Spotlight Program

Showcasing outstanding research by Swiss life scientists.

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We're proud to present the research of Swiss scientists working hard to improve our understanding of life.

Scroll down to read about them, their research, and the Promega technologies they use.

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Ana Belén Iglesias-Romero, Karolina Kaminska, Mathieu Quinodoz, Marc Folcher, Siying Lin, Gavin Arno, Joaquim Calado, Andrew R. Webster, Alexandre Moulin, Ana Berta Sousa, Luisa Coutinho-Santos, Cristina Santos, Carlo Rivolta

Bi-allelic variants in COQ8B, a gene involved in the biosynthesis of coenzyme Q10, lead to non-syndromic retinitis pigmentosa

Am J Hum Genet, 2024, Oct 3; 111(10):2299-2306; doi: 10.1016/j.ajhg.2024.08.005; PMID: 39226897

Inherited retinal diseases, such as retinitis pigmentosa (RP), are genetically heterogeneous diseases that cause progressive loss of the retina's photoreceptor cells, eventually leading to blindness. Although more than 100 gene variants have been associated with the pathogenesis of RP, the heritability and molecular mechanisms underlying this disease still present significant knowledge gaps. The authors of this study combined state-of-the-art genomic and protein analysis techniques to investigate the potential causes of retinal damage in RP patients.

Abstract

Retinitis pigmentosa (RP) is a Mendelian disease characterized by gradual loss of vision, due to the progressive degeneration of retinal cells. Genetically, it is highly heterogeneous, with pathogenic variants identified in more than 100 genes so far. Following a large-scale sequencing screening, we identified five individuals (four families) with recessive and non-syndromic RP, carrying as well bi-allelic DNA changes in COQ8B, a gene involved in the biosynthesis of coenzyme Q10. Specifically, we detected compound heterozygous assortments of five disease-causing variants (c.187C>T [p.Arg63Trp], c.566G>A [p.Trp189Ter], c.1156G>A [p.Asp386Asn], c.1324G>A [p.Val442Met], and c.1560G>A [p.Trp520Ter]), all segregating with disease according to a recessive pattern of inheritance. Cell-based analysis of recombinant proteins deriving from these genotypes, performed by target engagement assays, showed in all cases a significant decrease in ligand-protein interaction compared to the wild type. Our results indicate that variants in COQ8B lead to recessive non-syndromic RP, possibly by impairing the biosynthesis of coenzyme Q10, a key component of oxidative phosphorylation in the mitochondria.

Read the full publication online.

ana-grey

About Ana

Ana currently works as a postdoctoral researcher at the Institute of Molecular and Clinical Ophthalmology Basel (IOB), in the Ophthalmic Genetics group led by Prof. Carlo Rivolta. She applies her expertise in cellular and molecular biology, biochemistry, and microscopy to uncover the causes underlying monogenic and genetically complex ophthalmic diseases. Her aim is to decipher the molecular mechanisms that lead to blindness.

nanobret-ana

Promega Product Used

The NanoBRET® Target Engagement (TE) Intracellular Kinase Assays are based on the NanoBRET® System, an energy transfer technique designed to measure molecular proximity in living cells. The NanoBRET® TE Assays measure the apparent affinity of test compounds by competitive displacement of the NanoBRET® tracer, reversibly bound to a NanoLuc® luciferase-kinase fusion expressed in cells. In this study, measurement of the affinity of the tracer for wild-type versus mutant proteins was used as a proxy for normal enzymatic activity. Indeed, reduced binding might indicate a compromised or strongly modified catalytic pocket that can lead to functional defects.

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Lorenza P. Ferretti, Flurina Böhi, Deena M. Leslie Pedrioli, Phil F. Cheng, Elena Ferrari, Petra Baumgaertner, Abdiel Alvarado-Diaz, Federica Sella, Alessandra Cereghetti, Patrick Turko, Roni H. Wright, Katrien De Bock, Daniel E. Speiser, Roberto Ferrari, Mitchell P. Levesque, Michael O. Hottiger

Combinatorial Treatment with PARP and MAPK Inhibitors Overcomes Phenotype Switch-Driven Drug Resistance in Advanced Melanoma

Cancer Res., Dec. 2023; 1;83(23):3974-3988. doi: 10.1158/0008-5472.CAN-23-0485; PMID: 37729428

Resistance to targeted therapy constitutes a major challenge in the therapeutic management of melanoma, an aggressive form of skin cancer. The switch from proliferative to highly invasive forms of melanoma that can metastasize often drives the resistance to targeted drugs such as MAPK family inhibitors. Advancing current understanding of phenotype switching at the molecular level offers tremendous potential for developing innovative treatment approaches that will eventually improve the prognosis and treatment of metastatic melanoma.

Abstract

Metastatic melanoma is either intrinsically resistant or rapidly acquires resistance to targeted therapy treatments, such as MAPK inhibitors (MAPKi). A leading cause of resistance to targeted therapy is a dynamic transition of melanoma cells from a proliferative to a highly invasive state, a phenomenon called phenotype switching. Mechanisms regulating phenotype switching represent potential targets for improving treatment of patients with melanoma. Using a drug screen targeting chromatin regulators in patient-derived three-dimensional MAPKi-resistant melanoma cell cultures, we discovered that PARP inhibitors (PARPi) restore sensitivity to MAPKis, independent of DNA damage repair pathways. Integrated transcriptomic, proteomic, and epigenomic analyses demonstrated that PARPis induce lysosomal autophagic cell death, accompanied by enhanced mitochondrial lipid metabolism that ultimately increases antigen presentation and sensitivity to T-cell cytotoxicity. Moreover, transcriptomic and epigenetic rearrangements induced by PARP inhibition reversed epithelial–mesenchymal transition-like phenotype switching, which redirected melanoma cells toward a proliferative and MAPKi-sensitive state. The combination of PARP and MAPKis synergistically induced cancer cell death both in vitro and in vivo in patient-derived xenograft models. Therefore, this study provides a scientific rationale for treating patients with melanoma with PARPis in combination with MAPKis to abrogate acquired therapy resistance.

Significance: PARP inhibitors can overcome resistance to MAPK inhibitors by activating autophagic cell death and reversing phenotype switching, suggesting that this synergistic combination could help improve the prognosis of patients with melanoma.

Read the full publication online: https://aacrjournals.org/cancerres/article/83/23/3974/730142/Combinatorial-Treatment-with-PARP-and-MAPK

lorenza-white

About Lorenza

Lorenza worked as a URPP fellow in translational cancer research and postdoctoral researcher at the University of Zurich (UZH) and University Hospital Zurich (USZ). She is currently exploring opportunities to advance her scientific career. Utilizing her extensive expertise in molecular biology, she applied multidisciplinary approaches to unravel the complexity of melanoma biology. Lorenza is dedicated to pursuing innovative approaches advancing melanoma treatments and aims to make a significant impact on patients' lives.

cell-titer

Promega Product Used

CellTiter-Glo® 3D Cell Viability Assay uses the same reliable chemistry as the classic CellTiter-Glo® Assay and has been optimized to accurately determine cell viability in 3D models. By quantifying ATP levels using a high sensitivity luminescence-based readout, it is an ideal tool to assess drug toxicity in spheroids.

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Charlotte Sutter, Annabelle Marks, Livia Seiler, Fabian Baron, Zsuzsanna Varga, Cordula Haas, Jacqueline Neubauer

Methylation-based age estimation of different types of bones

Conference abstract. This project was presented at the 44th Spurenworkshop in Frankfurt (March 2024).

Accurate age estimation from forensically relevant traces, for instance using DNA methylation analysis, is essential for supporting forensic casework. While relevant DNA methylation markers and predictive models have been extensively validated for tissues such as blood or saliva, datasets derived from bone samples are comparatively small and existing models remain understudied. To ensure reliable age determination from bones, there is a need for the validation and optimization of available forensic DNA phenotyping models.

Abstract (EN)

Age estimation using DNA methylation from forensically relevant traces is an at the moment intensively researched application in the field of Forensic DNA Phenotyping. As it is currently being implemented in forensic casework in an increasing number of laboratories across Europe, it is important to thoroughly test the various available models for their reliability in application.
As generally known, different tissue types require different markers and models to achieve the highest possible age estimation accuracy. One forensically relevant tissue that has received comparatively less attention in DNA methylation analyses than, for example, blood or saliva is bone tissue. Although markers and models for bones have been investigated with various technologies (e.g., MPS or SNaPshot), the datasets are often comparatively small, and the sample collection used is not always described in great detail.

In our study, we are testing an existing MPS-based age estimation model for bones on five different types of bones (rib, clavicle, femur, petrous bone and pelvic crest). To optimally compare the age estimations of these different bones, all five bone types were collected from each autopsied individual.

Our research question is whether different types of bones in the markers we investigated exhibit the same methylation patterns and whether we find different estimation accuracies for each bone type. Accordingly, we will compare the estimated age between the different bone types, in order to adjust and optimize the model or the selection of CpG sites within the investigated markers if necessary.

Abstract (DE)

Die Altersschätzung mittels DNA-Methylierung aus forensisch relevanten Spuren ist eine derzeit intensiv erforschte Anwendung im Bereich der Forensischen DNA Phänotypisierung. Da sie aktuell in immer mehr Laboren europaweit in die forensische Fallarbeit implementiert wird, ist es wichtig die verschiedenen verfügbaren Modelle gründlich auf ihre Zuverlässigkeit in der Anwendung zu testen.

Wie allgemein bekannt ist, erfordern unterschiedliche Gewebetypen unterschiedliche Marker und Modelle, um die höchstmögliche Schätzgenauigkeit zu erreichen. Ein forensisch relevantes Gewebe, das vergleichsweise weniger Aufmerksamkeit bei DNA-Methylierungsanalysen erhalten hat als beispielsweise Blut oder Speichel, ist Knochengewebe. Obwohl für Knochen bereits Marker erforscht und Modelle für unterschiedliche Technologien (z.B. MPS oder SNaPshot) entwickelt wurden, sind die Datensätze oft vergleichsweise klein, und die verwendete Probensammlung ist nicht immer detailliert beschrieben.
In unserer Studie testen wir ein existierendes MPS-basiertes Altersschätzungsmodell für Knochen an fünf verschiedenen Knochentypen (Rippe, Schlüsselbein, Oberschenkelknochen, Felsenbein und Beckenkamm). Um die Schätzungen der unterschiedlichen Knochen optimal miteinander vergleichen zu können, wurden von jeder obduzierten Person alle fünf Knochentypen gesammelt.

Unsere Fragestellung ist, ob verschiedene Knochentypen in den von uns untersuchten Markern die gleichen Methylierungsmuster aufweisen, und ob wir unterschiedliche Schätzgenauigkeiten für jeden Knochentyp finden. Entsprechend werden wir das geschätzte Alter zwischen den einzelnen Knochentypen vergleichen, um bei Bedarf das Modell bzw. die Auswahl der CpG sites innerhalb der untersuchten Marker anpassen und optimieren zu können.

charlotte

About Charlotte

Charlotte is currently working as a doctoral researcher at the Institute of Forensic Medicine at the University of Zurich, Switzerland. Using Promega's MethylEdge® Bisulfite Conversion System, she and her collaborators are investigating the relevance of using DNA methylation for age determination in different bone types. Fueled by her passion for forensic genetics, her aim is to advance current understanding of available forensic phenotyping methods and develop their applications for work with difficult or unusual sample types.

methyl

Promega Product Used

The MethylEdge® Bisulfite Conversion System provides a rapid, efficient method to perform bisulfite conversion with minimal DNA fragmentation in less than two hours. This all-inclusive kit produces intact, usable, DNA for many downstream applications, including qPCR, arrays, and sequencing. Requiring minimal preparation and hands-on time, it is an ideal companion for streamlined DNA methylation analysis workflows.

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Susanne Meile*, Jiemin Du*, Samuel Staubli, Sebastian Grossmann, Hendrik Koliwer-Brandl, Pietro Piffaretti, Lorenz Leitner, Cassandra I. Matter, Jasmin Baggenstos, Laura Hunold, Sonja Milek, Christian Guebeli, Marko Kozomara-Hocke, Vera Neumeier, Angela Botteon, Jochen Klumpp, Jonas Marschall, Shawna McCallin, Reinhard Zbinden, Thomas M. Kessler, Martin J. Loessner, Matthew Dunne, Samuel Kilcher

*These authors contributed equally.

Engineered reporter phages for detection of Escherichia coli, Enterococcus, and Klebsiella in urine

Nat Commun. 2023 Jul 20;14(1):4336. doi: 10.1038/s41467-023-39863-x. PMID: 37474554; PMCID: PMC10359277

Common bacterial infections often present complex, polymicrobial disease etiology and are therefore challenging to diagnose using standard methods. As a result, broad-range antibiotics are preventively prescribed to treat such infections, contributing to the antimicrobial resistance crisis. More sensitive detection techniques utilizing reporter bacteriophage constitute a promising alternative for the specific and reliable identification of certain types of bacterial pathogens in patients.

Abstract

The rapid detection and species-level differentiation of bacterial pathogens facilitates antibiotic stewardship and improves disease management. Here, we develop a rapid bacteriophage-based diagnostic assay to detect the most prevalent pathogens causing urinary tract infections: Escherichia coli, Enterococcus spp., and Klebsiella spp. For each uropathogen, two virulent phages were genetically engineered to express a nanoluciferase reporter gene upon host infection. Using 206 patient urine samples, reporter phage-induced bioluminescence was quantified to identify bacteriuria and the assay was benchmarked against conventional urinalysis. Overall, E. coli, Enterococcus spp., and Klebsiella spp. were each detected with high sensitivity (68%, 78%, 87%), specificity (99%, 99%, 99%), and accuracy (90%, 94%, 98%) at a resolution of ≥103 CFU/ml within 5 h. We further demonstrate how bioluminescence in urine can be used to predict phage antibacterial activity, demonstrating the future potential of reporter phages as companion diagnostics that guide patient-phage matching prior to therapeutic phage application.

Read the full publication online: https://www.nature.com/articles/s41467-023-39863-x

jiemin-headshot

About Jiemin

Jiemin is currently working as a doctoral researcher at the Institute of Food, Nutrition, and Health at ETH Zurich, Switzerland. Utilizing the Nanoluciferase reporter system, she and her colleagues have developed a diagnostic tool for the rapid and sensitive detection of bacterial pathogens in patient urine. Collaborating with partners from the University Hospital Zurich and University Hospital Balgrist, she is focused on advancing phage-based therapeutics to address urinary tract infections. Her goal is to integrate her expertise in molecular phage biology and genetic engineering to enhance patient care and combat the growing challenge of antimicrobial resistance.

nano-glo

Promega Product Used

The Nano-Glo® Luciferase Assay System provides a simple, single-addition reagent that generates a stable and long-lasting glow-type signal in the presence of NanoLuc® luciferase. Because of its small size, NanoLuc® luciferase reporter gene can be inserted into viral genomes without disrupting packaging or enzyme activities. This allows for easy monitoring of viral processes, such as infection of bacteria by reporter bacteriophages.

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Kristina Seiler, Sreoshee Rafiq, Mario P. Tschan

Isoform-specific, Semi-quantitative Determination of Highly Homologous Protein Levels via CRISPR-Cas9-mediated HiBiT Tagging

Bio Protoc. 2023 Jul 20;13(14):e4777. doi: 10.21769/BioProtoc.4777. PMID: 37497448; PMCID: PMC10366989

Genetic redundancy between protein family members is essential to maintain continuous cellular function. However, extensive sequence homology also constitutes a major obstacle in the detection and quantification of distinct protein isoforms. Novel approaches to specifically tag endogenous protein homologs can facilitate their analysis in cells and overcome certain limitations of standard methods relying on isoform-specific antibodies.

Abstract

Many protein families consist of multiple highly homologous proteins, whether they are encoded by different genes or originating from the same genomic location. Predominance of certain isoforms has been linked to various pathological conditions, such as cancer. Detection and relative quantification of protein isoforms in research are commonly done via immunoblotting, immunohistochemistry, or immunofluorescence, where antibodies against an isoform-specific epitope of particular family members are used. However, isoform-specific antibodies are not always available, making it impossible to decipher isoform-specific protein expression patterns. Here, we describe the insertion of the versatile 11 amino acid HiBiT tag into the genomic location of the protein of interest. This tag was developed and is distributed by Promega (Fitchburg, WI, USA). This protocol describes precise and specific protein expression analysis of highly homologous proteins through expression of the HiBiT tag, enabling protein expression quantification when specific antibodies are missing. Protein expression can be analyzed through traditional methods such as western blotting or immunofluorescence, and also in a luciferase binary reporter system, allowing for reliable and fast relative expression quantification using a plate reader.

Read the full publication online: https://bio-protocol.org/en/bpdetail?id=4777&type=0

kristina

About Kristina

Kristina is currently working as a postdoctoral research scientist at the University of Utah in Salt Lake City (USA). She completed her MD-PhD studies at the University of Bern (CH) and Scripps Research La Jolla (USA), where she focused on the role of hexokinase 3 (HK3) in the development of acute myeloid leukemia (AML). Using the HiBiT protein tagging system, she and her colleagues were able to discover a novel role for HK3 in mediating cell death during the treatment of AML cells. In her current role, Kristina is putting her expertise in cellular energy metabolism to use and researching how mitochondrial energy production is regulated in health and disease.

hibit

Promega Product Used

The HiBiT protein tagging system allows for simple and sensitive bioluminescent protein quantitation. The 11 amino acid HiBiT tag can be added easily to a protein of interest using CRISPR-mediated genome editing. The total amount of HiBiT-tagged protein can be evaluated in live cells or cellular lysates through the reconstitution of NanoBiT® enzyme in the presence of LgBiT protein. In addition to this direct detection method, HiBiT-tagged proteins can also be detected via immunostaining using the anti-HiBiT monoclonal antibody.

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Bozhidar-Adrian Stefanov, Maysam Mansouri, Ghislaine Charpin-El Hamri, Martin Fussenegger

Sunlight-Controllable Biopharmaceutical Production for Remote Emergency Supply of Directly Injectable Therapeutic Proteins

Biopharmaceutical manufacturing requires specialized facilities and a long-range cold supply chain for the delivery of the therapeutics to patients. In order to produce biopharmaceuticals in locations lacking such infrastructure, a production process is designed that utilizes the trigger-inducible release of large quantities of a stored therapeutic protein from engineered endocrine cells within minutes to generate a directly injectable saline solution of the protein.
Abstract
Biopharmaceutical manufacturing requires specialized facilities and a long-range cold supply chain for the delivery of the therapeutics to patients. In order to produce biopharmaceuticals in locations lacking such infrastructure, a production process is designed that utilizes the trigger-inducible release of large quantities of a stored therapeutic protein from engineered endocrine cells within minutes to generate a directly injectable saline solution of the protein. To illustrate the versatility of this approach, it is shown that not only insulin, but also glucagon-like peptide 1 (GLP-1), nanoluciferase (NLuc), and the model biopharmaceutical erythropoietin (EPO) can be trigger-inducibly released, even when using biologically inactive insulin as a carrier. The facilitating beta cells are engineered with a controllable TRPV1-mediated Ca2+ influx that induces the fusion of cytoplasmic storage vesicles with the membrane, leading to the release of the stored protein. When required, the growth medium is exchanged for saline solution, and the system is stimulated with the small molecule capsaicin, with a hand-warming pack, or simply by using sunlight. Injection of insulin saline solution obtained in this way into a type-1 diabetes mouse model results in the regulation of blood glucose levels. It is believed that this system will be readily adaptable to deliver various biopharmaceutical proteins at remote locations.

Read the full paper online: https://onlinelibrary.wiley.com/doi/10.1002/smll.202202566
adrian

About Adrian

During his studies in Molecular Health Science, Adrian Stefanov developed an interest in personalized medicine and unconventional therapeutic approaches. This inspired him for a PhD at ETH Zurich where he applied specially modified human cells for diabetes therapy. He established a gene switch that enables electronic devices to be interfaced with the engineered cells for a digital fine-tuning of the insulin amounts released from the cells into the body. In addition to that, he developed a manufacturing strategy for ready-to-use therapeutic protein solutions at remote locations, as described in the article above.

nano-glo-luciferase-assay-system

Promega Product Used

The Nano-Glo® Luciferase Assay System provides a simple, single-addition reagent that generates a glow-type signal in the presence of NanoLuc® luciferase with a half-life of approximately 120 minutes in commonly used tissue culture media.

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Bruscaggin A, di Bergamo LT, Spina V, Hodkinson B, Forestieri G, Bonfiglio F, Condoluci A, Wu W, Pirosa MC, Faderl MR, Koch R, Schaffer M, Alvarez JD, Fourneau N, Gerber B, Stussi G, Zucca E, Balasubramanian S, Rossi D.

Circulating tumor DNA for comprehensive noninvasive monitoring of lymphoma treated with ibrutinib plus nivolumab

Blood Adv. 2021 Nov 23;5(22):4674-4685. doi: 10.1182/bloodadvances.2021004528. PMID: 34500472; PMCID: PMC8759132.

To advance the use of circulating tumor DNA (ctDNA) applications, their broad clinical validity must be tested in different treatment settings, including targeted therapies.
Abstract

To advance the use of circulating tumor DNA (ctDNA) applications, their broad clinical validity must be tested in different treatment settings, including targeted therapies.

Using the prespecified longitudinal systematic collection of plasma samples in the phase 1/2a LYM1002 trial (registered on www.clinicaltrials.gov as NCT02329847), we tested the clinical validity of ctDNA for baseline mutation profiling, residual tumor load quantification, and acquisition of resistance mutations in patients with lymphoma treated with ibrutinib+nivolumab. Inclusion criterion for this ancillary biological study was the availability of blood collected at baseline and cycle 3, day 1.

Overall, 172 ctDNA samples from 67 patients were analyzed by the LyV4.0 ctDNA Cancer Personalized Profiling Deep Sequencing Assay. Among baseline variants in ctDNA, only TP53 mutations (detected in 25.4% of patients) were associated with shorter progression-free survival; clones harboring baseline TP53 mutations did not disappear during treatment. Molecular response, defined as a >2-log reduction in ctDNA levels after 2 cycles of therapy (28 days), was achieved in 28.6% of patients with relapsed diffuse large B-cell lymphoma who had ≥1 baseline variant and was associated with best response and improved progression-free survival.

Clonal evolution occurred frequently during treatment, and 10.3% new mutations were identified after 2 treatment cycles in nonresponders. PLCG2 was the topmost among genes that acquired new mutations. No patients acquired the C481S BTK mutation implicated in resistance to ibrutinib in CLL.

Collectively, our results provide the proof of concept that ctDNA is useful for noninvasive monitoring of lymphoma treated with targeted agents in the clinical trial setting.

Read the full publication online: https://ashpublications.org/bloodadvances/article/5/22/4674/476850/Circulating-tumor-DNA-for-comprehensive

alessio

About Alessio

Since 2016, Alessio Bruscaggin has worked as a senior Post-doc in the Laboratory of Experimental Hematology of the Institute of Oncology Research in Bellinzona, Switzerland, where he coordinates next-generation sequencing projects in lymphoproliferative disorders.

He has a large experience in mature B-cell tumor genetics and in the development of ultra-deep next-generation sequencing pipelines, which will represent the methodological platform of all the mutation analysis. He actively participated in several projects aiming at the characterization of the molecular pathogenesis of B-cell tumors and at the translation of biological information into markers for disease diagnosis, prognostication, and treatment. He also contributed to the characterization of the splenic marginal zone lymphoma and CLL genomes, and to the development of plasma cell-free DNA as a tool to inform on tumor genetics in lymphomas.

Promega Product Used

Maxwell®️ instruments are used together with cartridge-based purification kits to quickly extract DNA or RNA from many different sample types.

The automated purification process consistently delivers quality nucleic acid, freeing up scientists’ time for other important work. The Maxwell RSC LV cfDNA kit purifies circulating cell-free DNA from up to 8ml or more of plasma.

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Nikolai Püllen,a Hailey Gahlon,a Shana J. Sturlaa*

Removal of Common Alterations in Genomic DNA for Accurate Damage Sequencing

The structural integrity of DNA is constantly altered by exposure to metabolic byproducts, chemicals or radiation. Persisting DNA damage can result in mutations and genome instability. To better understand biological influences of DNA damage formation, new DNA damage sequencing methods are rapidly emerging.

*e-mail: sturlas@ethz.ch

aDept. of Health Sciences and Technology, ETH Zurich, Schmelzbergstr. 9, 8092 Zurich,Switzerland;

Abstract
One common strategy for single-nucleotide resolution damage sequencing relies on having a reactive 3′-hydroxyl group at the damage position of interest. Such targeted 3′-hydroxyl ends are generated through enzymes to specifically excise damage products and produce interim apurinic sites and single strand breaks. However, such generic damage sites are by nature abundant in genomic DNA, making the possibility to uncover low abundance damage patterns without an effective background removal strategy impossible. Therefore, we used a ligation-mediated fluorescent probe-based damage quantitation approach to develop a strategy to minimize background damage in genomic DNA. Free 3′-hydroxyl groups in DNA were labeled by enzymatic incorporation of an alkyne-modified nucleobase and subsequently reacted with a fluorescent azide by click chemistry. By this approach, we could accurately detect enzyme-induced single strand breaks in oligonucleotide DNA in concentrations as low as 20 pM. We similarly processed genomic DNA and could detect elevated levels of 3′-hydroxyl groups on the basis of increased fluorescence intensity between enzymatically treated vs. native DNA. With an aim to remove pre-existing damage, we used an optimized enzyme mixture capable of repairing apurinic sites, gaps and single strand breaks in genomic DNA samples and validated the strategy by observing decreases in fluorescence signal compared to native genomic DNA. In conclusion, we developed an effective and general method for the quantitation and removal of adventitious common DNA damage products. Furthermore, the fluorescence-based ligation strategy used to optimize the enzymatic clean-up procedure could have wide use for developing sample preparation protocols for reliable DNA damage sequencing analysis.

Acknowledgment: We acknowledge funding from the Swiss National Science Foundation.

References

(1) Mingard, C. et al. Chem. Soc. Rev. 2020, 49 (20), 7354–7377.
nikolai

About Nikolai

Nikolai Püllen graduated from the University of Münster, Germany, with a Master in Chemistry. He joined Johnson and Johnson R&D in Zurich, as an industrial research intern. Currently, he is a Ph.D. student at the ETH in Zurich working on DNA damage sequencing in the Laboratory of Toxicology. Nikolai enjoys research as part of understanding how life works and as a mean to engage in scientific communication. He is curious, creative and also a project management enthusiast, which helps when conducting research.

dna-size

Promega Product Used

The ProNex® Size-Selective Purification System enables the rapid and efficient magnetic resin-based purification of double-stranded DNA (dsDNA) for next-generation sequencing (NGS), polymerase chain reaction (PCR) and general molecular biology applications.

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Vujić Tatjana, Schvartz Domitille & Sanchez Jean‑Charles

Paraquat-induced cholesterol biosynthesis proteins dysregulation in human brain microvascular endothelial cells

Despite Paraquat (PQ) being banned in several countries, it is still one of the most commonly used herbicides in agriculture. This compound is known to induce damaging effects on human and animal brain cells by generating Reactive Oxygen Species (ROS). However, there is few evidence of PQ effect on Human Brain Microvascular Endothelial Cells (HBMECs), one of the major component of the Blood–Brain Barrier (BBB).
Abstract
The present study aimed at unraveling biological mechanisms associated to the exposure of 1, 10 and 100 μM of PQ for 24 h on HBMECs. High-throughput mass spectrometry-based proteomics using data-independent acquisition (DIA) was applied. Biological pathway enrichment and cellular assays such as mitochondrial respiration and cholesterol level were performed to verify proteomics results. A total of 3753 proteins were quantified out of which 419 were significantly modulated by paraquat exposure. Biological pathway enrichment revealed the ubiquinone metabolism, a pathway directly linked to mitochondrial complex I proteins, confirming the well-known mechanism of PQ inducing oxidative stress. Additionally, this study also described the cholesterol biosynthesis modulation on HBMECs not yet described. In conclusion, our data indicate the toxic effect of PQ on HBMECs by downregulating proteins involved in mitochondrial complex I and cholesterol pathways.
tatjana

About Tatjana

Tatjana Vujić earned her Master's Degree in Pharmaceutical Sciences at the University of Geneva in Switzerland. During her Master's Degree, she joined the Nestlé Research Center R&D in the Vitamins and Phytonutrients Department in Lausanne. Currently doing her Ph.D. thesis in the Translational Biomarker Group at the University of Geneva, she studies the xenobiotic effects on human brain endothelial cells based on protein modulations, including cholesterol proteins. Persistent, curious, and optimistic by nature, Tatjana enjoys facing and meet the challenges of scientific discovery.

cholesterol

Promega Product Used

The Cholesterol/Cholesterol Ester-Glo™ Assay is a bioluminescent assay for rapid and sensitive measuring of cholesterol and cholesterol esters in cultured cell lysates and other biological samples, such as lipoprotein fractions, cell culture medium, serum and tissue homogenates. Cholesterol is an essential lipid involved in steroidogenesis, bile acid synthesis, cell signaling and maintenance of membrane structure.

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annalazarro

Anna Lazzaro

Scientific Collaborations Specialist
anna.lazzaro@promega.com

Email Anna
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