Search bioRxiv⌕ Search

Biology subjects

Fay, M.

Publications and source records attributed to Fay, M..

8 recordsLinked to original sources

Noise-referenced multi-shell diffusion-weighted imaging for regional cerebrospinal fluid thermometry

We developed a multi-shell diffusion-weighted imaging approach for separate ventricular and subarachnoid cerebrospinal fluid thermometry. The approach uses measured image noise to assess agreement among temperature estimates. In 12 participants, temperature was estimated from four non-zero diffusion weightings. For each voxel, disagreement between these estimates was compared with that expected from image noise, accounting for their shared reference image. Voxels meeting this consistency criterion were retained for regional analysis. Mean diffusion-derived temperature ({+/-} SD) was 38.4 {+/-} 0.4 {degrees}C in the lateral ventricles and 36.0 {+/-} 1.1 {degrees}C in the subarachnoid space. Ventricular estimates were consistently higher than subarachnoid estimates across all participants, with a mean difference of 2.4 {+/-} 1.2 {degrees}C (95% confidence interval 1.6 -3.1 {degrees}C). This difference persisted under alternative noise models and temperature estimators. Subarachnoid estimates increased with retained voxel count; in a post hoc analysis of the six participants with the largest retained counts, ventricular estimates remained higher by 1.6 {+/-} 0.7 {degrees}C. Absolute temperature accuracy and the physiological origin of the regional difference require independent validation. This approach provides an internal consistency check for CSF thermometry and supports separate assessment of ventricular and subarachnoid temperatures.

neuroscience↗

Hybrid Solid-Liquid Optics Enable Scalable, High-Resolution, Multi-Immersion Light-Sheet Microscopy

Modern biology increasingly depends on data-driven discovery, requiring scalable and affordable high-content 3D imaging across molecular to organ scales. Although tissue clearing, expansion microscopy, and light-sheet microscopy (LSM) enable subcellular-resolution imaging of intact specimens, their scalability remains fundamentally limited by detection optics: immersion objectives deliver high-resolution, aberration-free imaging but with short working distances, high cost, and multi-immersion incompatibility, while air objectives offer long working distances and portability at lower cost but suffer from severe aberrations and reduced photon collection when imaging immersed samples. We introduce the Hybrid Solid-Liquid Immersion Lens (HySIL) framework, which pairs an off-the-shelf solid optical component with a refractive index-matched liquid to precompensate aberrations and enhance resolution. Building on HySIL, we developed SCOPE and Super-SCOPE, objective-agnostic imaging devices achieving submicron lateral resolution (<0.75 {micro}m) across centimeter-scale samples using inexpensive air objectives with >30 mm working distances. Integration with a low-cost LSM platform yielded a compact, scalable system demonstrated for multi-immersion, multi-color, subcellular-resolution mapping of cleared or expanded mouse, salamander, and cavefish brains, human iPSC-derived organoids, and 3D histopathology of breast tissue. HySIL and SCOPE establish an accessible foundation for scalable, high-resolution volumetric imaging, advancing data-driven biological discovery.

bioengineering↗

ATR inhibition using gartisertib enhances cell death and synergises with temozolomide and radiation in patient-derived glioblastoma cell lines

Glioblastoma cells can restrict the DNA-damaging effects of temozolomide (TMZ) and radiation therapy (RT) using the DNA damage response (DDR) mechanism which activates cell cycle arrest and DNA repair pathways. Ataxia-telangiectasia and Rad3-Related protein (ATR) plays a pivotal role in the recognition of DNA damage induced by chemotherapy and radiation causing downstream DDR activation. Here, we investigated the activity of gartisertib, a potent ATR inhibitor, alone and in combination with TMZ and/or RT in 12 patient-derived glioblastoma cell lines. We showed that gartisertib alone potently reduced the cell viability of glioblastoma cell lines, where sensitivity was associated with the frequency of DDR mutations and higher expression of the G2 cell cycle pathway. ATR inhibition significantly enhanced cell death in combination with TMZ and RT and was shown to have higher synergy than TMZ+RT treatment. MGMT promoter unmethylated and TMZ+RT resistant glioblastoma cells were also more sensitive to gartisertib. Analysis of gene expression from gartisertib treated glioblastoma cells identified the upregulation of innate immune-related pathways. Overall, this study identifies ATR inhibition as a strategy to enhance the DNA-damaging ability of glioblastoma standard treatment, while providing preliminary evidence that ATR inhibition induces an innate immune gene signature that warrants further investigation.

cancer biology↗

Platelet proteo-transcriptomic profiling validates mediators of thrombosis and proteostasis in patients with myeloproliferative neoplasms

Patients with chronic Myeloproliferative Neoplasms (MPN) including polycythemia vera (PV) and essential thrombocythemia (ET) exhibit unique clinical features, such as a tendency toward thrombosis and hemorrhage, and risk of disease progression to secondary bone marrow fibrosis and/or acute leukemia. Although an increase in blood cell lineage counts (quantitative features) contribute to these morbid sequelae, the significant qualitative abnormalities of myeloid cells that contribute to vascular risk are not well understood. Here, we address this critical knowledge gap via a comprehensive and untargeted profiling of the platelet proteome in a large (n= 140) cohort of patients (from two independent sites) with an established diagnosis of PV and ET (and complement prior work on the MPN platelet transcriptome from a third site). We discover distinct MPN platelet protein expression and confirm key molecular impairments associated with proteostasis and thrombosis mechanisms of potential relevance to MPN pathology. Specifically, we validate expression of high-priority candidate markers from the platelet transcriptome at the platelet proteome (e.g., calreticulin (CALR), Fc gamma receptor (Fc{gamma}RIIA) and galectin-1 (LGALS1) pointing to their likely significance in the proinflammatory, prothrombotic and profibrotic phenotypes in patients with MPN. Together, our proteo-transcriptomic study identifies the peripherally-derived platelet molecular profile as a potential window into MPN pathophysiology and demonstrates the value of integrative multi-omic approaches in gaining a better understanding of the complex molecular dynamics of disease. HighlightsMPN patient platelet proteome identifies key pathobiological mediators of thrombosis and proteostasis. The MPN platelet proteomic profile validates our prior findings from the platelet transcriptome. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=134 SRC="FIGDIR/small/563619v2_ufig1.gif" ALT="Figure 1"> View larger version (20K): org.highwire.dtl.DTLVardef@1cb6290org.highwire.dtl.DTLVardef@1b3ec3eorg.highwire.dtl.DTLVardef@15b0c8eorg.highwire.dtl.DTLVardef@9575b2_HPS_FORMAT_FIGEXP M_FIG C_FIG

pathology↗

The Origin And Speciation Of Orchids

Orchids constitute one of the most spectacular radiations of flowering plants. However, their geographical origin, historical spread across the globe, and hotspots of speciation remain uncertain due to the lack of a broad phylogenomic framework. We present a new Orchidaceae phylogeny based on high-throughput and Sanger sequencing datasets, covering all five subfamilies, 17/22 tribes, 40/49 subtribes, 285/736 genera, and [~]7% (1,921) of the currently 29,524 accepted species. We then use it to infer geographic range evolution, diversity, and speciation patterns by adding curated geographical distribution data through the World Checklist of Vascular Plants. Orchids most recent common ancestor is traced back to the Late Cretaceous in Laurasia. The modern Southeast Asian range of subfamily Apostasioideae is interpreted as relictual, matching the history of numerous clades that went extinct at higher latitudes following the global climate cooled during the Oligocene. Despite their ancient origins, modern orchid species diversity mainly originated over the last 5 Ma, with the fastest speciation rates found in south-eastern Central America. Our results substantially alter our understanding of the geographic origin of orchids, previously proposed as Australian, and further pinpoint the role of Central American as a region of recent and explosive speciation.

evolutionary biology↗

High-resolution genome-wide mapping of chromosome-arm-scale truncations induced by CRISPR-Cas9 editing

CRISPR-Cas9 editing is a scalable technology for mapping of biological pathways, but it has been reported to cause a variety of undesired large-scale structural changes to the genome. We performed an arrayed CRISPR-Cas9 scan of the genome in primary human cells, targeting 17,065 genes for knockout with 101,029 guides. High-dimensional phenomics reveals a "proximity bias" in which CRISPR knockouts bear unexpected phenotypic similarity to knockouts of biologically-unrelated genes on the same chromosome arm, recapitulating both canonical genome structure and structural variants. Transcriptomics connects proximity bias to chromosome-arm truncations. Analysis of published large-scale knockout and knockdown experiments confirms that this effect is general across cell types, labs, Cas9 delivery mechanisms, and assay modalities, and suggests proximity bias is caused by DNA double-strand-breaks with cell cycle control in a mediating role. Finally, we demonstrate a simple correction for large-scale CRISPR screens to mitigate this pervasive bias while preserving biological relationships.

genomics↗

Biological Cartography: Building and Benchmarking Representations of Life

1The continued scaling of genetic perturbation technologies combined with high-dimensional assays such as cellular microscopy and RNA-sequencing has enabled genome-scale reverse-genetics experiments that go beyond single-endpoint measurements of growth or lethality. Datasets emerging from these experiments can be combined to construct perturbative "maps of biology", in which readouts from various manipulations (e.g., CRISPR-Cas9 knockout, CRISPRi knockdown, compound treatment) are placed in unified, relatable embedding spaces allowing for the generation of genome-scale sets of pairwise comparisons. These maps of biology capture known biological relationships and uncover new associations which can be used for downstream discovery tasks. Construction of these maps involves many technical choices in both experimental and computational protocols, motivating the design of benchmark procedures to evaluate map quality in a systematic, unbiased manner. Here, we (1) establish a standardized terminology for the steps involved in perturbative map building, (2) introduce key classes of benchmarks to assess the quality of such maps, (3) construct maps from four genome-scale datasets employing different cell types, perturbation technologies, and data readout modalities, (4) generate benchmark metrics for the constructed maps and investigate the reasons for performance variations, and (5) demonstrate utility of these maps to discover new biology by suggesting roles for two largely uncharacterized genes. 2 Author SummaryWith the proliferation of genetic perturbation, laboratory robotics, computer vision and sequencing technologies, a growing number of researchers are producing datasets that capture digital readouts of cellular responses to genetic perturbations at the full-genome-scale. Since each of these efforts utilizes different cellular models, experimental approaches, terminology, code bases, analysis methods and quality metrics, it is exceptionally difficult to reason through the pros and cons of possible design choices or even discuss the primary considerations when embarking on such an endeavor. These datasets can be powerful discovery tools to look at known biological relationships and uncover new associations in an unbiased manner, but only when paired with a computational pipeline to assemble the data into a digestible format. Moreover, there is great promise in looking across these data to highlight commonalities and differences that may be attributed to experimental or analytical approaches or the biological context. Therefore, a unified framework is necessary to align this nascent field and speed progress in assessing technologies and methods. In this work we define a unified framework for building and benchmarking these perturbative maps, benchmark four different datasets assembled into 18 different maps, explore the impact of different design decisions and demonstrate how these maps can be used to elucidate gene functions. The framework we propose highlights the necessary steps for building any such map - embedding, filtering, aligning, aggregating and relating the data across perturbations. For benchmarking, we propose two main types of metrics and give examples which highlight the impact of different processing pipelines. Finally, we explore these maps to demonstrate their utility for confirming known biological relationships and nominating annotations for genes with unknown function. We expect that this work will positively impact the nascent field of perturbative map building by enabling easier comparisons within and between technologies and methods through a shared language. Additionally, the associated code base is openly available and flexible enough to be easily extended with new methods, so we hope that it will become a resource for future researchers working on developing both laboratory and computational methodology. While there are too many confounding variables to make recommendations on the strengths of different technologies and cellular models at this time, highlighting that fact may prompt studies designed with the goal of directly comparing methods while holding other confounding variables fixed. Moreover, as the number of perturbative maps grows, the field will naturally consider the advantages of combining maps across modalities and the framework provided here can also help guide the evaluation of those efforts.

bioinformatics↗

Stress promotes RNA G-quadruplex folding in human cells

Guanine-rich nucleic acids can fold into G-quadruplex (G4) structures. Although endogenous RNAs contain sequences that can fold into RNA G4s (rG4s) in vitro, their folding and functions in vivo are not well understood. We show that the folding of putative rG4s in human cells into bona fide rG4 structures is dynamically regulated by stress. By using a high-throughput approach based on differential reactivity of dimethyl sulfate (DMS) towards Gs within folded vs unfolded rG4s, we identified hundreds of endogenous rG4s whose folding is promoted by cellular stress and validated them using a newly developed rG4-specific ligand. Stress-dependent rG4s are enriched in mRNA 3'-untranslated regions, suggesting their role in regulating mRNA stability under stress. Lastly, rG4 folding is reversible upon stress removal or adaptation. Our study show that rG4s function as regulatory elements in regulating mRNA stability and cellular stress response. One-Sentence SummaryRNA G-quadruplexes assemble under stress in human cells

molecular biology↗