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Mann, D.

Publications and source records attributed to Mann, D..

At least 19 recordsLinked to original sources

Discovery of Covalent Wild-Type Isocitrate Dehydrogenase 1 (IDH1) Inhibitors Targeting Cys269

Isocitrate dehydrogenase 1 (IDH1) catalyses the interconversion of isocitrate and -ketoglutarate and is overexpressed in several cancers, supporting tumour survival and treatment resistance. Inhibitors targeting the oncogenic mutant forms of IDH1 also inhibit the wild-type (WT) protein, but lose substantial potency due to greater competition with native substrates (isocitrate and Mg2+). We hypothesised that a covalent inhibitor may be more effective at overcoming the higher substrate affinity of wild-type IDH1. Here, a covalent fragment-based approach was used to develop IDH1-C269 selective inhibitors which prevent the key regulatory segment from forming an -helix required for catalytic competency. Following the identification of C269-selective fragments, we used X-ray crystallography to characterise IDH1-fragment bound complexes and guide structure-based design efforts. Inspired by the unexpected detection of bound isocitrate molecule in an X-ray crystal structure, fragment expansion yielded a series of compounds exploiting both an adjacent site and a unique water-mediated hydrogen bonding network. This series achieved strong potency (reaching IC50 = 47.5 nM, a 155-fold improvement in potency relative to the original fragment), retained activity in the presence of competing Mg2+, showed selectivity against IDH2 and reduced NADPH concentrations in a relevant PDAC cell model. Together, these findings present a mechanistic rationale for the covalent targeting of wild-type IDH1 and provide structurally validated inhibitors for further development.

cancer biology↗

Discovery of stereoselective targeted covalent inhibitors of the RAB27-effector protein-protein interaction

RAB27A and RAB27B are homologous small GTPases that regulate intracellular vesicle trafficking, orchestrating endocytic and exocytic processes that affect cellular communication, immune responses, and dynamics of the cellular microenvironment. Through their interactions with effector proteins, RAB27A/B play roles in tumor metastasis and chronic inflammation. However, pharmacological modulation of their activity faces challenges typical of small GTPases, including a lack of well-defined pockets outside the conserved GTP binding site, and large RAB27-effector protein-protein interaction (PPI) surfaces. Here, we present the discovery and development of the first cell-active, rationally designed covalent inhibitors of the RAB27-effector interaction, targeting a non-conserved cysteine residue flanking the PPI interface. An electrophile-first biochemical screen led to a novel class of acrylamide covalent inhibitors, and X-ray crystallography structure-guided design led to optimized inhibitors and probes that enantioselectively target RAB27A/B-Cys123 in cells. Potency and selectivity were confirmed through biochemical and cellular assays, including chemical proteomics and phenotype recapitulation in melanocytes alongside a matched inactive enantioprobe control. In contrast, a previously reported compound, Nexinhib-20, was found to be toxic and to exert its activity through non-selective reactivity. This work provides the first toolbox of cell-active chemical probes for RAB27 which can be used in future studies to shed light on the function of this protein and its potential as a therapeutic target.

biochemistry↗

Targeting RUNX1 in Macrophages Facilitates Cardiac Recovery

Despite advances in disease treatment, our understanding of how damaged organs recover and the mechanisms governing this process remain poorly defined. Here, we mapped the transcriptional and regulatory landscape of human cardiac recovery using single cell multiomics. Macrophages emerged as the most reprogrammed cell type. Deep learning identified the transcription factor RUNX1 as a key regulator of this process. Macrophage-specific Runx1 deletion recapitulated the human cardiac recovery phenotype in a chronic heart failure model. Runx1 deletion reprogrammed macrophages to a reparative phenotype, reduced fibrosis, and promoted cardiomyocyte adaptation. RUNX1 chromatin profiling revealed a conserved regulon that diminished during recovery. Mechanistically, the epigenetic reader BRD4 controlled Runx1 expression in macrophages. Chromatin activity mapping, combined with CRISPR perturbations, identified the precise regulatory element governing Runx1 expression. Therapeutically, small molecule Runx1 inhibition was sufficient to promote cardiac recovery. Our findings uncover a druggable RUNX1 epigenetic mechanism that orchestrates recovery of heart function.

immunology↗

Clinical and molecular characterisation of primary refractoriness to atezolizumab plus bevacizumab in patients with unresectable hepatocellular carcinoma.

BackgroundDespite improved outcomes with atezolizumab plus bevacizumab (A+B) in hepatocellular carcinoma (HCC), primary refractoriness (PRef), characterised by early progression or short-lived disease stabilisation following treatment, remains a significant and poorly understood clinical challenge. MethodsWe analysed 1296 patients with HCC and Child-Pugh A liver cirrhosis treated with frontline A+B (AB-real) and validated findings in 645 trial participants recruited to IMbrave150 and GO30140. PRef was defined by Society for the Immunotherapy of Cancer (SITC) criteria as progressive disease in the first 6 months after treatment initiation. Patients who achieved complete response, partial response or stable disease for [&ge;] 6 months were classified as responders. We performed a multi-parametric analysis of pre-treatment tumour tissue including machine learning-based quantification of tumour-infiltrating lymphocytes, imaging mass cytometry and RNA sequencing (RNAseq) to evaluate differences in the tumour microenvironment (TME) of PRef versus responding patients. We employed conditional inference tree analyses to provide a hierarchical organisation of determinants of PRef. ResultsAmong 677 AB-real and 378 trial patients evaluable by SITC criteria, PRef identified inferior median OS in comparison with responding patients (AB-real: 7.3 vs. 31.5 months, HR 3.7, 95%CI 2.8-8.5, p<0.001; Trials: 10.8 vs. NR, HR 4.6, 95%CI 3.3-6.3, p<0.001). PRef patients exhibited higher baseline systemic inflammation (neutrophil-to-lymphocyte ratio, NLR [&ge;]3), a distinctively immunosuppressive TME enriched in CD163+ tumour-associated macrophages and a higher Treg/Teff ratio. RNAseq of tumour tissue demonstrated lower intrinsic immunogenicity in PRef samples, characterised by repressed IFN-{gamma} and Teff signatures, with elevated myeloid infiltration. Conditional inference tree analysis identified IFN-{gamma} signature downregulation combined with NLR [&ge;]3 as the strongest contributor of PRef. ConclusionsPRef to A+B identifies a distinct biological entity characterised by unopposed systemic inflammation, myeloid cell infiltration and T-cell depletion. Targeting myeloid-mediated immunosuppression, particularly in patients with low IFN-{gamma} signature expression and elevated NLR might enhance responsiveness to A+B. HighlightsO_LIPrimary refractoriness to atezolizumab plus bevacizumab in hepatocellular carcinoma, as defined by SITC criteria, is associated with poor clinical outcomes. C_LIO_LITumour microenvironment profiling reveals an immunosuppressive phenotype characterized by high myeloid infiltration, reduced interferon-{gamma} signalling, and T-cell depletion. C_LIO_LIThe combination of systemic inflammation and low IFN-{gamma} signature expression strongly predicts primary refractoriness and may inform therapeutic decision-making. C_LI

cancer biology↗

Structure of the complete extracellular bacterial flagellum reveals mechanism for flagellin incorporation

The bacterial flagellum is essential for motility, adhesion, and colonization in pathogens like Salmonella enterica and Campylobacter jejuni. Its extracellular structure comprises the hook, hook-filament junction, filament, and filament cap. The native structures of the hook-filament junction and the cap remain elusive, leaving the molecular details of cap-mediated filament assembly largely uncharacterized. Here, we report the structure of the complete extracellular flagellum, encompassing the hook, hook-filament junction, filament, and cap. This structure reveals intermediates of filament assembly, providing a molecular blueprint for flagellin folding and insertion at the filament tip. Mutagenesis and functional assays demonstrate the crucial roles of the caps terminal regions in flagellin incorporation, and of the structural integrity of the hook-filament junction. Finally, the structure of the cap and hook-filament junction prior to filament assembly reveals the structural basis for the initiation of filament assembly. Collectively, this study provides comprehensive insights into flagellum assembly and how flagellin incorporation is coupled with its secretion.

microbiology↗

Ex-vivo mouse precision cut tumour slices for modelling hepatocellular carcinoma; A 3Rs solution for at-scale drug screening

Disease modelling is vital for improving knowledge of disease mechanisms and for development of new therapeutic molecules and strategies. Modelling the intact living tumour microenvironment (TME) is increasingly considered to be vital not only for gaining a better understanding of the biology of cancer but for examining the efficacy of novel oncology drugs. To date, pre-clinical mouse models of cancer have represented the mainstay methodology for studying the evolving TME and for determining the effects of potential therapeutic molecules on tumour evolution and growth. Regarding drug screening, in vivo mouse models are expensive, require the use of large cohorts of mice and involve the administration of drugs with unknown toxicities to animals which often result in adverse effects that can cause animal suffering and the discontinuation of drug investigations. Hepatocellular carcinoma (HCC) is a primary cancer of the liver for which there is an urgent need for improved systemic treatments due to the disease usually being diagnosed at an advanced stage and current treatments having limited efficacy. To provide a practical solution to the screening of drugs for their likely efficacy in HCC we have developed an ex-vivo model in which orthotopic tumours are excised from the liver and subsequently processed to generate precision-cut tumour slices (PCTS) which provide an intact culture model of the HCC-TME. We describe simplified culture conditions that maintain the viability and metabolic activity of live PCTS which maintain the architecture, cellular complexity, drug sensitivity and responsiveness to immunotherapy of the original tumour. Importantly, we show that HCC derived PCTS can be miniaturised to 96-well scale and modified to express soluble luciferase, which in combination enabled non-destructive screening of a library of 26 drugs at two doses using just 5 tumours as the source for PCTS. This screen identified two small molecules, salinomycin and rottlerin, that have potent anti-tumour activities in HCC-PCTS and subsequently validated salinomycin as effective in vivo. In summary, we report a 3Rs (reduction, refinement and replacement) solution for study of HCC biology and for 96-well-scale screening of potential therapeutic agents in the context of an intact, metabolically active TME.

cancer biology↗

Damaging mutations in LXRα uncouple lipogenesis from hepatotoxicity and implicate hepatic cholesterol sensing in human liver health

The nuclear receptor Liver X Receptor- (LXR) activates lipogenic gene expression in hepatocytes. Its inhibition has therefore been proposed as a strategy to treat metabolic-dysfunction-associated steatotic liver disease (MASLD). In order to understand the impact of reducing LXR activity on human health we first examined the association between the carriage of rare loss of function mutations in NR1H3 (encoding LXR) and metabolic and hepatic phenotypes. We identified 63 rare predicted damaging variants in the ligand binding domain of LXR in 454,787 participants in UK Biobank. On functional characterisation, 42 of these were found to be severely impaired. Consistent with loss of the lipogenic actions of LXR, carriers of damaging mutations in LXR had reduced serum triglycerides ({beta}=-0.13 s.d. {+/-}0.03, P=2.7x10-5, N(carriers)=971). Surprisingly, these carriers also had elevated concentrations of serum liver enzymes (e.g. ALT: {beta}=0.17s.d. {+/-}0.03, P=1.1x10-8, N(carriers)=972) with a 35% increased risk of clinically significant elevations in ALT (OR=1.32, 95%CI:1.15-1.53, P=1.2x10-4, N(carriers)=972), suggestive of hepatotoxicity. We generated a knock-in mouse carrying one of the most severely damaging mutations (Nr1h3 p.W441R) which we demonstrated to have dominant negative properties. Homozygous knock-in mice rapidly developed severe hepatitis and fibrotic liver injury following exposure to western diet despite markedly reduced steatosis, liver triglycerides and lipogenic gene expression. This phenotype was completely rescued by viral over-expression of wildtype LXR specifically in hepatocytes, indicating a cell-autonomous effect of the mutant on hepatocyte health. While homozygous LXR knockout mice showed some evidence of hepatocyte injury under similar dietary conditions, the phenotype of the LXRW441R/W441R mouse was much more severe, suggesting that dominant negative mutations that actively co-repress target genes can result in pathological impacts significantly more severe than those seen with simple absence of the receptor. In summary, our results show that loss of function mutations in LXR occur in at least 1/450 people and are associated with evidence of liver dysfunction. These findings implicate LXR in the maintenance of human liver health, identify a new murine model of rapidly progressive fibrotic liver disease and caution against LXR antagonism as a therapeutic strategy for MASLD.

genetics↗

Metabolic resistance of Abeta3pE-42, epitope of the anti-Alzheimer therapeutic antibody, donanemab.

The amyloid {beta} peptide (A{beta}) starting with pyroglutamate (pE) at position 3 and ending at position 42 (A{beta}3pE-42) is a dominant species that accumulates in the Alzheimers disease (AD) brain. Consistently, a therapeutic antibody raised against this species, donanemab, has been shown to be effective in recent clinical trials. While the primary A{beta} species produced physiologically is A{beta}1-40/42, an explanation for how and why this physiological A{beta} is converted to the pathological form has remained elusive. The conversion of A{beta}1-42 to A{beta}3pE-42 is likely to take place after deposition of A{beta}1-42 given that A{beta}3pE-42 plaques arise significantly later than A{beta}1-42 deposition in the brains of single App knock-in and APP-transgenic mice. Here, we present experimental evidence that accounts for the aging-associated A{beta}3pE-42 deposition: [1] A{beta}3pE-42 is metabolically more stable than other A{beta}X-42 species; [2] Deficiency of neprilysin (NEP), the major A{beta}-degrading enzyme, induces a relatively selective deposition of A{beta}3pE-42 in APP-Tg mice. [3] A{beta}3pE-42 deposition always colocalizes with cored plaques in both APP-Tg and App knock-in mouse brains; [4] A{beta}3E-42, an immediate precursor of A{beta}3pE-42, as well as A{beta}2A-42 and A{beta}4F-42 are more short-lived than A{beta}1-42 in vivo, indicating that simple N-terminal truncation that can arise enzymatically or spontaneously makes A{beta}X-42 easier to catabolize. Consistently, newly generated knock-in mice, AppNL-({Delta}DA)-F and AppNL-({Delta}DA)-Q-F, showed no detectable A{beta} pathology even after aging, indicating that the A{beta}3E-42 and A{beta}3Q-42 species are extremely labile to the in vivo catabolic system and that the E/Q cyclase activity present in mouse brain is insufficient for A{beta}3pE-42 generation. In addition, a deficiency of NEP facilitated A{beta}3pE-42 deposition. Of note, we identified a trace amount of A{beta}3pE-42 and its immediate precursor, A{beta}3E-42, in the insoluble fraction of NEP-deficient APP-Tg mouse brains. A{beta}3pE-42 is thus likely to be a probabilistic by-product of A{beta}1-42 metabolism that selectively accumulates over a long-time range of brain aging. It is likely produced in the solid state or at the solid-liquid interface. Our findings suggest that anti-A{beta} therapies will probably be most effective if given before A{beta}3pE-42 deposition takes place.

neuroscience↗

Identification of a P62-TIF-IA axis that drives nucleolar fusion and the senescence associated secretory phenotype

Two key characteristics of senescent cells are nucleolar fusion and secretion of a plethora of pro-inflammatory cytokines called the senescence-associated secretory phenotype (SASP). The SASP is dependent on NF-{kappa}B but the initial trigger, and links with nucleoli, are unclear. Using multiple in vitro and in vivo models, we show that an early response to oncogene- and therapy-induced senescence (OIS and TIS) is nuclear/nucleolar accumulation of the PolI complex component, TIF-IA. This accumulation is essential for nucleolar fusion, the SASP and senescence, independent of rDNA transcription. We show that in steady state, TIF-IA is targeted for autophagic degradation by the p62 cargo receptor and that accumulation in senescence occurs as a consequence of ATM activation, which disrupts the p62-TIF-IA interaction. In mice, TIF-IA accumulates in colonic mucosa with age, which is further enhanced in the nfkb1-/- model of accelerated ageing. Together, these results reveal a p62-TIF-IA nucleolar stress axis that regulates the SASP and senescence, and that warrants further investigation as an anti-ageing target.

molecular biology↗

Optical ice thickness measurement in the VitroJet for time-efficient single particle structure determination

Embedding biomolecules in vitreous ice of optimal thickness is critical for structure determination by cryo-electron microscopy. Ice thickness assessment and selection of suitable holes for data collection are currently part of time-consuming preparatory routines performed on expensive electron microscopes. To address this challenge, a routine has been developed to measure ice thickness during sample preparation using an optical camera integrated in the VitroJet. This method allows to estimate the ice thickness with an error below {+/-} 20 nm for ice layers in the range of 0 - 70 nm. Additionally, we implemented pin printing to reproduce and control sample deposition in the VitroJet. The median ice thickness can be reproduced with a standard deviation below {+/-} 11 nm for thicknesses up to 75 nm. Therefore, the ice thickness of buffer-suspended holes on an EM grid can be tuned and measured within the working range relevant for single particle cryo-EM. Single particle structures of apoferritin were determined at two distinct thicknesses of 30 nm and 70 nm. These reconstructions demonstrate the importance of ice thickness for time-efficient cryo-EM structure determination. HighlightsO_LIMethods in the VitroJet allow for on-the-fly ice thickness tuning and measurement C_LIO_LIThe optical camera can estimate ice thickness ranging from 0 - 70 {+/-} 20 nm C_LIO_LIPin printing enables to reproduce and control median ice thickness up to 75 {+/-} 11 nm C_LIO_LIStructures of apoferritin require 3.7 x fewer particles in 30 compared to 70 nm ice C_LI

molecular biology↗

Structural plasticity of Atg18 oligomers: organization of assembled tubes and scaffolds at the isolation membrane

Autophagy-related protein 18 (Atg18) participates in the elongation of early autophagosomal structures in concert with Atg2 and Atg9 complexes. How Atg18 contributes to the structural coordination of Atg2 and Atg9 at the isolation membrane remains to be understood. Here, we determined the cryo-EM structures of Atg18 organized in helical tubes as well as soluble oligomers. The helical assembly is composed of Atg18 tetramers forming a lozenge cylindrical lattice with remarkable structural similarity to the COPII outer coat. When reconstituted with lipid membranes, using subtomogram averaging we determined tilted Atg18 dimer structures bridging two juxtaposed lipid membranes spaced apart by 80 [A]. Together with an AlphaFold Atg18-Atg2 model, we propose that Atg18 oligomers form a structural scaffold coordinating the Atg2 membrane bridge. The observed structural plasticity of Atg18s oligomeric organization and membrane binding provide a molecular framework for the positioning of downstream components of the autophagy machinery.

biophysics↗

Single-particle cryo-EM analysis of the shell architecture and internal organization of an intact α-carboxysome

Carboxysomes are proteaceous bacterial microcompartments (BMCs) that sequester the key enzymes for carbon fixation in cyanobacteria and some proteobacteria. They consist of a virus-like icosahedral shell, encapsulating carbonic anhydrase and ribulose 1,5-bisphosphate carboxylase/oxygenase (RuBisCO), which catalyses the dehydration of bicarbonate into CO2, the first step of the Calvin-Benson-Bassham cycle. Despite their significance in carbon fixation and great bioengineering potentials, the structural characterization of native carboxysomes, including the shell and the internal organization, is currently limited to low-resolution tomography studies. Notably, the degree of heterogeneity of the shell, and the internal arrangement of enzymes, remain poorly understood. Here, we report the structural characterization of a native -carboxysome from a marine cyanobacterium by single-particle cryo-EM. We determine the structure of RuBisCO enzyme at 2.9 [A] resolution. In addition, we obtain low-resolution maps of the icosahedral protein shell and the concentric interior organisation. In combination with artificial intelligence (AI)-driven modelling approaches, we exploited these maps to propose a complete atomic model of an intact carboxysome. This study provides insight into carboxysome structure and protein-protein interactions involved in carboxysome assembly. Advanced knowledge about carboxysome architecture and structural plasticity is critical for not only a better understanding of biological carbon fixation mechanism but also repurposing carboxysomes in synthetic biology for biotechnological applications.

biophysics↗

Improving Lab Culture Through Self-Assessment: A Case Study

PurposeMotivated by perceived dissatisfaction within our labs changed working environment brought about by the COVID-19 pandemic, we performed a self-assessment of our lab culture through anonymous surveys and live sessions. MethodsIn Survey 1, we asked each lab member to identify and rank up to 10 values that are important for a healthy lab environment. They were then asked to rate how well the lab embodied those values at two time points: before the COVID-19 pandemic while working onsite, and at the time of the survey while working remotely (10 months into the pandemic). In a series of live group sessions, we reviewed relevant literature and the survey results to finalize ten themes. We then reflected on each theme and proposed action items to address any deficiencies. Finally, we conducted Survey 2 after the self-assessment to judge the groups finalized themes, implemented changes, and overall satisfaction with the assessment process. ResultsThemes identified were attitude, accountability, teamwork/collaboration, communication, diversity/inclusion, emotional intelligence, integrity, training, well-being, and adaptability in crisis-management. All lab members liked the self-assessment process and felt their voices were heard. On average, there was a 12% increase in satisfaction across all themes from the start to end of the lab assessment. ConclusionWe successfully assessed the culture of our lab and subsequently improved lab member satisfaction. The success of this team project suggests that other scientific labs could benefit from similar interactive self-assessments.

scientific communication and education↗

The cryo-EM structure of the bacterial type I DNA segregation ATPase filament reveals its conformational plasticity upon DNA binding.

The efficient segregation of replicated genetic material is an essential step for cell division. In eukaryotic cells, sister chromatids are separated via the mitotic spindles. In contrast, bacterial cells use several evolutionarily-distinct genome segregation systems. The most common of these is the Type I Par system. It consists of an adapter protein, ParB, that binds to the DNA cargo via interaction with the parS DNA sequence; and an ATPase, ParA, that binds nonspecific DNA and mediates cargo transport. However, the molecular details of how this system functions are not well understood. Here, we report the cryo-EM structure of a ParA filament bound to its DNA template, using the chromosome 2 (Chr2) of Vibrio cholerae as a model system. We also report the crystal structures of this protein in various nucleotide states, which collectively offer insight into its conformational changes from dimerization through to DNA binding and filament assembly. Specifically, we show that the ParA dimer is stabilized by nucleotide binding, and forms a left-handed filament using DNA as a scaffold. Our structural analyses also reveal dramatic structural rearrangements upon DNA binding and filament assembly. Finally, we show that filament formation is controlled by nucleotide hydrolysis. Collectively, our data provide the structural basis for ParAs cooperative binding to DNA and the formation of high ParA density regions on the nucleoid, and suggest a role for its filament formation.

biophysics↗

PspA maintains membrane integrity by an ESCRT-like membrane remodeling activity

PspA is the main effector of the phage shock protein (Psp) system and preserves the bacterial inner membrane integrity and function. Here, we present the 3.6 [A] resolution cryo-EM structure of PspA assembled in helical rods. PspA monomers adopt a canonical ESCRT-III fold in an extended open conformation. PspA rods are capable of enclosing lipids and generate positive membrane curvature. Using cryo-EM we visualized how PspA remodels membrane vesicles into m-sized structures and how it mediates the formation of internalized vesicular structures. Hot spots of these activities are zones derived from PspA assemblies, serving as lipid transfer platforms and linking previously separated lipid structures. These membrane fusion and fission activities are in line with the described functional properties of bacterial PspA/IM30/LiaH proteins. Our structural and functional analyses reveal that bacterial PspA belongs to the evolutionary ancestry of ESCRT-III proteins involved in membrane remodeling.

microbiology↗

Structural basis for lipid transport by the MLA complex

Multi-resistant bacteria are a major threat in modern medicine. The gram-negative coccobacillus Acinetobacter baumannii currently leads the WHO list of pathogens in critical need for new therapeutic development. The maintenance of lipid asymmetry (MLA) protein complex is one of the core machineries that transport lipids from/to the outer membrane in gram-negative bacteria. It also contributes to broad-range antibiotic resistance in several pathogens, most prominently in A. baumannii. Nonetheless, the molecular details of its role in lipid transport has remained largely elusive. Here, we report the cryo-EM structures of the core MLA complex, MlaBDEF, from the pathogen A. baumannii, in the apo-, ATP- and ADB-bound states. These structures reveal multiple lipid binding sites, in the cytosolic and periplasmic side of the complex. Molecular dynamics simulations suggest their potential trajectory across the membrane. Collectively with the recently-reported structures of the E.coli orthologue, these data also allows us to propose a molecular mechanism of lipid transport by the MLA system.

biochemistry↗

Visualising G-quadruplex DNA dynamics in live cells by fluorescence lifetime imaging microscopy

Guanine rich regions of oligonucleotides fold into quadruple-stranded structures called G-quadruplexes (G4). Increasing evidence suggests that these G4 structures form in vivo and play a crucial role in cellular processes. However, their direct observation in live cells remains a challenge. Here we demonstrate that a fluorescent probe (DAOTA-M2) in conjunction with Fluorescence Lifetime Imaging Microscopy (FLIM) can identify G4 within nuclei of live and fixed cells. We present a new FLIM-based cellular assay to study the interaction of non-fluorescent small molecules with G4 and apply it to a wide range of drug candidates. We also demonstrate that DAOTA-M2 can be used to study G4 stability in live cells. Reduction of FancJ and RTEL1 expression in mammalian cells increases the DAOTA-M2 lifetime and therefore suggests an increased number of G4 in these cells, implying that FancJ and RTEL1 play a role in resolving G4 structures in cellulo.

biophysics↗

Augmenting biologging with supervised machine learning to study in situ behavior of the medusa Chrysaora fuscescens

Zooplankton occupy critical roles in marine ecosystems, yet their fine-scale behavior remains poorly understood due to the difficulty of studying individuals in situ. Here we combine biologging with supervised machine learning (ML) to demonstrate a pipeline for studying in situ behavior of larger zooplankton such as jellyfish. We deployed the ITAG, a biologging package with high-resolution motion sensors designed for soft-bodied invertebrates, on 8 Chrysaora fuscescens in Monterey Bay, using the tether method for retrieval. Using simultaneous video footage of the tagged jellyfish, we develop ML methods to 1) identify periods of tag data corrupted by the tether method, which may have compromised prior research findings, and 2) classify jellyfish behaviors. Our tools yield characterizations of fine-scale jellyfish activity and orientation over long durations, and provide evidence that developing behavioral classifiers on in situ rather than laboratory data is essential.\n\nSummary StatementHigh-resolution motion sensors paired with supervised machine learning can be used to infer fine-scale in situ behavior of zooplankton for long durations.

animal behavior and cognition↗