Biology subjects

Cartailler, J.-P.

Publications and source records attributed to Cartailler, J.-P..

At least 19 recordsLinked to original sources

bioRxiv2026

Integrin α3β1 is required for alveolar-capillary barrier formation through regulation of epithelial differentiation

Laminin-binding integrins regulate critical morphogenic processes, but their specific roles in lung development are unknown. In this study, we combined an in vivo model of epithelial 3 subunit deletion in the murine lung with a multiomics approach to investigate the role of the epithelial 3{beta}1 integrin during murine lung development. We demonstrate that 3{beta}1 integrin is dispensable for airway branching morphogenesis due to delayed epithelial expression. Instead, in vivo deletion of 3{beta}1 integrin impaired alveolar epithelial cell differentiation and disrupted alveolar-capillary barrier formation, functionally limiting gas exchange. A discontinuous alveolar BM contained abnormal collagen IV and laminin networks and widened the gap between epithelial and endothelial cells in the alveolar-capillary barrier niche. Mechanistically, mice deficient in epithelial 3{beta}1 integrin possessed an intracellular trafficking and secretion defect for BM components. Thus, integrin 3{beta}1 orchestrates the temporal maturation of alveolar epithelial cells required for organization of the alveolar-capillary barrier.

developmental biology↗

bioRxiv2026

PanKbase Integrated Single-Cell Map: A Comprehensive Atlas of Human Pancreatic Islets

Single-cell RNA sequencing (scRNA-seq) of human pancreatic islet tissue is a powerful tool for investigating type 1 diabetes (T1D). However, individual datasets are limited in size and fragmented across donors, laboratories, and experimental conditions. To address this, we constructed a comprehensive, integrated scRNA-seq atlas of isolated human pancreatic islets by collating publicly available data generated from tissue provided by resources including the Human Pancreas Analysis Program, the Integrated Islet Distribution Program, and Prodo Labs. Systematic quality controls were implemented to select high-quality samples, reads, and cells. During integration, we accounted for important variables such as age, sex, body mass index, origin study, treatments, islet distribution resources, and sequencing chemistry. Our single-cell atlas comprises 191 high-quality samples from 140 donors (59 female, 81 male) across five phenotypic groups: no diabetes (controls, n=69), autoantibody positivity without diabetes (n=12), pre-diabetes (n=11), T1D (n=12), and type 2 diabetes (T2D) (n=36). In total, the atlas contains 448,935 cells, capturing 13 distinct populations, including alpha cells (43.3%) and beta cells (26.8%), as well as groups such as immune cells (0.6%). Publicly available at www.pankbase.org, this atlas provides a platform for hypothesis-driven investigation of diabetes pathophysiology and, given rigorous quality control, is well-suited for downstream machine-learning applications. Article HighlightsO_LICurrent scRNA-seq datasets of pancreatic islet tissue are limited in size and scattered across donors, laboratories, and experimental conditions, underscoring the need for a consolidated resource. C_LIO_LIWe harmonized datasets from multiple sources to build a comprehensive single-cell map of isolated human pancreatic islets. C_LIO_LIOur atlas captures 448,935 cells from 191 high-quality samples across 140 donors and multiple phenotypic groups, identifying 13 distinct cell populations. C_LIO_LIAvailable at www.pankbase.org, the atlas provides a scalable, rigorously curated platform to support hypothesis-driven diabetes research and can enable a broad range of downstream computational applications. C_LI

genomics↗

bioRxiv2026

Adipose tissue as a site of immune activation and dysfunction in individuals with obesity and asthma

Obesity increases local inflammatory responses in adipose tissue. Individuals with obesity have increased asthma incidence and severity and reduced responses to asthma therapeutics through unknown mechanisms. To identify mechanisms by which increased fat mass augments asthma pathogenesis, single cell RNA sequencing of the immune-rich stromovascular fraction of subcutaneous adipose tissue was conducted from well-characterized adults with obesity-associated asthma matched to adults without asthma. Individuals with asthma had increased abundance of perivascular macrophages and lymphoid-associated macrophages (LAMs) and reduced abundance of classical monocytes and CD4+ and CD8+ naive T cells. Pseudo-bulk differential expression (DE) identified upregulation of cellular metabolism, specifically oxidative phosphorylation, and decreased immune homeostatic pathways in asthma across immune cell subsets. Cell type specific DE analysis of effector cell subtypes identified significant induction of metallothionein gene expression in asthma, a signature of immune cell dysfunction characterized by both an activation and exhaustion phenotype. Gene co-expression analysis identified gene modules associated with asthma diagnosis, lung function, and biomarkers of type 2 inflammation were enriched in effector cells. These data identify adipose tissue dysfunction occurs in obesity-associated asthma and support adipose tissue as therapeutic target to address the enhanced asthma risk among those with obesity. Grant SupportNIH U01AI155299, P30DK020593, R01AI182159, K23HL159351, UL1RR024975-03, P30CA68485, P30EY08126, G20RR030956, 5UL1TR002243, KL2TR002245, P30AI110527, DK020593, American Heart Association 17SFRN33520017.

immunology↗

bioRxiv2026

Microvascular architecture and dynamics of the choroid plexus brain barrier

The choroid plexus is a specialized blood-cerebrospinal fluid barrier that supports cerebrospinal fluid production, immune surveillance, and molecular exchange between the circulation and the central nervous system, yet its vascular bed remains poorly understood. Here, we combine whole-tissue clearing and light-sheet imaging, single-nucleus transcriptomic reanalysis, and live calcium imaging of intact murine explants to define the structural and functional organization of choroid plexus endothelial networks across development. Three-dimensional imaging and reconstruction highlights a dense, epithelial-ensheathed vascular plexus that is continuous with the broader cerebrovasculature and organized into anatomically distinct inflow and ventricular margin regions. Transcriptomic analysis identified developmentally stratified endothelial subtypes, with embryonic populations enriched for proliferative, motor, and membrane remodeling programs and adult and aged populations enriched for adhesion, extracellular matrix, transport, and mechanosensory pathways. Endothelial subsets across stages expressed genes linked to flow sensing and calcium-dependent mechanotransduction, including Piezo1, Piezo2, and Trpv4. Consistent with these signatures, intact explants exhibited spontaneous, spatially graded calcium oscillations, and pharmacologic activation by Piezo1, triggered robust network-wide calcium responses in embryonic and adult tissue with distinct temporal dynamics. Piezo1 activation also promoted stabilization of PECAM1-associated endothelial adhesion under ex vivo flow conditions. Together, these findings establish the choroid plexus endothelium as a structurally specialized, developmentally dynamic, and mechanosensitive vascular network and provide a framework for investigating endothelial contributions to blood-cerebrospinal fluid barrier function in health and disease.

neuroscience↗

bioRxiv2026

Calorie Restriction Up-regulates Islet PD-L1 Signaling and Decreases the Risk of Auto-immune Diabetes Onset in NOD Mice.

Type 1 diabetes (T1D) is an autoimmune disease where beta cells are destroyed by cytotoxic T cells. Calorie restriction (CR) enhances glucose homeostasis and promotes beta cell longevity and was used as therapeutic strategy for T1D prior to the discovery of insulin. However, a significant knowledge gap remains regarding its effects on beta cells during the pathogenesis of autoimmunity. We demonstrate that CR enhances glucose homeostasis, reduces beta cell load, and delays T1D onset in NOD mice. CR induced a largely post-mitotic beta cell state marked by selective loss of beta cell identity markers, reduced DNA damage and beta cell senescence, and increased PD-L1 within the islet microenvironment. This beta cell phenotype correlates with anti-inflammatory and exhausted immune cell states in the NOD islet. Together, these findings indicate that CR improves glucose homeostasis and remodels the islet microenvironment to promote beta cell longevity via a pro-tolerogenic immune microenvironment that reduces the risk for autoimmune diabetes.

cell biology↗

bioRxiv2025

Warmer temperature accelerates senescence by modifying the aging-dependent changes in the mosquito transcriptome, altering immunity, metabolism, and DNA repair

BackgroundGlobal environmental temperatures are rising, which is increasing the body temperature of mosquitoes. This increase in body temperature is accelerating senescence, thereby weakening immune responses and reproductive processes, and shortening lifespan. To determine how warmer temperature and aging, individually and interactively, shape the transcriptome of the African malaria mosquito, Anopheles gambiae, we conducted RNA-sequencing and network-analysis in naive and immune-induced mosquitoes that had been reared at 27C, 30C or 32C and were 1, 5, 10 or 15 days into adulthood. Results: We demonstrate that immune induction, warmer temperature, and aging alter the transcriptome. Notably, the transcriptome of 1-day-old mosquitoes is pronouncedly different from older mosquitoes, and importantly, warmer temperature modifies the aging-dependent changes to accelerate senescence. For example, warmer temperature amplifies the aging-dependent decrease in immune gene expression but dampens both the aging-dependent decrease in metabolic gene expression and the aging-dependent increase in DNA repair gene expression. ConclusionsAltogether, warmer temperature accelerates senescence, shaping the transcriptome in ways that alter the mosquitos ability to fight infection and survive in a warming environment.

zoology↗

bioRxiv2025

peakScout - a user-friendly and reversible peak-to-gene translator for genomic peak calling results

SummarypeakScout is a command line and web-based bioinformatics tool designed to quickly and easily bridge the gap between genomic peak data and gene annotations, enabling researchers to understand the relationship between measurements of regulatory elements and their target genes. At its core, peakScout processes genomic peak files obtained through various means chromatin profiling and maps them to nearby genes using reference genome annotations. The workflow begins with input processing, where peak files are standardized and reference GTF files are decomposed into chromosome-specific feature collections. The core analysis modules then perform bidirectional mapping: peak-to-gene identifies which genes are potentially regulated by specific genomic regions, while gene-to-peak reveals which regulatory elements might influence particular genes of interest. Throughout this process, nearest-feature detection algorithms handle the complex spatial relationships between genomic elements, considering factors like distance constraints and feature overlaps. Finally, the results are formatted into researcher-friendly CSV and Excel outputs, providing a comprehensive view of the genomic landscape that connects regulatory elements to their potential gene targets. Availability and implementationThe web version of peakScout is available at https://vandydata.github.io/peakScout/. The command line version is available at https://github.com/vandydata/peakScout and archived on Zenodo (URL to be provided upon version 1.0 release) under the GNU Affero General Public License v3.0. Installation instructions, example datasets, and detailed usage examples are provided in the GitHub repository README file. peakScout is implemented in Python and is platform independent, but the web version is implemented in Amazon Web Services and thus uses proprietary infrastructure.

bioinformatics↗

bioRxiv2025

Sustained Yap/Taz activation promotes aberrant alveolar epithelial cell differentiation and drives persistent fibrotic remodeling

YAP/TAZ signaling is required for initiation of lung alveolar repair, yet previous studies in idiopathic pulmonary fibrosis (IPF) predicted increased YAP/TAZ signaling in alveolar epithelial cells (AECs). We investigated whether persistent YAP/TAZ AEC signaling contributes to failed epithelial repair and persistent fibrotic remodeling. In IPF lungs, we identified increased YAP+/TAZ+ AECs and increased expression of YAP/TAZ transcriptional targets compared to donor control lungs. In human lung organoids, pharmacological YAP/TAZ activation resulted in phenotype shifts of AECs into aberrant transitional states. In mice with Yap/Taz activation (YTactive) resulting from deletion of Hippo-kinases Stk3/4 in alveolar-type 2 (AT2) cells, resulted in persistent fibrotic remodeling at 28- and 56-days post-bleomycin injury. Gene promoter activity associated with transitional cell markers (Krt19, Hopx, and Runx2) was increased in YTactive AT2 cells. Immunofluorescent staining showed a loss of AT2 associated Cebpa and increased Krt19 in YTactive lineage traced AT2 cells 28 days post-injury. Inhibition of Yap/Taz using Verteporfin resulted in improved lung repair in YTactive mouse lungs, including increased Cebpa and decreased Krt19+ transitional cells. These findings demonstrate sustained Yap/Taz activation drives abnormal alveolar repair and persistent fibrotic remodeling. Blocking aberrant persistent Yap/Taz activity promotes adaptive repair and has potential as a therapeutic strategy for PF.

molecular biology↗

bioRxiv2025

Genetic background influences the heterogeneous phenotypes driven by the MAFAS64F MODY variant in male mice

Pancreatic {beta}-cells require the coordinated expression of transcription factors such as MAFA to dynamically secrete insulin to maintain euglycemia. A naturally occurring mutation in MAFA (MAFAS64F) produces a long-lived variant protein which predisposes carriers to dichotomous conditions of either maturity (adult)-onset diabetes of the young (MODY) or hypoglycemia in a sex-dependent manner. Here we show that genetic background modulates disease penetrance in MafAS64F/+ male mice. Specifically, MafAS64F/+ males backcrossed to a C57/Bl6J ("C57") background prevented dysglycemia, while C57 MafAS64F/+ males bred one generation to an SJL/J background ("mixed") manifested overt diabetes, impaired insulin secretion, and accelerated {beta}-cell senescence. MafA protein levels, phosphorylation status, and target gene expression in C57 MafAS64F/+ male islets were more comparable to wildtype males. RNA sequencing of C57 MafAS64F/+ male islets revealed fewer differentially expressed genes than mixed background male islets, including transcriptional signatures of {beta}-cell senescence. In addition, retinoic acid signaling, another signature of cellular aging, was uniquely downregulated in C57 MafAS64F/+ male islets. Indeed, core retinoic acid signaling receptor RAR and known target genes were downregulated in C57 MafAS64F/+ male islets. CUT&RUN mapping revealed that MafA directly impacted retinoic acid receptor alpha Rara expression. In sum, these data show that genetic factors can impact unique pathways to modulate disease penetrance in mice modeling MAFA-MODY. Article HighlightsO_LIGenetic background in mice or ancestry in humans can profoundly influence diabetes susceptibility. C_LIO_LIWe asked whether diabetes penetrance in our robust mouse model of MAFA-MODY on a mixed genetic background was impacted when backcrossed to C57/Bl6J ("C57"). C_LIO_LIHere we show that C57 MafAS64F/+ males have wildtype glucose-sensing properties, compared to overt diabetes which could be reproducibly re-created on a mixed background. Further analysis disclosed more muted gene expression changes in C57 MafAS64F/+ male islets including unique downregulation of senescence and retinoic acid signaling. C_LIO_LIThese results illustrate the influence of genetic landscape on {beta}-cell function in response to a pathogenic MODY variant. C_LI

physiology↗

bioRxiv2024

Mapping histological and functional maturation of human endocrine pancreas across early postnatal periods

Human endocrine cell differentiation and islet morphogenesis play critical roles in determining islet cell mass and function, but the events and timeline of these processes are incompletely defined. To better understand early human islet cell development and maturation, we collected 115 pediatric pancreata and mapped morphological and spatiotemporal changes from birth through the first ten years of life. Using quantitative analyses and a combination of complementary tissue imaging approaches, including confocal microscopy and whole-slide imaging, we developed an integrated model for endocrine cell formation and islet architecture, including endocrine cell type heterogeneity and abundance, endocrine cell proliferation, and islet vascularization and innervation. We also assessed insulin and glucagon secretory profiles in isolated islet preparations from pediatric donors aged 2 months to 10 years and found a temporal difference in the maturation of insulin secretion compared to glucagon secretion. This comprehensive summary of postnatal and pediatric pancreatic islet development provides a framework for future studies and integration of emerging genetic and genomic data related to islet biology and diabetes risk.

developmental biology↗

bioRxiv2024

Heterogeneous endocrine cell composition defines human islet functional phenotypes

Phenotyping and genotyping initiatives within the Integrated Islet Distribution Program (IIDP), the largest source of human islets for research in the U.S., provide standardized assessment of islet preparations distributed to researchers, enabling the integration of multiple data types. Data from islets of the first 299 organ donors without diabetes, analyzed using this pipeline, highlights substantial heterogeneity in islet cell composition associated with hormone secretory traits, sex, reported race and ethnicity, genetically predicted ancestry, and genetic risk for type 2 diabetes (T2D). While and {beta} cell composition influenced insulin and glucagon secretory traits, the abundance of {delta} cells showed the strongest association with insulin secretion and was also associated with the genetic risk score (GRS) for T2D. These findings have important implications for understanding mechanisms underlying diabetes heterogeneity and islet dysfunction and may provide insight into strategies for personalized medicine and {beta} cell replacement therapy.

physiology↗

bioRxiv2024

Building a literature knowledge base towards transparent biomedical AI

As artificial intelligence (AI) continues to advance and scale up in biomedical research, concerns about AIs trustworthiness and transparency have grown. There is a critical need to systematically bring accurate and relevant biomedical knowledge into AI applications for transparency and provenance. Knowledge graphs have emerged as a powerful tool that integrates heterogeneous knowledge by explicitly describing biomedical knowledge as entities and relationships between entities. However, PubMed, the largest and most comprehensive repository of biomedical knowledge, exists primarily as unstructured text and is under utilized for advanced machine learning tasks. To address the challenge, we developed LiteralGraph, a computational framework to extract biomedical terms and relationships from PubMed literature into a unified knowledge graph. Using this framework, we established the Genomic Literature Knowledge Base (GLKB), which consolidates 14,634,427 biomedical relationships between 3,276,336 biomedical terms from over 33 million PubMed abstracts and nine well-established biomedical repositories. The database is coupled with RESTful APIs and a user-friendly web interface that makes it accessible to researchers for various usages. We demonstrated the broad utility of GLKB towards transparent AI in three distinct application scenarios. In the LLM grounding scenario, we developed a Retrieval Augmented Generation (RAG) agent to reduce LLM hallucination in biomedical question answering. In the hypothesis generation scenario, we elucidated the potential functions of RFX6 in type 2 diabetes (T2D) using the vast evidence from PubMed articles. In the machine learning scenario, we utilized GLKB to provide semantic knowledge in predictive tasks and scientific fact-checking.

bioinformatics↗

bioRxiv2024

SCN gene expression plasticity in response to photoperiod

Seasonal daylength, or circadian photoperiod, is a pervasive environmental signal that profoundly influences physiology and behavior. In mammals, the central circadian clock resides in the suprachiasmatic nuclei (SCN) of the hypothalamus where it receives retinal input and synchronizes, or entrains, organismal physiology and behavior to the prevailing light cycle. The process of entrainment induces sustained plasticity in the SCN, but the molecular mechanisms underlying SCN plasticity are incompletely understood. Entrainment to different photoperiods persistently alters the timing, waveform, period, and light resetting properties of the SCN clock and its driven rhythms. To elucidate novel molecular mechanisms of photoperiod plasticity, we performed RNAseq on whole SCN dissected from mice raised in Long (LD 16:8) and Short (LD 8:16) photoperiods. Fewer rhythmic genes were detected in Long photoperiod and in general the timing of gene expression rhythms was advanced 4-6 hours. However, a few genes showed significant delays, including Gem. There were significant changes in the expression clock-associated gene Timeless and in SCN genes related to light responses, neuropeptides, GABA, ion channels, and serotonin. Particularly striking were differences in the expression of the neuropeptide signaling genes Prokr2 and Cck, as well as convergent regulation of the expression of three SCN light response genes, Dusp4, Rasd1, and Gem. Transcriptional modulation of Dusp4 and Rasd1, and phase regulation of Gem, are compelling candidate molecular mechanisms for plasticity in the SCN light response through their modulation of the critical NMDAR-MAPK/ERK-CREB/CRE light signaling pathway in SCN neurons. Modulation of Prokr2 and Cck may critically support SCN neural network reconfiguration during photoperiodic entrainment. Our findings identify the SCN light response and neuropeptide signaling gene sets as rich substrates for elucidating novel mechanisms of photoperiod plasticity.

neuroscience↗

bioRxiv2023

From goal to outcome: analyzing the progression of biomedical sciences PhD careers in a longitudinal study using an expanded taxonomy

Biomedical sciences PhDs pursue a wide range of careers inside and outside academia. However, there is little data regarding how career interests of PhD students relate to the decision to pursue postdoctoral training or to their eventual career outcomes. Here, we present the career goals and career outcomes of 1,452 biomedical sciences PhDs who graduated from Vanderbilt University between 1997-2021. We categorized careers using an expanded three-tiered taxonomy and flags that delineate key career milestones. We also analyzed career goal changes between matriculation and defense, and the reasons why students became more- or less-interested in research-intensive faculty careers. We linked students career goal at defense to whether they did a postdoc, the duration of time between defense and the first non-training position, the career area of the first non-training position, and the career area of the job at ten years after graduation. Finally, we followed individual careers for ten years after graduation to characterize movement between different career areas over time. We found that most students changed their career goal during graduate school, declining numbers of alumni pursued postdoctoral training, many alumni entered first non-training positions in a different career area than their goal at defense, and the career area of the first non-training position was a good indicator of the job that alumni held 10 years after graduation. Our findings emphasize that students need a wide range of career development opportunities and career mentoring during graduate school to prepare them for futures in research and research-related professions.

scientific communication and education↗

bioRxiv2023

The MODY-associated TALK-1 L114P mutation causes islet α-cell overactivity and β-cell inactivity resulting in transient neonatal diabetes and glucose dyshomeostasis in adults

The gain-of-function mutation in the TALK-1 K+ channel (p.L114P) is associated with maturity-onset diabetes of the young (MODY). TALK-1 is a key regulator of {beta}-cell electrical activity and glucose-stimulated insulin secretion. The KCNK16 gene encoding TALK-1 is the most abundant and {beta}-cell-restricted K+ channel transcript. To investigate the impact of KCNK16 L114P on glucose homeostasis and confirm its association with MODY, a mouse model containing the Kcnk16 L114P mutation was generated. Heterozygous and homozygous Kcnk16 L114P mice exhibit increased neonatal lethality in the C57BL/6J and the CD-1(ICR) genetic background, respectively. Lethality is likely a result of severe hyperglycemia observed in the homozygous Kcnk16 L114P neonates due to lack of glucose-stimulated insulin secretion and can be reduced with insulin treatment. Kcnk16 L114P increased whole-cell {beta}-cell K+ currents resulting in blunted glucose-stimulated Ca2+ entry and loss of glucose-induced Ca2+ oscillations. Thus, adult Kcnk16 L114P mice have reduced glucose-stimulated insulin secretion and plasma insulin levels, which significantly impairs glucose homeostasis. Taken together, this study shows that the MODY-associated Kcnk16 L114P mutation disrupts glucose homeostasis in adult mice resembling a MODY phenotype and causes neonatal lethality by inhibiting islet insulin secretion during development. These data suggest that TALK-1 is an islet-restricted target for the treatment for diabetes. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=135 SRC="FIGDIR/small/545631v3_ufig1.gif" ALT="Figure 1"> View larger version (48K): org.highwire.dtl.DTLVardef@19031e9org.highwire.dtl.DTLVardef@1bccc49org.highwire.dtl.DTLVardef@803e1org.highwire.dtl.DTLVardef@36c584_HPS_FORMAT_FIGEXP M_FIG Graphical Summary C_FIG

physiology↗

bioRxiv2021

Combinatorial transcription factor profiles predict mature and functional human islet α and β cells

Islet-enriched transcription factors (TFs) exert broad control over cellular processes in pancreatic and {beta} cells and changes in their expression are associated with developmental state and diabetes. However, the implications of heterogeneity in TF expression across islet cell populations are not well understood. To define this TF heterogeneity and its consequences for cellular function, we profiled >40,000 cells from normal human islets by scRNA-seq and stratified and {beta} cells based on combinatorial TF expression. Subpopulations of islet cells co-expressing ARX/MAFB ( cells) and MAFA/MAFB ({beta} cells) exhibited greater expression of key genes related to glucose sensing and hormone secretion relative to subpopulations expressing only one or neither TF. Moreover, all subpopulations were identified in native pancreatic tissue from multiple donors. By Patch-seq, MAFA/MAFB co-expressing {beta} cells showed enhanced electrophysiological activity. Thus, these results indicate combinatorial TF expression in islet and {beta} cells predicts highly functional, mature subpopulations.

genomics↗

bioRxiv2020

Human iPSC-derived cerebral organoids model features of Leigh Syndrome and reveal abnormal corticogenesis

Leigh syndrome (LS) is a rare, inherited neurometabolic disorder that presents with bilateral brain lesions, caused by defects in the mitochondrial respiratory chain and associated nuclear-encoded proteins. We generated iPSCs from three patient-derived LS fibroblast lines and identified, by whole-exome and mitochondrial sequencing, unreported mutations in pyruvate dehydrogenase (GM0372, PDH; GM13411, MT-ATP6/PDH) and dihydrolipoyl dehydrogenase (GM01503, DLD). LS-derived iPSC lines were viable and generally capable of differentiating into key progenitor populations, but we identified several abnormalities in three-dimensional differentiation models of brain development. LS-derived cerebral organoids showed defects in neural epithelial bud generation, size, and cortical architecture at 100 days. The double mutant MT-ATP6/PDH line produced organoid neural progenitor cells with abnormal mitochondrial morphology characterized by fragmentation and disorganization and showed an increased generation of astrocytes. These studies aim to provide a comprehensive phenotypic characterization of available patient-derived cell lines that can be used as LS model systems.

cell biology↗

bioRxiv2020

Pancreatlas: a comprehensive and interactive image atlas of the human pancreas in health and disease

Human tissue phenotyping generates complex spatial information from numerous imaging modalities, yet images typically become static figures for publication and original data and metadata are rarely available. While comprehensive image maps exist for some organs, most resources have limited support for multiplexed imaging or have non-intuitive user interfaces. Therefore, we built a Pancreatlas resource that integrates several technologies into a novel interface, allowing users to access richly annotated web pages, drill down to individual images, and deeply explore data online. The current version of Pancreatlas contains over 800 unique images acquired by whole-slide scanning, confocal microscopy, and imaging mass cytometry, and is available at https://www.pancreatlas.org. To create this human pancreas-specific biological imaging resource, we developed a React-based web application and Python-based application programming interface, collectively called Flexible Framework for Integrating and Navigating Data (FFIND), which can be adapted beyond Pancreatlas to meet countless imaging or other structured data management needs.

cell biology↗