sEVs) derived from A549 lung adenocarcinoma and BEAS-2B non-tumorigenic epithelial cell lines. Principal component analysis and hierarchical clustering revealed that all three profiles are highly dependent on the origin of sEV, highlighting fundamental differences not only at the proteomic but also at the N-glycopeptide and CS/DS levels. Protein expression differences were primarily associated with the upregulation of cell cycle regulation, DNA repair, metabolism, and protein synthesis, while immune-related processes were predominantly downregulated. Proteomics revealed differential expressions of 5 CS proteoglycans, anticipating that their CS profile may also change. N-glycoproteomics highlighted a shift from complex to hybrid N-glycans in cancer sEVs, alongside a significant decrease in fucosylation. Prominent glycoproteins characterized with multiple glycosylation sites included versican, galectin-3-binding protein and laminins. The total amount of CS/DS increased 3.4-fold in cancer sEVs, while the ratio of the two monosulfated disaccharides changed 2-fold, suggesting altered sulfation mechanisms. These findings highlight the potential of N-glycoproteomics and GAG profiling to enhance biomarker discovery and EV-based cancer diagnostics. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=121 SRC="FIGDIR/small/643059v1_ufig1.gif" ALT="Figure 1"> View larger version (23K): org.highwire.dtl.DTLVardef@c2dfdeorg.highwire.dtl.DTLVardef@1f79452org.highwire.dtl.DTLVardef@12a9dbborg.highwire.dtl.DTLVardef@d992da_HPS_FORMAT_FIGEXP M_FIG C_FIG Proteomic, N-glycoproteomic and chondroitin/dermatan sulfate disaccharide profiles differ between A549 lung adenocarcinoma and BEAS-2B non-tumorigenic epithelial cell derived small extracellular vesicles.

cancer biology↗

Psychedelic-mediated Reversal of General Anesthesia and Restoration of Brain Dynamics in Rat

Serotonergic psychedelics enhance neurophysiological complexity and the repertoire of brain states, whereas general anesthetics produce opposite effects. Serotonergic psychedelics are also known to increase wakefulness and reduce sleep time in rodents. Therefore, we hypothesized that 2,5-dimethoxy-4-iodopamphetamine (DOI), a serotonergic psychedelic, will reverse general anesthesia and restore neurophysiological conditions associated with normal wakefulness. We demonstrate that intravenous administration of DOI in rats under general anesthesia induced wakefulness despite ongoing delivery of the anesthetics, propofol or isoflurane. Behavioral arousal was accompanied by recovery of directional and non-directional high gamma (125-165Hz) functional connectivity and restoration of functional brain network structure. These behavioral and neurophysiological effects were blocked by a 5-HT2A antagonist, volinanserin. Intravenous administration of a non-psychedelic 5-HT2A agonist, lisuride, failed to restore wakefulness or brain dynamics in anesthetized rats. To our knowledge, these results provide the first evidence of psychedelic-mediated reversal of general anesthesia and concurrent restoration of brain dynamics associated with normal wakefulness.

neuroscience↗

Proximity to Explosive Synchronization Determines Network Collapse and Recovery Trajectories in Neural and Economic Crises

When complex systems move away from criticality--a balance between order and chaos--they are no longer optimized. Furthermore, when criticality is lost too quickly, or recovery is delayed, system damage can result. However, the mechanism for these abnormally fast or slow critical transitions remains unknown. Here, we show that the proximity of a complex network to explosive synchronization (ES), a first-order phase transition, determines the trajectories of criticality loss and recovery after perturbations. Our computational models revealed characteristic dynamics based on network proximity to ES, enabling us to infer network phase transition types from empirical data and predict criticality transition patterns. We validated our predictions using empirical data from the human brain under anesthesia and the stock market during an economic crisis, demonstrating that early and prolonged recoveries can be systematically predicted. This study has implications for designing resilient networks that withstand perturbations and recover quickly.

systems biology↗

Combined analysis of somatic mutations and gene expression reveals nuclear speckles-associated enhanced stemness in gingivobuccal carcinoma under DNA damage response

Smokeless tobacco chewing habits in India lead to a high prevalence of Gingivobuccal oral squamous cell carcinoma (OSCC-GB). Cancer stem cells (CSCs) are a sub-population of cancer cells within a tumor with stem-like properties and are believed to contribute to tumor initiation, progression, increased resistance to drug therapy, and promote post-therapeutic cancer relapse. An RNA-seq data-based integrative analysis of somatic mutation and gene expression was performed to explore the role of CSCs in disease progression using the novel Indian-origin OSCC-GB cell line IIOC019 from a patient with tobacco-chewing habit. The identified DNA damage-related known mutational signature (ID1, SBS5) indicates the impact of smokeless tobacco-related carcinogens in the IIOC019 cell line. The differentially expressed somatic variants, functional impact predictions, and survival analysis reveal the role of DNA damage response (DDR)-related genes in OSCC-GB, with the SON gene as a significant player. The study suggests that the loss of function in a somatic variant of the SON gene is associated with enhanced stemness and increased risk of disease progression in OSCC-GB under DDR conditions. The newly identified CSC-associated somatic variants appear to promote cancer spread, local recurrence, and resistance to chemotherapy or radiotherapy, contributing to the high mortality rates among Indian OSCC-GB patients.

genomics↗

Regulation of REM Sleep Onset and Homeostasis by Preoptic Glutamatergic Neurons

The preoptic area of the hypothalamus is key for the control of sleep onset and sleep homeostasis. Although traditionally considered exclusively somnogenic, recent studies identified a group of preoptic glutamatergic neurons that promote wakefulness. Specifically, our previous investigations demonstrated that chemogenetic stimulation of glutamatergic neurons within the medial-lateral preoptic area (MLPO_VGLUT2) promotes wakefulness, fragments non-rapid eye movement sleep (NREMs), and suppresses REM sleep (REMs). This evidence is further supported by recent work showing that preoptic glutamatergic neurons are activated during microarousals that fragment sleep in response to stress, and optogenetic stimulation of these neurons promotes microarousals and wakefulness. Thus, while the wake-promoting function of MLPO_VGLUT2 is clear, their role in sleep homeostasis has not been assessed. We tested the hypothesis that MLPO_VGLUT2 are wake-active, and their activation will increase wakefulness and disrupt sleep homeostasis via projections to arousal-promoting systems. Using fiber photometry, we found that MLPO_VGLUT2 were highly active during REMs, wakefulness and brief arousals, and remained minimally active during NREMs. Chemogenetic stimulation of MLPO_VGLUT2 inhibited REMs onset and suppressed the REMs homeostatic response after total sleep deprivation. Chemogenetic inhibition of MLPO_VGLUT2 increased REMs time (during the light phase only) but did not influence REMs and NREMs homeostasis. Anterograde projection mapping revealed that MLPO_VGLUT2 innervate central regions that promote wakefulness and inhibit REMs. We conclude that MLPO_VGLUT2 powerfully suppress REMs and that exogenous --and possibly pathologic-- activation of these neurons disrupts REMs recovery, presumably by directly or indirectly activating REMs-inhibitory mechanisms. SIGNIFICANCE STATEMENTThe preoptic area of the hypothalamus has been extensively studied and its role in sleep regulation is well-established. Importantly, recent work identified a group of preoptic glutamatergic neurons (MLPO_VGLUT2) that are wake-active and promote wakefulness. However, whether these neurons influence sleep homeostasis remains unknown. We demonstrate that MLPO_VGLUT2 are maximally active during REM sleep (REMs), wakefulness and brief arousals from sleep, and innervate wake-promoting and REMs-inhibitory regions. MLPO_VGLUT2 stimulation inhibits REMs and REMs rebound after sleep deprivation, whereas their inactivation increases REMs but does not alter REMs homeostatic response. We thus identified a preoptic mechanism that powerfully suppresses REMs, which we propose may engage during normal sleep-to-wake transitions to block REMs intrusions into subsequent wakefulness.

neuroscience↗

Predicting immune checkpoint therapy response in three independent metastatic melanoma cohorts

While Immune checkpoint inhibition (ICI) therapy shows significant efficacy in metastatic melanoma, only about 50% respond, lacking reliable predictive methods. We introduce a panel of six proteins aimed at predicting response to ICI therapy. Evaluating previously reported proteins in two untreated melanoma cohorts, we used a published predictive model (EaSIeR score) to identify potential proteins distinguishing responders and non-responders. Six proteins initially identified in the ICI cohort correlated with predicted response in the untreated cohort. Additionally, three proteins correlated with patient survival, both at the protein, and at the transcript levels, in an independent immunotherapy treated cohort. Our study identifies predictive biomarkers across three melanoma cohorts, suggesting their use in therapeutic decision-making. O_FIG O_LINKSMALLFIG WIDTH=164 HEIGHT=200 SRC="FIGDIR/small/592032v1_ufig1.gif" ALT="Figure 1"> View larger version (63K): org.highwire.dtl.DTLVardef@754668org.highwire.dtl.DTLVardef@1616263org.highwire.dtl.DTLVardef@827009org.highwire.dtl.DTLVardef@1899ba7_HPS_FORMAT_FIGEXP M_FIG C_FIG

cancer biology↗

Neurochemical and Neurophysiological Effects of Intravenous Administration of N,N-dimethyltryptamine in Rats

N,N-dimethyltryptamine (DMT) is a serotonergic psychedelic that is being investigated clinically for the treatment of psychiatric disorders. Although the neurophysiological effects of DMT in humans are well-characterized, similar studies in animal models as well as data on the neurochemical effects of DMT are generally lacking, which are critical for mechanistic understanding. In the current study, we combined behavioral analysis, high-density (32-channel) electroencephalography, and ultra-high-performance liquid chromatography-tandem mass spectrometry to simultaneously quantify changes in behavior, cortical neural dynamics, and levels of 17 neurochemicals in medial prefrontal and somatosensory cortices before, during, and after intravenous administration of three different doses of DMT (0.75 mg/kg, 3.75 mg/kg, 7.5 mg/kg) in male and female adult rats. All three doses of DMT produced head twitch response with most twitches observed after the low dose. DMT caused dose-dependent increases in serotonin and dopamine levels in both cortical sites along with a reduction in EEG spectral power in theta (4-10 Hz) and low gamma (25-55 Hz), and increase in power in delta (1-4 Hz), medium gamma (65-115 ), and high gamma (125-155 Hz) bands. Functional connectivity decreased in the delta band and increased across the gamma bands. In addition, we provide the first measurements of endogenous DMT in these cortical sites at levels comparable to serotonin and dopamine, which together with a previous study in occipital cortex, suggests a physiological role for endogenous DMT. This study represents one of the most comprehensive characterizations of psychedelic drug action in rats and the first to be conducted with DMT. Significance StatementN,N-dimethyltryptamine (DMT) is a serotonergic psychedelic with potential as a tool for probing the neurobiology of consciousness and as a therapeutic agent for psychiatric disorders. However, the neurochemical and neurophysiological effects of DMT in rat, a preferred animal model for mechanistic studies, are unclear. We demonstrate that intravenous DMT caused a dose-dependent increase in serotonin and dopamine in medial prefrontal and somatosensory cortices, and simultaneously increased gamma functional connectivity. Similar effects have been shown for other serotonergic and atypical psychedelics, suggesting a shared mechanism of drug action. Additionally, we report DMT during normal wakefulness in two spatially and functionally distinct cortical sites -- prefrontal, somatosensory -- at levels comparable to those of serotonin and dopamine, supporting a physiological role for endogenous DMT.

neuroscience↗

Psilocybin induces dose-dependent changes in functional network organization in rat cortex

Psilocybin produces an altered state of consciousness in humans and is associated with complex spatiotemporal changes in brain networks. Given the emphasis on rodent models for mechanistic studies, there is a need for characterization of the effect of psilocybin on brain-wide network dynamics. Previous rodent studies of psychedelics, using electroencephalogram, have primarily been done with sparse electrode arrays that offered limited spatial resolution precluding network level analysis, and have been restricted to lower gamma frequencies. Therefore, in the study, we used electroencephalographic recordings from 27 sites (electrodes) across rat cortex (n=6 male, 6 female) to characterize the effect of psilocybin (0.1 mg/kg, 1 mg/kg, and 10 mg/kg delivered over an hour) on network organization as inferred through changes in node degree (index of network density) and connection strength (weighted phase-lag index). The removal of aperiodic component from the electroencephalogram localized the primary oscillatory changes to theta (4-10 Hz), medium gamma (70-110 Hz), and high gamma (110-150 Hz) bands, which were used for the network analysis. Additionally, we determined the concurrent changes in theta-gamma phase-amplitude coupling. We report that psilocybin, in a dose-dependent manner, 1) disrupted theta-gamma coupling [p<0.05], 2) increased frontal high gamma connectivity [p<0.05] and posterior theta connectivity [p[&le;]0.049], and 3) increased frontal high gamma [p<0.05] and posterior theta [p[&le;]0.046] network density. The medium gamma frontoparietal connectivity showed a nonlinear relationship with psilocybin dose. Our results suggest that high-frequency network organization, decoupled from local theta-phase, may be an important signature of psilocybin-induced non-ordinary state of consciousness.

neuroscience↗

Curtailed CaSR expression in peripheral blood mononuclear cells is associated with hypertension

The calcium-sensing receptor (CaSR) is a GPCR family member. CaSR is abundantly expressed in the parathyroid gland and controls calcium homeostasis. There are no particular discoveries involving CaSR expression in hypertensive peripheral blood mononuclear cells. We investigated lower CaSR expression in hypertensive human and animal models. Nitric oxide (NO) has an important role in vascular function. Impaired NO production disrupts CaSR-mediated fine adjustment of the intra- and extracellular [Ca2+] gradients. According to the law Ca2+ transportation through Ca channels maintains its connection from the circulatory micro-vascular bed to interstitial space, influenced by capillary and interstitial fluid hydrostatic pressure, as well as oncotic pressure. In that situation, the alterations in Ca2+ microenvironment and dynamics remain unknown. CaSR on circulatory mononuclear cells may detect changes in the Ca2+ microenvironment in the ISF of endothelial cells-VSMC and endothelium lining in hypertension. In this experiment, the decreased expression of CaSR revealed a molecular sensor in the presence of elevated blood pressure.

biochemistry↗

Post-GWAS Prioritization of Genome-Phenome Associations in Sorghum

Genome-Wide Association Studies (GWAS) are widely used to infer the genetic basis of traits in organisms, yet selecting appropriate thresholds for analysis remains a significant challenge. In this study, we developed the Sequential SNP Prioritization Algorithm (SSPA) to elucidate the genetic underpinnings of two key phenotypes in Sorghum bicolor: maximum canopy height and maximum growth rate. Utilizing a subset of the Sorghum Bioenergy Association Panel cultivated at the Maricopa Agricultural Center in Arizona, our objective was to employ GWAS with specific permissive-filtered thresholds to identify the genetic markers associated with these traits, allowing for a broader collection of explanatory candidate genes. Following this, our proposed method incorporates a feature engineering approach based on statistical correlation coefficient to reveal patterns between phenotypic similarity and genetic proximity across 274 accessions. This approach helps prioritize Single Nucleotide Polymorphisms (SNPs) likely to be associated with the studied phenotype. Additionally, we evaluated the impact of SSPA by considering all variants (SNPs) as inputs, without any GWAS filtering, as a complementary analysis. Empirical evidence including ontology- based gene function, spatial and temporal expression, and similarity to known homologs, demonstrated that SSPA effectively prioritizes SNPs and genes influencing the phenotype of interest, providing valuable insights for functional genetics research.

genomics↗