Biology subjects

Morgan, R.

Publications and source records attributed to Morgan, R..

18 recordsLinked to original sources

bioRxiv2026

The HuBMAP Framework for Advancing Data FAIRness

Since publication of the FAIR Guiding Principles in 2016, the scientific community has increasingly sought to make experimental data findable, accessible, interoperable, and reusable. Operationalizing the FAIR principles in routine scientific workflows remains challenging without a standardized, workable infrastructure. With over 10,000 datasets from over 40 institutions, spanning more than 50 diverse assay types ranging from single-cell sequencing technologies to 2D and 3D spatial omics, the U.S. National Institutes of Health (NIH) Human Bio-Molecular Atlas Program (HuBMAP) consortium has been ideally situated to create a FAIR ecosystem. With the goal of achieving data "FAIRness," HuBMAP developed and implemented well-defined, community-endorsed metadata reporting standards across the research lifecycle. These reporting standards include detailed schemas, harmonized across a multitude of assays, that define the metadata associated with a dataset and the organization of the corresponding data files. These standards ensure documentation of the data collection process, of the data themselves, and of the manner in which the data are packaged for sharing, while remaining compliant with the Health Insurance Portability and Accountability Act (HIPAA). The use of these reporting standards, in tandem with technology to foster adherence, allows HuBMAP to fulfill its goal of generating FAIR data for open dissemination through its Data Portal and Human Reference Atlas. The procedures and simple workflow adopted by HuBMAP investigators serve as a model for other scientific communities aiming to maximize the value of varied datasets addressing a shared research question. The HuBMAP end-to-end, metadata-centered workflow has been replicated and enhanced by the NIH Cellular Senescence Network (SenNet) consortium and is readily available through open-source technology for others to utilize.

cell biology↗

bioRxiv2025

Identification of chemicals targeting dementia genes and pathways using the Comparative Toxicogenomics Database

IntroductionDementia is a public health challenge and exposures likely contribute to risk, though many have not been evaluated. We screened chemicals for enrichment with dementia genes and related pathways. MethodsWe obtained gene lists from the Comparative Toxicogenomics Database for 1,008 chemicals and nine dementia-related pathways (e.g., Alzheimers disease, tauopathies). We tested pairwise chemical-dementia gene enrichment using Fishers exact tests and proportional reporting ratios (PRR), accounting for multiple comparisons with false discovery rate (FDR<1x10-6). ResultsOf the chemicals tested, 742 (73.6%) were enriched for at least one dementia pathway and 15 with all nine pathways, including benzo(a)pyrene, ethanol, paraquat, and particulate matter. We observed 295 chemicals enriched for Alzheimers disease, including sodium arsenite (PRR = 57.9) and 305 enriched for tauopathies, including bisphenol A (PRR=37.7). DiscussionWe identified chemicals enriched for dementia pathways, suggesting broad classes of chemicals contribute to dementia.

genomics↗

bioRxiv2025

The IFN I response in tumor cells is shaped by PARP7-p300/CBP interactions through distinct loss- and gain-of-function mechanisms

PARP7, a mono-ADP-ribosyl (MAR) transferase, is a key suppressor of the type I interferon (IFN-I) IFN{beta} in various tumor cells and a validated drug target. This negative regulation is reversed by small-molecule inhibitors of PARP7 catalytic activity, resulting in increased IFN-{beta} expression. Yet, the mechanism of action of PARP7 inhibitors remains unclear because the relevant substrates of PARP7-mediated MARylation are unknown. Using an optimized analog- sensitive chemical genetic (ASCG) approach, we identified the co-activators, p300 and CBP, as nuclear PARP7 substrates. We identified an -helical domain in PARP7 essential for p300/CBP interaction, MARylation, and proteasome degradation. Disrupting PARP7-p300/CBP interaction prevents PARP7s suppression of IFN{beta} in colorectal cancer cells. p300/CBP reciprocally regulate PARP7s activity and nuclear localization. Intriguingly, treatment with PARP7 inhibitors increased IFN{beta} expression more than PARP7 knockout in a p300/CBP-dependent manner. Our findings suggest that in some contexts, IFN{beta} induction by PARP7 inhibitors occurs via two mechanisms: inhibiting MARylation of p300/CBP (loss-of-function) and stabilizing the PARP7- p300/CBP complex (gain-of-function). TeaserChemical genetics discovery of p300 and CBP as substrates of PARP7 that are essential for PARP7-mediated regulation of IFN{beta} via a dual mechanism.

cancer biology↗

bioRxiv2025

Status of Florida's pillar coral population: in situ declines and ex situ successes

The population of the pillar coral, Dendrogyra cylindrus, in Florida was decimated from 2013-2020, primarily by the emergence of stony coral tissue loss disease (SCTLD). Monitoring of survivors from 2021 - early 2025 showed that the population underwent an additional 96% decline in live tissue, 78% loss in living colonies, and 57% loss of genotypes. SCTLD continued to be the primary cause of these losses. Though some surviving tissue isolates exhibited small amounts of growth, the population remains extremely small, with only an estimated 9.6 square meters of tissue remaining on 23 colonies (15 genotypes). Additionally, colonies are far too dispersed to successfully fertilize spawned gametes. The further declines in the population since 2020 highlight the instability of the remnant population, as well as the value of the pillar coral rescue program and ongoing propagation efforts. As of February 2025, eight different in situ and ex situ facilities were caring for rescued D. cylindrus. Experimental fragmentation at one in situ nursery identified variable, but continually increasing, growth rates across multiple fragmentation events. Sexual propagation efforts at an ex situ nursery documented 105 different rescue fragments spawning across five years. The smallest fragment was 9 x 7 x 9 cm, establishing a potential "minimum colony size" for reproductive capacity for this species. From these spawning events, 82 juveniles were being raised ex situ in early 2025. Two of these sexually propagated juveniles spawned six years after settlement, thus establishing a potential minimum age for reproduction.

ecology↗

bioRxiv2024

A reliance on human habitats is key to the success of an introduced predatory reptile

Understanding the success of animals in novel environments is increasingly important as human-mediated introductions continue to move species far beyond their natural ranges. Alongside these introductions, inhabited and agricultural areas are spreading, and correspondingly most animal introductions occur in populated areas. Commensal species which can live alongside humans by making use of specific conditions, structures, or prey, have a significant advantage. Introduced mammal species often use anthropogenic features in their environment and demonstrate a higher tolerance of human disturbance, but their importance remains understudied in ectotherms. The Aesculapian snake (Zamenis longissimus) is an ectotherm which has been introduced beyond the northern extremities of its natural range. To understand their persistence, we radio-tracked snakes daily over two active seasons, including high-frequency tracking of a subset of males. We investigated snake home range size using Autocorrelated Kernel Density Estimators (AKDE). Using AKDE-weighted Habitat Selection Functions we identified preferences for habitat features in a mosaic of habitats, and we used Integrated Step Selection Functions to further explore how these features influence movement. We revealed a particular preference for buildings in male snakes, while females preferred woodland. We demonstrate that the success of this ectothermic predator is likely tied to a willingness to use human features of the landscape.

animal behavior and cognition↗

bioRxiv2024

Carbonyl Reductase 1: a novel regulator of blood pressure in Down Syndrome

BackgroundApproximately one in every 800 children is born with the severe aneuploid condition of Down Syndrome (DS), a trisomy of chromosome 21. Low blood pressure (hypotension) is a common condition associated with DS and can have a significant impact on exercise tolerance and quality of life. Little is known about the factors driving this hypotensive phenotype and therefore therapeutic interventions are limited. Carbonyl reductase 1 (CBR1) is an enzyme contributing to the metabolism of prostaglandins, glucocorticoids, reactive oxygen species and neurotransmitters, encoded by a gene (CBR1) positioned on chromosome 21 with potential to impact blood pressure. MethodsUtilising genetically modified mice and telemetric blood pressure measurement, we tested the hypothesis that CBR1 influences blood pressure and that its overexpression contributes to hypotension in DS. ResultsIn a mouse model of DS (Ts65Dn), which exhibit hypotension, CBR1 activity was increased and pharmacological inhibition of CBR1 increased blood pressure. Mice heterozygous null for Cbr1 had reduced CBR1 enzyme activity and elevated blood pressure. Further experiments indicate that the underlying mechanisms include alterations in sympathetic tone and prostaglandin metabolism. ConclusionsWe conclude that CBR1 activity contributes to blood pressure homeostasis and inhibition of CBR1 may present a novel therapeutic opportunity to correct symptomatic hypotension in DS.

physiology↗

bioRxiv2024

DNA methylation differences between the female and male X chromosomes in human brain

The mechanisms of X chromosome inactivation suggest fundamental epigenetic differences between the female and male X chromosomes. However, DNA methylation studies often exclude the X chromosomes. In addition, many previous studies relied on techniques that examine non-randomly selected subsets of positions such as array-based methods, rather than assessing the whole X chromosome. Consequently, our understanding of X chromosome DNA methylation lags behind that of autosomes. Here we addressed this gap of knowledge by studying X chromosome DNA methylation using 89 whole genome bisulfite sequencing (WGBS) maps from neurons and oligodendrocytes. Using this unbiased and comprehensive data, we show that DNA methylation of the female X chromosomes is globally reduced (hypomethylated) across the entire chromosome compared to the male X chromosomes and autosomes. On the other hand, the majority of X-linked promoters were more highly methylated (hypermethylated) in females compared to males, consistent with the role of DNA methylation in X chromosome inactivation and dosage compensation. Remarkably, hypermethylation of female X promoters was limited to a group of previously lowly methylated promoters. The other group of highly methylated promoters were both hyper- and hypo-methylated in females with no obvious association with gene expression. Therefore, X chromosome inactivation by DNA methylation was exclusive to a subset of promoters with distinctive epigenetic feature. Apart from this group of promoters, differentially methylated regions in the female and male X chromosomes were dominated by female hypomethylation. Our study furthers the understanding of X-chromosome dosage regulation by DNA methylation on the chromosomal level as well as on individual gene level.

genomics↗

bioRxiv2023

Genome assembly of the dyeing poison frog provides insights into the dynamics of transposable element and genome-size evolution

Genome size varies greatly across the tree of life and transposable elements are an important contributor to this variation. Among vertebrates, amphibians display the greatest variation in genome size, making them ideal models to explore the causes and consequences of genome size variation. However, high-quality genome assemblies for amphibians have, until recently, been rare. Here, we generate a high-quality genome assembly for the dyeing poison frog, Dendrobates tinctorius. We compare this assembly to publicly-available frog genomes and find evidence for both large-scale conserved synteny and widespread rearrangements between frog lineages. Comparing conserved orthologs annotated in these genomes revealed a strong correlation between genome size and gene size. To explore the cause of gene-size variation, we quantified the location of transposable elements relative to gene features and find that the accumulation of transposable elements in introns has played an important role in the evolution of gene size in D. tinctorius, while estimates of insertion times suggest that many insertion events are recent and species-specific. Finally, we show that the diversity and abundance of transposable elements in poison frog genomes can complicate genotyping efforts that rely on repetitive elements as sequence anchors. Our results show that transposable elements have clearly played an important role in the evolution of large genome size in D. tinctorius. Future studies are needed to fully understand the dynamics of transposable element evolution and to optimise primer or bait design for cost-effective population-level genotyping in species with large, repetitive genomes. SignificanceAmphibians display more variation in genome size than any other vertebrate lineage. Complexities associated with large genomes frequently hamper genome assembly and population genetic studies. Here we use long-read HiFi sequences to generate a high-quality 6.3 Gbp genome assembly of the poison frog Dendrobates tinctorius. We use this genome and leverage comparative genomics and de novo annotations to quantify aspects of genome evolution driven by repetitive transposable genetic elements. Our results provide support for the dynamic role that transposable elements play in driving the evolution of "genomic gigantism" in amphibians. We also show how transposable elements can be leveraged for cost-efficient population genetic studies using limited input material.

genetics↗

bioRxiv2023

A genome-wide cytotoxicity screen of Cluster F1 mycobacteriophage Girr reveals novel inhibitors of Mycobacterium smegmatis growth

Over the past decade, thousands of bacteriophage genomes have been sequenced and annotated. A striking observation from this work is that known structural features and functions cannot be assigned for >65% of the encoded proteins. One approach to begin experimentally elucidating the function of these uncharacterized gene products is genome-wide screening to identify phage genes that confer phenotypes of interest like inhibition of host growth. This study describes the results of a screen evaluating the effects of overexpressing each gene encoded by the temperate Cluster F1 mycobacteriophage Girr on the growth of the host bacterium Mycobacterium smegmatis. Overexpression of 29 of the 102 Girr genes ([~]28% of the genome) resulted in mild to severe cytotoxicity. Of the 29 toxic genes described, 12 have no known function (NKF) and are predominately small proteins of <125 amino acids. Overexpression of the majority of these 12 cytotoxic NKF proteins resulted in moderate to severe growth reduction and represent novel antimicrobial products. The remaining 17 toxic genes have predicted functions, encoding products involved in phage structure, DNA replication/modification, DNA binding/gene regulation, or other enzymatic activity. Comparison of this dataset with prior genome-wide cytotoxicity screens of mycobacteriophages Waterfoul and Hammy reveals some common functional themes, though several of the predicted Girr functions associated with cytotoxicity in our report, including genes involved in lysogeny, have not been described previously. This study, completed as part of the HHMI-supported SEA-GENES project, highlights the power of parallel, genome-wide overexpression screens to identify novel interactions between phages and their hosts.

microbiology↗

bioRxiv2022

A yeast-based system to study SARS-CoV-2 Mpro structure and to identify nirmatrelvir resistant mutations

The SARS-CoV-2 main protease (Mpro) is a major therapeutic target. The Mpro inhibitor, nirmatrelvir, is the antiviral component of Paxlovid, an orally available treatment for COVID-19. As Mpro inhibitor use increases, drug resistant mutations will likely emerge. We have established a non-pathogenic system, in which yeast growth serves as a proxy for Mpro activity, enabling rapid identification of mutants with altered enzymatic activity and drug sensitivity. The E166 residue is known to be a potential hot spot for drug resistance and yeast assays showed that an E166R substitution conferred strong nirmatrelvir resistance while an E166N mutation compromised activity. On the other hand, N142A and P132H mutations caused little to no change in drug response and activity. Standard enzymatic assays confirmed the yeast results. In turn, we solved the structures of Mpro E166R, and Mpro E166N, providing insights into how arginine may drive drug resistance while asparagine leads to reduced activity. The work presented here will help characterize novel resistant variants of Mpro that may arise as Mpro antivirals become more widely used.

microbiology↗

bioRxiv2022

Water salinity does not affect acute thermal tolerance (CTmax) in zebrafish (Danio rerio)

Tolerance against acute warming is an essential trait that can determine how organisms cope during heatwaves, yet the mechanisms underlying it remain elusive. Water salinity has previously been shown to modulate thermal tolerance and may therefore provide clues towards these limiting mechanisms. Here we tested whether short (2 hours) and long (10 days) term exposure to different water salinities (0-5 ppt) affected acute thermal tolerance in zebrafish (N=269). We found that water salinity did not affect the thermal tolerance of zebrafish at either time point, indicating that salinity does not affect the mechanism limiting acute thermal tolerance limits in zebrafish. We did, however, observe unexpected behaviour during the CTmax test in a subset of fish in the highest salinity treatment after 10 days (3 ppt), indicating some form of salinity-driven disturbance during warming.

physiology↗

bioRxiv2022

Vitamin D receptor cistrome-transcriptome analyses establishes quantitatively distinct receptor genomic interactions in African American prostate cancer regulated by BAZ1A

BackgroundAfrican American (AA) prostate cancer (PCa) appears uniquely sensitive to 1,25(OH)2D3 signaling, compared to European American (EA) PCa, but the extent and impact of vitamin D receptor genomic functions remain poorly defined. ResultsA panel of EA and AA prostate epithelial cells (EA: HPr1-AR, LNCaP, AA: RC43N, RC43T, RC77N, RC77T) were analyzed with RIME to reveal the cell-specific composition of the VDR- complex. 1,25(OH)2D3-dependent ATAC-Seq revealed the greatest impact on nucleosome positioning in RC43N and RC43T, with gain of nucleosome-free at enhancer regions. VDR ChIP-Seq identified stronger and more frequent VDR binding in RC43N and RC43T that was enriched for a larger and distinct motif repertoire, than EA cells. VDR binding significantly overlapped with core circadian rhythm transcription factors in AA cell line models. RNA-Seq also revealed significantly stronger 1,25(OH)2D3 dependent VDR transcriptional responses enriched for circadian rhythm and inflammation networks in AA cells. Whilst RC43N was most responsive, RC43T displayed distorted responses. Significantly reduced BAZ1A/SMARCA5 in AA PCa samples was identified, and restored BAZ1A expression uniquely and significantly increased 1,25(OH)2D3-regulated VDR targets in AA cells. These VDR- dependent cistrome-annotated genes were also uniquely and most significantly identified in three cohorts of AA PCa patients. ConclusionThese data suggest VDR transcriptional control in the prostate is more potent and dynamic in AA men, and primed to govern inflammatory and circadian pathways. Reduced BAZ1A/SMARCA5 expression and/or reduced environmentally-regulated serum vitamin D3 levels suppress these actions. Therefore, the VDR axis lies at the cross-roads of biopsychosocial processes including stress responses, access to quality early detection and treatment, social determinants and that collectively contribute to PCa health disparities.

cancer biology↗

bioRxiv2021

THERAPEUTIC EFFECTS OF HYPOXIC AND PRO-INFLAMMATORY PRIMING OF MESENCHYMAL STEM CELL-DERIVED EXTRACELLULAR VESICLES IN INFLAMMATORY ARTHRITIS

Novel biological therapies have revolutionised the management of Rheumatoid Arthritis (RA) but no cure currently exists. Mesenchymal stem cells (MSCs) immunomodulate inflammatory responses through paracrine signalling, including via secretion of extracellular vesicles (EVs) in the cell secretome. We evaluated the therapeutic potential of MSCs-derived small EVs in an antigen-induced model of arthritis (AIA). EVs isolated from MSCs cultured normoxically (21% O2, 5% CO2), hypoxically (2% O2, 5% CO2) or with a pro-inflammatory cytokine cocktail were applied into the AIA model. Disease pathology was assessed post-arthritis induction through swelling and histopathological analysis of synovial joint structure. Activated CD4+ T cells from healthy mice were cultured with EVs or MSCs to assess deactivation capabilities prior to application of standard EVs in vivo to assess T cell polarisation within the immune response to AIA. All EVs treatments reduced knee-joint swelling whilst only normoxic and pro-inflammatory primed EVs improved histopathological outcomes. In vitro culture with EVs did not achieve T cell deactivation. Polarisation towards CD4+ helper cells expressing IL17a (Th17) was reduced when normoxic and hypoxic EV treatments were applied in vitro. Normoxic EVs applied into the AIA model reduced Th17 polarisation and improved Th17:Treg homeostatic balance. Priming of MSCs in EV production can be applied to alter the therapeutic efficacy however normoxic EVs present the optimal strategy for broad therapeutic benefit. The varied outcomes observed in MSCs priming may promote EVs optimised for therapies targeted for specific therapeutic priorities. EVs present an effective novel technology with potential for cell-free therapeutic translation.

immunology↗

bioRxiv2020

Classification of ovarian cancer cell lines using transcriptional profiles defines the five major pathological subtypes

Epithelial ovarian cancer (EOC) is a heterogenous disease consisting of five major pathologically distinct subtypes: High-grade serous ovarian carcinoma (HGSOC), low-grade serous (LGS), endometrioid, clear cell and mucinous carcinoma. Although HGSOC is the most prevalent subtype, representing approximately 75% of cases, a 2013 landmark study from Domcke et al., found that many frequently used ovarian cancer cell lines were not genetically representative of HGSOC tissue samples from The Cancer Genome Atlas. Although this work subsequently identified several rarely used cell lines to be highly suitable as HGSOC models, cell line selection for ovarian cancer research does not appear to have altered substantially in recent years. Here, we find that application of non-negative matrix factorisation (NMF) to the transcriptional profiles of 45 commonly used ovarian cancer cell lines exquisitely clusters them into five distinct classes, representative of the five main subtypes of EOC. This methodology was in strong agreement with Domcke et al., in identification of cell lines most representative of HGSOC. Furthermore, this robust classification of cell lines, including some previously not annotated or miss-annotated in the literature, now informs selection of the most appropriate models for all five pathological subtypes of ovarian cancer. Furthermore, using machine learning algorithms trained using the classification of the current cell lines, we are able provide a methodology for future classification of novel EOC cell lines.

cancer biology↗

bioRxiv2020

PARG inhibition induces replication catastrophe in ovarian cancer cells with down-regulated DNA replication genes

The discovery that PARP1/2 inhibitors selectively kill BRCA mutant cells has led to a paradigm shift in the treatment of women with homologous recombination (HR)-deficient high-grade serous ovarian cancer (HGSOC), driving unprecedented improvements in progression-free and, more recently, overall survival. However, because most HGSOC cases are not HR-defective, and are therefore unlikely to benefit from PARPi-based therapies, additional strategies will be required to improve outcomes for women with HR-proficient disease. To develop novel therapeutic strategies, considerable attention is now being focused on inhibitors targeting PARG, the poly(ADP ribose) glycohydrolase that counterbalances PARP1/2 activity. Here we characterise ten ovarian cancer cell lines in response to the PARG inhibitor PDD00017273, hereafter PARGi. We demonstrate that six lines are resistant while four are sensitive, and that sensitivity correlates with several markers of persistent DNA replication stress, DNA damage and replication catastrophe, namely the accumulation of asymmetric DNA replication fibres, {gamma}H2AX and RPA foci, KAP1 and Chk1 phosphorylation, a pre-mitotic cell cycle block and, following prolonged exposure, a pan-nuclear {gamma}H2AX phenotype that indicates RPA exhaustion. We demonstrate that PARGi-sensitive cell lines have down-regulated DNA replication genes, including components of the fork protection complex, namely TIMELESS, TIPIN and CLASPIN. These observations suggest that a subset of HGSOC may respond to PARG inhibitors and that "replication stress" gene expression signature could serve as a predictive biomarker to guide the design of clinical trials.

cancer biology↗

bioRxiv2020

MSCs from syndecan-3 null mice exhibit enhanced adhesion to collagen type I, hyperactivation of the AKT pathway and increased efficacy in inflammatory arthritis

1Rheumatoid arthritis (RA) is a debilitating and painful inflammatory autoimmune disease characterised by the accumulation of leukocytes in the synovium, cartilage destruction and bone erosion. The immunomodulatory effects of bone marrow derived mesenchymal stem cells (MSCs) has been widely studied and the recent observations that syndecan-3 (SDC3) is selectively pro-inflammatory in the joint led us to hypothesise that SDC3 might play an important role in MSC biology. MSCs isolated from bone marrow of wild type and Sdc3-/- mice were used to assess immunophenotype, differentiation, adhesion and migration properties and cell signalling pathways. While both cell types show similar differentiation potential and forward scatter values, the cell complexity in wild type MSCs was significantly higher than in Sdc3-/- cells and was accompanied by lower spread surface area. Moreover, Sdc3-/- MSCs adhered more rapidly to collagen type I and showed a dramatic increase in AKT phosphorylation, accompanied by a decrease in ERK1/2 phosphorylation compared with control cells. In a mouse model of antigen-induced inflammatory arthritis, intraarticular injection of Sdc3-/- MSCs yielded enhanced recovery compared to injection of wild type MSCs. In conclusion, our data suggest that syndecan-3 regulates MSC adhesion and efficacy in inflammatory arthritis, likely via induction of the AKT pathway.

immunology↗

bioRxiv2019

Brain cooling marginally increases maximum thermal tolerance in Atlantic cod

The physiological mechanisms determining thermal limits in fishes are debated but remain elusive. It has been hypothesised that loss of motor function observed as a loss of equilibrium during an acute thermal challenge is due to direct thermal effects on brain neuronal function. To test this hypothesis, we mounted cooling plates on the head of Atlantic cod (Gadus morhua) and quantified whether local cooling of the brain increased whole-organism critical thermal maxima (CTmax). Brain cooling reduced brain temperature by 2-6{degrees}C and increased CTmax by 0.5-0.7{degrees}C relative to instrumented and uninstrumented controls, suggesting that direct thermal effects on brain neurons might contribute to setting upper thermal limits in fish. However, the improvement in CTmax with brain cooling was small relative to the difference in brain temperature, demonstrating that other mechanisms (e.g., failure of spinal and peripheral neurons, or muscle) may also contribute to controlling acute thermal tolerance in fishes.\n\nSummary statementWe tested whether brain temperature sets the upper thermal limit in a fish. Selectively cooling the brain during whole-organism thermal ramping marginally increased thermal tolerance.

physiology↗

bioRxiv2016

Starting from the end: what to do when restricted data is released

Repository managers can never be one hundred percent sure of the security ofhosted research data. Even assuming that human errors and technical faults will never happen, repositories can be subject to hacking attacks. Therefore, repositories accepting personal/sensitive data (or other forms of restricted data) should have workflows in place with defined procedures to be followed should things go wrong and restricted data is inappropriately released. In this paper wewill report on our considerations and procedures when restricted data from ourinstitution was inappropriately released.

scientific communication and education↗