Biology subjects

Lee, P.

Publications and source records attributed to Lee, P..

At least 19 recordsLinked to original sources

bioRxiv2026

Breast Cancer-derived PDGFB Remodels the CNS Vascular Niche to Promote Brain, Spinal and Leptomeningeal Metastasis

Background: Central nervous system (CNS) metastases are a major driver of breast cancer (BC) mortality. Recently, our group demonstrated that platelet-derived growth factor-B (PDGFB) and its receptor, platelet-derived growth factor receptor-beta (PDGFR{beta}), promote BC metastasis to the brain; however, the cellular/molecular mechanisms driving this process remain unclear. Here, we investigated tumor-derived PDGFB effects on the CNS vascular niche in regulating metastatic spread. Methods: Triple-negative BC cells were engineered to overexpress PDGFB and used to evaluate endothelial sprouting, blood-brain barrier (BBB) function, vascular permeability and experimental CNS metastasis. A novel retro-orbital (RO) injection model was used to study leptomeningeal/spinal experimental metastasis. Results: PDGFB enhanced human brain microvascular endothelial cell (HBMEC) sprouting, induced cell migration in BBB spheroids, increased permeability in 3D models, and disrupted tight junction proteins in HBMECs. Notably, alterations in vascular permeability were observed in both PDGFR{beta}-positive and PDGFR{beta}-negative endothelial systems, suggesting PDGFB can remodel the CNS vasculature through multiple mechanisms. In vivo, PDGFB increased CNS metastatic burden and altered tumor vasculature in xenograft and allograft models of BC. Furthermore, PDGFB promoted robust colonization of both spinal and leptomeningeal compartments, identifying a previously underappreciated role for this signaling pathway in a clinically devastating form of CNS metastasis. Analysis of patient transcriptomic datasets revealed enrichment of angiogenesis-related pathways in PDGFB-high tumors from patients who developed CNS metastases. Conclusions: Collectively, these findings identify tumor-derived PDGFB as a key regulator of CNS vascular remodeling and metastatic tropism, while introducing a new experimental framework to study spinal metastases and leptomeningeal disease in BC.

cancer biology↗

bioRxiv2026

Geothermal gradients restructure metabolism in hot spring microbial communities

Hot springs are employed as model systems for understanding how environmental stress structures microbial communities, yet the mechanisms by which geothermal stress reorganizes community metabolism remain poorly understood. Here we combined genome-resolved metagenomics, metatranscriptomics, aqueous geochemistry, and community metabolic modelling to investigate photosynthetic biofilms across the geothermal gradient of a hot spring in Singapore. We reconstructed community taxonomic and functional composition via metagenome-assembled genomes and identified three transcriptionally coordinated ecological guilds defined by convergent metabolic strategies rather than phylogeny. Community metabolic models revealed that increasing geothermal stress reorganized nutrient exchange networks, progressively reducing metabolic redundancy and increasing dependence on reciprocal interactions among thermophilic guilds. Increasing geothermal stress redirected relative modelled elemental demand from carbon-associated metabolism towards nitrogen and sulfur metabolism, highlighting nitrogen limitation and sulfur-linked bioenergetics as defining features of stress adaptation. Electron allocation modelling further demonstrated a systems-level transition from growth-oriented biosynthesis toward catabolic energy conservation, respiratory metabolism, and oxidative stress management under geothermal stress. These coordinated metabolic shifts indicate that hot spring communities become increasingly specialized and energetically constrained near their upper geothermal limits. Overall, the findings demonstrate how environmental stress restructures microbial ecosystems through guild-level metabolic partitioning and cooperative resource exchange and establishes an integrative systems biology framework for predicting microbial ecosystem function in extreme environments.

microbiology↗

bioRxiv2026

Statins and genetic inhibition of the mevalonate pathway activate an ATF3-STMN2 regenerative program

Loss of neuronal regenerative capacity is a common feature of neurodegenerative disease and axonal injury, yet the transcriptional programs governing this state remain poorly defined. Stathmin-2 (STMN2), a tubulin-binding protein essential for axon maintenance and repair, is profoundly depleted following loss of nuclear TDP-43 in neurodegenerative disease. Here, we identify statins as potent inducers of STMN2 expression. Pharmacological and genetic suppression of the mevalonate pathway, and subsequent prevention of protein geranylgeranylation, restored STMN2 levels in TDP-43 deficient cells and promoted neurite growth. STMN2 induction was abrogated when using a statin analogue unable to interact with HMG-CoA reductase, and through co-administration of mevalonate or geranylgeranyl diphosphate substrates. RNA-seq revealed that statins induce a coordinated pro-regenerative transcriptional response, including activation of the AP-1 transcription factor complex gene, ATF3. Loss of ATF3 attenuated STMN2 induction in vitro, and diminished injury-induced Stmn2 upregulation in spinal motor neurons in vivo. These results demonstrate statins as modulators of ATF3 and STMN2 expression and highlight their therapeutic potential in neurodegenerative disease.

neuroscience↗

bioRxiv2026

Hierarchical Phase-Contrast Tomography Imaging: Applicability in biomedical research

ObjectivesHierarchical Phase-Contrast Tomography (HiP-CT) enables non-destructive, multi-scale imaging of whole human organs. We describe how HiP-CT is utilized for biomedical research within the Human Organ Atlas Hub through three case studies: mapping the enteric nervous system (ENS) of the human colon, analysing myocardial and AV conduction architecture in Tetralogy of Fallot (TOF), and characterizing ductal organization in breast carcinoma. The challenges we faced with this novel biomedical data are discussed. MethodsWhole-organ and region-of-interest scans of three types of human organs were acquired at the European Synchrotron Radiation Facility (ESRF) with isotropic voxel sizes ranging from 20 {micro}m to 0.8 {micro}m. For the colon, voxel binning and RootPainter were employed to tackle data size to segment the ENS. For the heart, voxel-wise myocyte orientation mapping was calculated in terabyte-scale datasets with a high-performance computational framework (Cardiotensor). Breast carcinoma samples were correlated with histopathology for structure validation. ResultsHiP-CT revealed the large-scale organization of the ENS in the colon, enabling visualisation of the 3D structures of the ENS across the colon In TOF hearts, analysis uncovered abnormal myocardial structure and heterogeneous conduction system morphology. In breast carcinoma, HiP-CT resolved the full hierarchy of ductal structures and vascular relationships within tumour and peritumoral regions. ConclusionsHiP-CT provides unprecedented, hierarchical insight into intact human organ structure, bridging the gap between histology and radiology. Advances in knowledgeHiP-CT establishes a new ex vivo radiological modality capable of linking microscale pathology to whole-organ context, advancing translational research in neurogastroenterology, cardiology, and oncology

biophysics↗

bioRxiv2026

A glucocorticoid-responsive polygenic signature in the anterior cingulate cortex moderates the association of early-life adversity and vulnerability for depression

Stress exposure is a major risk factor for psychopathology, yet how stress mediators shape long-term psychiatric vulnerability in humans remains unclear. Glucocorticoids, central effectors of the stress response, regulate gene expression through tissue-specific transcriptional programs, suggesting that glucocorticoid-responsive networks may shape sensitivity to adversity. Using RNA-sequencing following chronic glucocorticoid exposure in a non-human primate model, we identified a gene co-expression network specific to the anterior cingulate cortex (ACC) that was highly preserved across human post-mortem brain datasets relevant to depression. We derived an expression-based polygenic score (ePGS) reflecting genetic variation in network activity and tested its interaction with adversity in the UK Biobank. The ACC-specific glucocorticoid-responsive ePGS moderated the association between adversity and depressive symptoms in adult females, with the strongest effects for early-life adversity. Network genes were enriched for neurodevelopmental processes and showed stronger co-expression during childhood, highlighting a developmentally sensitive, region-specific mechanism linking stress exposure to depression risk.

neuroscience↗

bioRxiv2025

A whole-organ multi-scale in silico framework for human kidney haemodynamics informed by hierarchical phase-contrast tomography

Studying human kidney haemodynamics has been limited by the absence of complete vascular maps of the whole organ. Here we utilise previously generated multi-resolution hierarchical phase-contrast tomography (HiP-CT) coupled with a hybrid anatomically-grounded synthetic reconstruction to generate a full arterial-glomerular network of an intact human kidney comprising 1.6 million vessels and over 800,000 glomeruli. Using this anatomically comprehensive structure, we apply physics-based zero-dimensional haemodynamic modelling to quantify blood pressure, flow and simulated filtration rate across the entire organ. We show that the reconstructed human kidney vascular network exhibits order-dependent branching behaviour similar to that of rat kidneys, and that physiologically plausible pressure and flow patterns are recovered only when the full vascular network is represented. We further demonstrate how the kidney responds to macrovascular and microvascular perturbations, including stenosis of the large renal arteries and narrowing or ablation of afferent arterioles. Stenosis and arteriole narrowing exhibit threshold-type behaviour, with kidney perfusion and simulated glomerular filtration rate remaining largely preserved up to [~]50% narrowing, followed by sharp nonlinear declines beyond [~]70%. These predictions emerge in the absence of autoregulatory mechanisms, indicating that vascular geometry and resistance scaling alone contribute to kidney functional deterioration. Together, our framework provides the first organ-wide, data-driven model of human kidney haemodynamics and offers a foundation for future studies of kidney physiology and disease.

bioengineering↗

bioRxiv2025

Electrodiffusion active pump model with asymmetric immersed chemical potentials

Electrodiffusion is essential in understanding the mechanisms of electrophysiology. Active exchange pumps are critical regarding volume homeostasis, and are also significant in the mechanisms of cell division, growth, and apoptosis. In the formalism of the immersed boundary (IB) method, we replace classical interface conditions across the membrane with regularized chemical potentials to control the permeation of each ionic species governed by the Poisson-Nernst-Planck equation. In asymmetry, to regulate ionic transport, continuous chemical potential barriers are augmented with energetic gradients represented by smoothed Heaviside kernels specifying the directions of active pumps. We obtain steady-state concentrations from electrodiffusion active pumps using Na+, K+, Cl- ionic species, with background charges in the entire unified domain under periodic boundary conditions. As a consequence of the model simulation, electroneutrality, except for the thin space charge layers along the membrane, is well satisfied. The electrodiffusion active pump model for the exchange of sodium and potassium (NKE) exhibits a good fit to the theoretical formula over a broad range of pertur-bations in ionic concentrations, ensuring volume conservation in the steady state only when active pumps are functioning. It is also shown that vant Hoffs law is satisfied without active pumps. This is a foundation for applying the IB electrodiffusion active pump model for subcellular transport of water and molecules, possibly involving cell motility and migration.

biophysics↗

bioRxiv2025

The HosA histone deacetylase regulates stress resistance, host cell interactions, and virulence in Aspergillus fumigatus

The capacity of Aspergillus fumigatus to cause invasive pulmonary aspergillosis depends on its ability to adapt to dynamic and stressful microenvironments within the host. Epigenetic regulation, including histone deacetylation, plays a critical role in fungal adaptation to stress. Here, we investigated the role of the class I histone deacetylase (HDAC) HosA in A. fumigatus stress resistance, host cell interactions, and virulence. A {Delta}hosA mutant had increased susceptibility to intracellular oxidant stress induced by menadione. It also had impaired capacity to invade and damage two pulmonary epithelial cell lines in vitro. In a corticosteroid-immunosuppressed mouse model of invasive aspergillosis, mice infected with the {Delta}hosA mutant survived significantly longer than those infected with the wild-type strain, despite having similar pulmonary fungal burden. The {Delta}hosA mutant also induced a weaker inflammatory response than the wild-type strain. Transcriptomic analysis revealed that HosA regulates genes involved in secondary metabolite biosynthesis and energy metabolism, functioning as both an activator and repressor of distinct gene sets. Collectively, these results indicate that HosA is a key epigenetic regulator that governs A. fumigatus interactions with host cells and virulence during invasive pulmonary aspergillosis. ImportanceEpigenetic modifications in A. fumigatus can be induced by environmental changes and stresses such as those induced by interaction with host cells. HosA, a class I histone deacetylase, has been shown to play a key role in regulating secondary metabolism in several Aspergillus species, but its function in A. fumigatus was previously unknown. We found that deletion of hosA increased susceptibility to intracellular, but not extracellular, oxidative stress. The {Delta}hosA mutant also exhibited significantly reduced pulmonary epithelial cell invasion and host cell damage, as well as attenuated virulence in immunosuppressed mice. Together, these findings indicate that HosA functions as a key epigenetic regulator that governs stress resistance, secondary metabolism, and fungal-host interactions. Defining the functions of HosA could provide critical insight into the epigenetic mechanisms that control fungal pathogenicity and may reveal a potential therapeutic target for invasive aspergillosis.

microbiology↗

bioRxiv2025

Non-synaptic Mechanism of Ocular Dominance Plasticity

Classic experiments showing that monocular visual disruption alters synaptic connections to binocular neurons established the fundamental concept of synaptic plasticity. Synaptic inputs that are activated coincidently with postsynaptic action potential firing are strengthened, and inputs from cells firing before or after the postsynaptic action potential are weakened. An implicit assumption, however, is that the speed of impulse transmission is not altered by visual deprivation. If so, spike time arrival at binocular neurons would be affected, thereby inducing synaptic plasticity. This possibility is tested here in adult mice by monocular eyelid suture and monocular action potential inhibition in retinal axons. The results show that spike time arrival in visual cortex is altered by monocular visual disruption in association with morphological changes in myelin (nodes of Ranvier) on axons in optic nerve and optic tract. This non-synaptic mechanism of ocular dominance plasticity, mediated by myelin-forming cells, supplements and may drive synaptic plasticity.

neuroscience↗

bioRxiv2025

Debiasing Sinkhorn divergence in optimal transport of cellular dynamics

Single-cell RNA-seq analysis characterizes developmental mechanisms of cellular differentiation, lineage determination, and reprogramming with differential conditioning of the microenvironment. In this article, the underlying dynamics are formulated via optimal transport with algorithms that calculate the transition probability of the state of cell dynamics over time. The algorithmic biases of optimal transport (OT) due to entropic regularization are balanced by Sinkhorn divergence, which normally de-biases the regularized transport by centering them. In the case of reprogramming mouse embryonic fibroblasts [1] with dense time points, Sinkhorn divergence is shown to improve the trajectories of targeted cell fates depending on the specific cell types. When the time points are filtered out with sparser 9 and 5 time points, some cell phenotypes show better outcomes from strong entropic regularization. For 9 time points with 2 days interval, Sinkhorn divergence shows a clear advantage with broad bandwith of optimal entropic regularization. For these derived time points, when the cell population is scaled down from n = 8000 to n = 2000, there comes no benefit from Sinkhorn divergence for some specific cell types. In the case of stratifying morphogenesis of the epidermis [2], the sparsity of time points makes it not significant to prescribe Sinkhorn divergence in the accuracy of transporting to the expected cell fates. Overall, whether to prescribe Sinkhorn divergence for the accurate prediction of lineages of single cells depends on temporal sparsity.

bioinformatics↗

bioRxiv2025

Serotonin inhibits sexual receptivity in female cichlid fish

Serotonin is involved in multiple diverse and complex biological processes. Selective serotonin reuptake inhibitors (SSRIs) are often used to test this, and fluoxetine, a commonly detected SSRI in aquatic ecosystems from pharmaceutical pollution, has been found to disrupt important behaviours and functions in organisms exposed to the antidepressant. Increased serotonin generally has an inhibitory effect on sexual behaviour and decreased serotonin has a facilitatory effect, however in the few existing studies on fish, either no effect or the opposite effect have been reported in females, with most studies focusing on male behaviour. The present research aims to examine the role of the serotonin pathway in female sexual receptivity in the cichlid fish Nyassachromis cf. microcephalus. The sexual dimorphism and lekking system of this species, where male-male competition is aggressive and female choice is important, make them an important and interesting evolutionary system. Serotonin levels were modulated using fluoxetine and after a three-week exposure to their respective treatments (control - 0{micro}g/L, low ecologically relevant dose - 0.54{micro}g/L, high dose - 5.4{micro}g/L), female sexual receptivity to male courtship was measured in a simulated lek mating arena where multiple males were presented simultaneously. Sexual receptivity was inhibited in females exposed to a high dose of fluoxetine. This behaviour change due to a disruption of the serotonin pathway could affect sexual selection in the long term, and in the short term highlights the potential for pollution to affect aquatic life by directly altering mating behaviour. Highlights- Disrupting the serotonin pathway reduces sexual receptivity in female cichlid fish - The inhibitory effect of fluoxetine on female receptivity is dose-dependent - The serotonin pathway could be important in the evolution of male mating strategies - SSRI pollution could cause behaviour changes that amplify freshwater biodiversity loss

animal behavior and cognition↗

bioRxiv2024

Evaluation of a Functional Portable Hemodialysis Machine, XKIDNEY

Chronic kidney failure and end-stage renal disease (ESRD) are increasing globally, but home hemodialysis offers a critical means of improving patient quality of life and reducing national healthcare costs. This study investigates the performance of a portable hemodialysis (HD) device named XKIDNEY. The efficacy and safety of the device were determined with focus on solute clearance, fluid balancing accuracy, and blood cell integrity in an ex-vivo test environment. A comparison of the performance of XKIDNEY and a conventional HD unit showed that XKIDNEY had superior balancing accuracy without any technical malfunction. In addition, low molecular weight solutes, such as urea and creatinine, were effectively removed. These findings demonstrate that XKIDNEY enhances treatment portability without compromising performance and indicate XKIDNEY is a feasible home hemodialysis option.

bioengineering↗

bioRxiv2024

Identification of potential sepsis therapeutic drugs using a zebrafish rapid screening approach

In the military, combat wound infections can progress rapidly to life-threatening sepsis. Discovery of effective small molecule drugs to prevent and/or treat sepsis is a priority. To identify potential sepsis drug candidates, we used an optimized larval zebrafish model of endotoxicity/sepsis (Philip et al., 2017) to screen commercial libraries of U.S. Food and Drug Administration (FDA)- approved drugs and other active pharmaceutical ingredients (API) known to affect pathways implicated in the initiation and progression of sepsis in humans (i.e., inflammation, mitochondrial dysfunction, coagulation, and apoptosis). We induced endotoxicity in 3- and 5-day post fertilization larval zebrafish (characterized by mortality and tail fin edema (vascular leakage)) by immersion exposure to Pseudomonas aeruginosa 60 g/mL lipopolysaccharide (LPS) for 24 hours, then screened for the rescue potential of 644 selected drugs simultaneously with LPS at 10 M. After LPS exposure, we used a neurobehavioral assay (light-dark test) to further evaluate rescue from endotoxicity and to determine possible off-target drug side effects. We identified 29 drugs with > 60% rescue of tail edema and mortality. Three drugs (Ketanserin, Tegaserod, and Brexpiprazole) produced 100% rescue and did not differ from the controls in the light-dark test, suggesting a lack of off-target neurobehavioral effects. Further testing of these three drugs at a nearly 100% lethal concentration of Klebsiella pneumoniae LPS (45 g/mL) showed 100% rescue from mortality and 88%-100% mitigation against tail edema. The success of the three identified drugs in a zebrafish endotoxicity/sepsis model warrants further evaluation in mammalian sepsis models.

pharmacology and toxicology↗

bioRxiv2024

The contribution of neutrophils to bacteriophage clearance and pharmacokinetics in vivo

With the increasing prevalence of antimicrobial-resistant bacterial infections, there is great interest in using lytic bacteriophages (phages) to treat such infections. However, the factors that govern bacteriophage pharmacokinetics in vivo remain poorly understood. Here, we have examined the contribution of neutrophils, the most abundant phagocytes in the body, to the pharmacokinetics of intravenously administered bacteriophage in uninfected mice. A single dose of LPS-5, an antipseudomonal bacteriophage recently used in human clinical trials, was administered intravenously to both wild-type BALB/c and neutropenic ICR mice. Phage concentrations were assessed in peripheral blood and spleen at 0.5, 1, 2, 4, 8, 12, and 24 hours after administration by plaque assay and qPCR. We observed that the phage clearance is only minimally affected by neutropenia. Indeed, the half-life of phages in blood in BALB/c and ICR mice is 3.45 and 3.66 hours, respectively. These data suggest that neutrophil-mediated phagocytosis is not a major determinant of phage clearance. Conversely, we observed a substantial discrepancy in circulating phage levels over time when measured by qPCR versus plaque assay, suggesting that substantial functional inactivation of circulating phages occurs over time. These data indicate that circulating factors, but not neutrophils, inactivate intravenously administered phages.

pharmacology and toxicology↗

bioRxiv2023

Gut microbiota-dependent increase in phenylacetic acid induces endothelial cell senescence during aging

Endothelial cell (EC) senescence plays a crucial role in the development of cardiovascular diseases in aging population. Gut microbiota alterations are emerging as significant factors present in cellular senescence associated with aging. However, little is known about how aging-related changes in gut microbiota are causally implicated in EC senescence. Here we show that gut microbiota-dependent phenylacetic acid (PAA) and its derivative, phenylacetylglutamine (PAGln), are elevated in a human aging cohort (TwinsUK, n=7,303) and in aged mice. Metagenomic analyses revealed a marked increase in the abundance of PAA-producing microbial pathways (PPFOR and VOR), which were positively associated with the abundance of Clostridium sp. ASF356, higher circulating PAA concentrations, and endothelial dysfunction in old mice. We found that PAA potently induces EC senescence and attenuates angiogenesis. Mechanistically, PAA increases mitochondrial H2O2 generation, which aggravates IL6-mediated HDAC4 translocation and thereby upregulates VCAM1. In contrast, exogenous acetate, which was reduced in old mice, rescues the PAA-induced EC senescence and restores angiogenic capacity through markedly alleviating the SASP and epigenetic alteration. Our studies provide direct evidence of PAA-mediated crosstalk between aging gut microbiota and EC senescence and suggest a microbiota-based therapy for promoting healthy aging. HighlightsO_LIAging-related gut microbiota alterations contribute to a marked elevation of plasma PAA and PAGln in humans and mice C_LIO_LIClostridium sp. ASF356 contributes to PPFOR-mediated PAA formation in aged mice C_LIO_LIGut-derived PAA promotes endothelial senescence and impairs angiogenesis C_LIO_LIPAA induces mitochondrial H2O2 generation, by which drives epigenetic alterations and SASP in ECs C_LIO_LIAcetate rescues PAA-induced EC senescence and mitochondrial dysfunction C_LIO_LIAcetate improves angiogenesis by reducing HDAC4 phosphorylation and SASP C_LI

cell biology↗

bioRxiv2023

Neuronal Tau Pathology Worsens Late Phase White Matter Degeneration After Traumatic Brain Injury in Transgenic Mice

Traumatic brain injury (TBI) causes diffuse axonal injury which can produce chronic white matter pathology and subsequent post-traumatic neurodegeneration with poor patient outcomes. Tau modulates axon cytoskeletal functions and undergoes phosphorylation and mis-localization in neurodegenerative disorders. The effects of tau pathology on neurodegeneration after TBI are unclear. We used mice with neuronal expression of human mutant tau to examine effects of pathological tau on white matter pathology after TBI. Adult male and female hTau.P301S (Tg2541) transgenic and wild type (Wt) mice received either moderate single TBI (s-TBI) or repetitive mild TBI (r-mTBI; once daily x 5), or matched sham procedures. Acutely, s-TBI produced more extensive axon damage in the corpus callosum (CC) as compared to r-mTBI. After s-TBI, significant CC thinning was present at 6 weeks and 4 months post-injury in Wt and transgenic mice, with homozygous tau expression producing additional pathology of late demyelination. In contrast, r-mTBI did not produce significant CC thinning except at the chronic time point of 4 months in homozygous mice, which exhibited significant CC atrophy (-29.7%) with increased CC microgliosis, but not astrogliosis. Serum biomarker quantification demonstrated neurofilament light detection of early axonal damage one day post-injury in Wt and homozygous mice. At 4 months, high tau and neurofilament in homozygous mice implicated tau in chronic axon pathology. Conclusions: Neuronal tau pathology differentially exacerbated CC pathology based on injury severity and chronicity. Ongoing CC atrophy from s-TBI became accompanied by late demyelination. Pathological tau significantly worsened CC atrophy during the chronic phase after r-mTBI.

neuroscience↗

bioRxiv2022

Territorial aggression in male bower-building cichlids Nyassachromis cf. microcephalus is disrupted by exposure to environmental concentrations of fluoxetine

Selective serotonin reuptake inhibitors (SSRIs) are commonly prescribed drugs for treating human depression, but the role of serotonin--often called the happy chemical--is complex, associated with the regulation of appetite, anxiety, aggression, and more. With such psychoactive pharmaceuticals being increasingly detected in aquatic environments and their effects on non-target species an uncertainty, this study seeks to investigate how inhibiting the serotonin pathway with the SSRI fluoxetine affects territorial aggression, using the cichlid fish Nyassachromis cf. microcephalus as a model. Males of this sand-dwelling Lake Malawi species build bowers to attract females within a lekking system, where male-male competition is intense. Being aggressive in defending against intruders would serve to maximise mating opportunities and reproductive success for the territory holding male. However, after a one-week exposure to fluoxetine at environmentally relevant concentrations, a decline in aggression was observed in the male cichlids. This implies the serotonergic system plays an important role in modulating aggression and therefore sexual selection in cichlid fishes, and that environmental pollution has the potential to disrupt these behaviours.

animal behavior and cognition↗

bioRxiv2022

Building an Open Representation for Biological Protocols

Laboratory protocols are critical to biological research and development, yet difficult to communicate and reproduce across projects, investigators, and organizations. While many attempts have been made to address this challenge, there is currently no available protocol representation that is unambiguous enough for precise interpretation and automation, yet simultaneously abstract enough to enable reuse and adaptation. The Protocol Activity Markup Language (PAML) is a free and open protocol representation aiming to address this gap, building on a foundation of UML, Autoprotocol, and SBOL RDF. PAML provides a representation both for protocols and for records of their execution and the resulting data, as well as a framework for exporting from PAML for execution by either humans or laboratory automation. PAML is currently implemented in the form of an RDF knowledge representation, specification document, and Python library, can be exported for execution as either a manual "paper protocol" or Autoprotocol, and is being further developed as an open community effort.

synthetic biology↗