diff --git a/_bibliography/citations-eu.bib b/_bibliography/citations-eu.bib index 11239123..93d054b5 100644 --- a/_bibliography/citations-eu.bib +++ b/_bibliography/citations-eu.bib @@ -3369,6 +3369,33 @@ @article{fatima_book_2023 year = {2023} } +@article{faulstich_evidence_2024, + abstract = {ABSTRACT + + +Reef-building corals depend on symbiosis with photosynthetic algae that reside within their cells. As important as this relationship is for maintaining healthy reefs, it is strikingly delicate. When ocean temperatures briefly exceed the average summer maximum, corals can bleach, losing their endosymbionts. Although the mechanisms governing bleaching are unknown, studies implicate uncoupling of coral and algal cell divisions at high temperatures. Still, little is known regarding the coordination of host and algal cell divisions. Control of nutrient exchange is one likely mechanism. Both nitrogen and phosphate are necessary for dividing cells, and although nitrogen enrichment is known to increase symbiont density in the host, the consequences of phosphate enrichment are poorly understood. Here, we examined the effects of phosphate depletion on symbiont growth in culture and compared the physiology of phosphate-starved symbionts in culture to symbionts that were freshly isolated from a host. We found that available phosphate is as low in freshly isolated symbionts as it is in phosphate-starved cultures. Furthermore, RNAseq revealed that phosphate-limited and freshly isolated symbionts have similar patterns of gene expression for phosphate-dependent genes, most notably upregulation of phosphatases, which is consistent with phosphate recycling. Similarly, lipid profiling revealed a substantial decrease in phospholipid abundance in both phosphate-starved cultures and freshly isolated symbionts. These findings are important because they suggest that limited access to phosphate controls algal cell divisions within a host. + + +IMPORTANCE +The corals responsible for building tropical reefs are disappearing at an alarming rate as elevated sea temperatures cause them to bleach and lose the algal symbionts they rely on. Without these symbionts, corals are unable to harvest energy from sunlight and, therefore, struggle to thrive or even survive in the nutrient-poor waters of the tropics. To devise solutions to address the threat to coral reefs, it is necessary to understand the cellular events underpinning the bleaching process. One model for bleaching proposes that heat stress impairs algal photosynthesis and transfer of sugar to the host. Consequently, the host’s demands for nitrogen decrease, increasing nitrogen availability to the symbionts, which leads to an increase in algal proliferation that overwhelms the host. Our work suggests that phosphate may play a similar role to nitrogen in this feedback loop. + +, +The corals responsible for building tropical reefs are disappearing at an alarming rate as elevated sea temperatures cause them to bleach and lose the algal symbionts they rely on. Without these symbionts, corals are unable to harvest energy from sunlight and, therefore, struggle to thrive or even survive in the nutrient-poor waters of the tropics. To devise solutions to address the threat to coral reefs, it is necessary to understand the cellular events underpinning the bleaching process. One model for bleaching proposes that heat stress impairs algal photosynthesis and transfer of sugar to the host. Consequently, the host’s demands for nitrogen decrease, increasing nitrogen availability to the symbionts, which leads to an increase in algal proliferation that overwhelms the host. Our work suggests that phosphate may play a similar role to nitrogen in this feedback loop.}, + author = {Faulstich, Nathan G. and Deloach, Alexis R. and Ksor, Ykok B. and Mesa, Gabriel H. and Sharma, Daiven S. and Sisk, Sebastian L. and Mitchell, Geoffrey C.}, + doi = {10.1128/mbio.01059-24}, + editor = {McFall-Ngai, Margaret J. and Weis, Virginia}, + issn = {2150-7511}, + journal = {mBio}, + keywords = {{\textgreater}UseGalaxy.eu}, + language = {en}, + month = {August}, + pages = {e01059--24}, + title = {Evidence for phosphate-dependent control of symbiont cell division in the model anemone \textit{{Exaiptasia} diaphana}}, + url = {https://journals.asm.org/doi/10.1128/mbio.01059-24}, + urldate = {2024-08-09}, + year = {2024} +} + @article{feldker_genome-wide_2020, abstract = {Abstract Invasion, metastasis and therapy resistance are the major cause of cancer-associated deaths, and the EMT-inducing transcription factor ZEB1 is a crucial stimulator of these processes. While work on ZEB1 has mainly focused on its role as a transcriptional repressor, it can also act as a transcriptional activator. To further understand these two modes of action, we performed a genome-wide ZEB1 binding study in triple-negative breast cancer cells. We identified ZEB1 as a novel interactor of the AP-1 factors FOSL1 and JUN and show that, together with the Hippo pathway effector YAP, they form a transactivation complex, predominantly activating tumour-promoting genes, thereby synergising with its function as a repressor of epithelial genes. High expression of ZEB1, YAP, FOSL1 and JUN marks the aggressive claudin-low subtype of breast cancer, indicating the translational relevance of our findings. Thus, our results link critical tumour-promoting transcription factors: ZEB1, AP-1 and Hippo pathway factors. Disturbing their molecular interaction may provide a promising treatment option for aggressive cancer types.}, author = {Feldker, Nora and Ferrazzi, Fulvia and Schuhwerk, Harald and Widholz, Sebastian A and Guenther, Kerstin and Frisch, Isabell and Jakob, Kathrin and Kleemann, Julia and Riegel, Dania and Bönisch, Ulrike and Lukassen, Sören and Eccles, Rebecca L and Schmidl, Christian and Stemmler, Marc P and Brabletz, Thomas and Brabletz, Simone}, @@ -4109,6 +4136,26 @@ @article{glaros_limited_2021 year = {2021} } +@article{godbole_multiomic_2024, + abstract = {Medulloblastomas (MBs) are malignant pediatric brain tumors that are molecularly and clinically heterogenous. The application of omics technologies—mainly studying nucleic acids—has significantly improved MB classification and stratification, but treatment options are still unsatisfactory. The proteome and their N-glycans hold the potential to discover clinically relevant phenotypes and targetable pathways. We compile a harmonized proteome dataset of 167 MBs and integrate findings with DNA methylome, transcriptome and N-glycome data. We show six proteome MB subtypes, that can be assigned to two main molecular programs: transcription/translation (pSHHt, pWNT and pG3myc), and synapses/immunological processes (pSHHs, pG3 and pG4). Multiomic analysis reveals different conservation levels of proteome features across MB subtypes at the DNA methylome level. Aggressive pGroup3myc MBs and favorable pWNT MBs are most similar in cluster hierarchies concerning overall proteome patterns but show different protein abundances of the vincristine resistance-associated multiprotein complex TriC/CCT and of N-glycan turnover-associated factors. The N-glycome reflects proteome subtypes and complex-bisecting N-glycans characterize pGroup3myc tumors. Our results shed light on targetable alterations in MB and set a foundation for potential immunotherapies targeting glycan structures.}, + author = {Godbole, Shweta and Voß, Hannah and Gocke, Antonia and Schlumbohm, Simon and Schumann, Yannis and Peng, Bojia and Mynarek, Martin and Rutkowski, Stefan and Dottermusch, Matthias and Dorostkar, Mario M. and Korshunov, Andrey and Mair, Thomas and Pfister, Stefan M. and Kwiatkowski, Marcel and Hotze, Madlen and Neumann, Philipp and Hartmann, Christian and Weis, Joachim and Liesche-Starnecker, Friederike and Guan, Yudong and Moritz, Manuela and Siebels, Bente and Struve, Nina and Schlüter, Hartmut and Schüller, Ulrich and Krisp, Christoph and Neumann, Julia E.}, + copyright = {2024 The Author(s)}, + doi = {10.1038/s41467-024-50554-z}, + issn = {2041-1723}, + journal = {Nature Communications}, + keywords = {{\textgreater}UseGalaxy.eu, CNS cancer, Data integration, Glycomics, Proteomics, Tumour heterogeneity}, + language = {en}, + month = {July}, + note = {Publisher: Nature Publishing Group}, + number = {1}, + pages = {6237}, + title = {Multiomic profiling of medulloblastoma reveals subtype-specific targetable alterations at the proteome and {N}-glycan level}, + url = {https://www.nature.com/articles/s41467-024-50554-z}, + urldate = {2024-07-27}, + volume = {15}, + year = {2024} +} + @article{goossens_obligate_2023, abstract = {Hyaloperonospora arabidopsidis (Hpa) is an obligately biotrophic downy mildew that is routinely cultured on Arabidopsis thaliana hosts that harbour complex microbiomes. We hypothesized that the culturing procedure proliferates Hpa-associated microbiota (HAM) in addition to the pathogen and exploited this model system to investigate which microorganisms consistently associate with Hpa. Using amplicon sequencing, we found nine bacterial sequence variants that are shared between at least three out of four Hpa cultures in the Netherlands and Germany and comprise 34\% of the phyllosphere community of the infected plants. Whole-genome sequencing showed that representative HAM bacterial isolates from these distinct Hpa cultures are isogenic and that an additional seven published Hpa metagenomes contain numerous sequences of the HAM. Although we showed that HAM benefit from Hpa infection, HAM negatively affect Hpa spore formation. Moreover, we show that pathogen-infected plants can selectively recruit HAM to both their roots and shoots and form a soil-borne infection-associated microbiome that helps resist the pathogen. Understanding the mechanisms by which infection-associated microbiomes are formed might enable breeding of crop varieties that select for protective microbiomes.}, author = {Goossens, Pim and Spooren, Jelle and Baremans, Kim C. M. and Andel, Annemiek and Lapin, Dmitry and Echobardo, Nakisa and Pieterse, Corné M. J. and Van den Ackerveken, Guido and Berendsen, Roeland L.}, @@ -4166,6 +4213,25 @@ @article{greenfield_modification_2020 year = {2020} } +@article{gress_prostaglandin_2024, + abstract = {Increased production of Prostaglandin D2 (PGD2) is linked to development and progression of asthma and allergy. PGD2 is rapidly degraded to its metabolites, which initiate type 2 innate lymphoid cells (ILC2) migration and IL-5/IL-13 cytokine secretion in a PGD2 receptor 2 (DP2)-dependent manner. Blockade of DP2 has shown therapeutic benefit in subsets of asthma patients. Cellular mechanisms of ILC2 activity in response to PGD2 and its metabolites are still unclear. We hypothesized that ILC2 respond non-uniformly to PGD2 metabolites. ILC2s were isolated from peripheral blood of patients with atopic asthma. ILC2s were stimulated with PGD2 and four PGD2 metabolites (Δ12-PGJ2, Δ12-PGD2, 15-deoxyΔ12,14-PGD2, 9α,11β-PGF2) with or without the selective DP2 antagonist fevipiprant. Total RNA was sequenced, and differentially expressed genes (DEG) were identified by DeSeq2. Differential gene expression analysis revealed an upregulation of pro-inflammatory DEGs in ILC2s stimulated with PGD2 (14 DEGs), Δ12-PGD2 (27 DEGs), 15-deoxyΔ12,14-PGD2 (56 DEGs) and Δ12-PGJ2 (136 DEGs), but not with 9α,11β-PGF2. Common upregulated DEGs were i.e. ARG2, SLC43A2, LAYN, IGFLR1, or EPHX2. Inhibition of DP2 via fevipiprant mainly resulted in downregulation of pro-inflammatory genes such as DUSP4, SPRED2, DUSP6, ETV1, ASB2, CD38, ADGRG1, DDIT4, TRPM2, or CD69. DEGs were related to migration and various immune response-relevant pathways such as “chemokine (C-C motif) ligand 4 production”, “cell migration”, “interleukin-13 production”, “regulation of receptor signaling pathway via JAK-STAT”, or “lymphocyte apoptotic process”, underlining the pro-inflammatory effects of PGD2 metabolite-induced immune responses in ILC2s as well as the anti-inflammatory effects of DP2 inhibition via fevipiprant. Furthermore, PGD2 and metabolites showed distinct profiles in ILC2 activation. Overall, these results expand our understanding of DP2 initiated ILC2 activity.}, + author = {Gress, Christina and Fuchs, Maximilian and Carstensen-Aurèche, Saskia and Müller, Meike and Hohlfeld, Jens M.}, + doi = {10.1371/journal.pone.0307750}, + issn = {1932-6203}, + journal = {PLOS ONE}, + keywords = {{\textgreater}UseGalaxy.eu, Asthma, Cell metabolism, Cytokines, Gene expression, Immune response, Metabolic pathways, Metabolites, RNA sequencing}, + language = {en}, + month = {July}, + note = {Publisher: Public Library of Science}, + number = {7}, + pages = {e0307750}, + title = {Prostaglandin {D2} receptor 2 downstream signaling and modulation of type 2 innate lymphoid cells from patients with asthma}, + url = {https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0307750}, + urldate = {2024-07-29}, + volume = {19}, + year = {2024} +} + @article{gress_transcriptomic_2024, abstract = {Segmental instillation of lipopolysaccharide (LPS) by bronchoscopy safely induces transient airway inflammation in human lungs. This model enables investigation of pulmonary inflammatory mechanisms as well as pharmacodynamic analysis of investigational drugs. The aim of this work was to describe the transcriptomic profile of human segmental LPS challenge with contextualization to major respiratory diseases. Pre-challenge bronchoalveolar lavage (BAL) fluid and biopsies were sampled from 28 smoking, healthy participants, followed by segmental instillation of LPS and saline as control. Twenty-four hours post instillation, BAL and biopsies were collected from challenged lung segments. Total RNA of cells from BAL and biopsy samples were sequenced and analysed for differentially expressed genes (DEGs). After challenge with LPS compared with saline, 6316 DEGs were upregulated and 241 were downregulated in BAL, but only one DEG was downregulated in biopsy samples. Upregulated DEGs in BAL were related to molecular functions such as “Inflammatory response” or “chemokine receptor activity”, and upregulated pro-inflammatory pathways such as “Wnt-"/“Ras-"/“JAK-STAT” “-signaling pathway”. Furthermore, the segmental LPS challenge model resembled aspects of the five most prevalent respiratory diseases chronic obstructive pulmonary disease (COPD), asthma, pneumonia, tuberculosis and lung cancer and featured similarities with acute exacerbations in COPD (AECOPD) and community-acquired pneumonia. Overall, our study provides extensive information about the transcriptomic profile from BAL cells and mucosal biopsies following LPS challenge in healthy smokers. It expands the knowledge about the LPS challenge model providing potential overlap with respiratory diseases in general and infection-triggered respiratory insults such as AECOPD in particular.}, author = {Gress, Christina and Litzenburger, Tobias and Schmid, Ramona and Xiao, Ke and Heissig, Florian and Muller, Meike and Gupta, Abhya and Hohlfeld, Jens M.}, @@ -5691,7 +5757,7 @@ @article{kohler_msstatsshiny_2023 year = {2023} } -@article{kojima_cytochrome_nodate, +@article{kojima_cytochrome_2024, abstract = {Austocystin D is a natural compound that induces cytochrome P450 (CYP) monooxygenase-dependent DNA damage and growth inhibition in certain cancer cell lines. Cancer cells exhibiting higher sensitivity to austocystin D often display elevated CYP2J2 expression. However, the essentiality and the role of CYP2J2 for the cytotoxicity of this compound remain unclear. In this study, we demonstrate that CYP2J2 depletion alleviates austocystin D sensitivity and DNA damage induction, while CYP2J2 overexpression enhances them. Moreover, the investigation into genes involved in austocystin D cytotoxicity identified POR and PGRMC1, positive regulators for CYP activity, and KAT7, a histone acetyltransferase. Through genetic manipulation and analysis of multiomics data, we elucidated a role for KAT7 in CYP2J2 transcriptional regulation. These findings strongly suggest that CYP2J2 is crucial for austocystin D metabolism and its subsequent cytotoxic effects. The potential use of austocystin D as a therapeutic prodrug is underscored, particularly in cancers where elevated CYP2J2 expression serves as a biomarker.}, author = {Kojima, Yukiko and Fujieda, Saki and Zhou, Liya and Takikawa, Masahiro and Kuramochi, Kouji and Furuya, Toshiki and Mizumoto, Ayaka and Kagaya, Noritaka and Kawahara, Teppei and Shin-ya, Kazuo and Dan, Shingo and Tomida, Akihiro and Ishikawa, Fuyuki and Sadaie, Mahito}, copyright = {© 2024 The Author(s). Cancer Science published by John Wiley \& Sons Australia, Ltd on behalf of Japanese Cancer Association.}, @@ -5700,12 +5766,12 @@ @article{kojima_cytochrome_nodate journal = {Cancer Science}, keywords = {{\textgreater}UseGalaxy.eu, DNA damage, austocystin D, cytotoxicity, gene expression, knockout screening}, language = {en}, + month = {July}, note = {\_eprint: https://onlinelibrary.wiley.com/doi/pdf/10.1111/cas.16289}, - number = {n/a}, title = {Cytochrome {P450} {2J2} is required for the natural compound austocystin {D} to elicit cancer cell toxicity}, url = {https://onlinelibrary.wiley.com/doi/abs/10.1111/cas.16289}, urldate = {2024-07-19}, - volume = {n/a} + year = {2024} } @article{kolosov_malpighian_2019, @@ -6937,7 +7003,7 @@ @article{mcdonald_ultraviolet_2022 year = {2022} } -@article{mcdonald_ultraviolet_2022, +@article{mcdonald_ultraviolet_2022-1, author = {McDonald, Marisa S. and Palecanda, Sitara and Cohen, Jonathan H. and Porter, Megan L.}, doi = {10.1242/jeb.243256}, journal = {Journal of Experimental Biology}, @@ -7339,6 +7405,22 @@ @article{mootapally_sediment_2021 year = {2021} } +@article{moraga-fernandez_impact_2024, + abstract = {There are currently no vaccines available to prevent and control of Anaplasma phagocytophilum, an intracellular bacterial pathogen transmitted by ticks that occurs in many regions of the world and causes disease in a wide range of domestic and wild hosts, including humans. Vaccines induce long-lasting immunity and could prevent or reduce transmission of this pathogen. Understanding how vaccines induce a protective response can be difficult due to the complexity of the immune system, which operates at many levels throughout the organism. New perspectives in vaccinology, based on systems biology approaches, integrate many scientific disciplines to fully understand the biological responses to vaccination, where a transcriptomic approach could reveal relevant information of the host immune system, allowing profiling for rational design of vaccine formulations, administration, and potential protection. In the present study we report the gene expression profiles by RNA-seq followed by functional analysis using whole blood samples from rabbits immunized with a recombinant chimeric protein containing peptides from the MSP4 protein of A. phagocytophilum, which showed satisfactory results in terms of potential protection. Transcriptomic analysis revealed differential expression of 720 genes, with 346 genes upregulated and 374 genes downregulated. Overrepresentation of biological and metabolic pathways correlated with immune response, protein signaling, cytoskeleton organization and protein synthesis were found. These changes in gene expression could provide a complete and unique picture of the biological response to the epitope candidate vaccine against A. phagocytophilum in the host.}, + author = {Moraga-Fernández, Alberto and de Sousa-Blanco, María and Marques, João Pedro and Queirós, João and Fernández-Melgar, Rubén and García-Álvarez, Olga and Alves, Paulo C. and Contreras, Marinela}, + doi = {10.1016/j.rvsc.2024.105370}, + issn = {0034-5288}, + journal = {Research in Veterinary Science}, + keywords = {{\textgreater}UseGalaxy.eu, Immune response, MSP4, Tick-borne pathogen, Transcriptomic analysis, Vaccination}, + month = {October}, + pages = {105370}, + title = {Impact of vaccination with the \textit{{Anaplasma} phagocytophilum} {MSP4} chimeric antigen on gene expression in the rabbit host}, + url = {https://www.sciencedirect.com/science/article/pii/S0034528824002376}, + urldate = {2024-08-08}, + volume = {178}, + year = {2024} +} + @article{morandi_evolutionary_2020, abstract = {Background: Ultra-conserved non-coding elements (UCNEs) are genomic sequences that exhibit \> 95\% sequence identity between humans, mammals, birds, reptiles, and fish. Recent findings reported their functional role in cancer. The aim of this study was to evaluate the DNA methylation modifications of UNCEs in squamous cell carcinoma (SCC) from different mammal species. Methods: Fifty SCCs from 26 humans, 17 cats, 3 dogs, 1 horse, 1 bovine, 1 badger, and 1 porcupine were investigated. Fourteen feline stomatitis and normal samples from 36 healthy human donors, 7 cats, 5 dogs, 5 horses, 2 bovines and 1 badger were collected as normal controls. Bisulfite next generation sequencing evaluated the DNA methylation level from seven UCNEs (uc.160, uc.283, uc.416, uc.339, uc.270, uc.299, and uc.328). Results: 57/59 CpGs were significantly different according to the Kruskal\–Wallis test (p \< 0.05) comparing normal samples with SCC. A common DNA hypermethylation pattern was observed in SCCs from all the species evaluated in this study, with an increasing trend of hypermethylation starting from normal mucosa, through stomatitis to SCC. Conclusions: Our findings indicate that UCNEs are hypermethylated in human SCC, and this behavior is also conserved among different species of mammals.}, author = {Morandi, Luca and Sabattini, Silvia and Renzi, Andrea and Rigillo, Antonella and Bettini, Giuliano and Dervas, Eva and Schauer, Alexandria and Morandi, Marco and Gissi, Davide B. and Tarsitano, Achille and Evangelisti, Stefania and Tonon, Caterina}, @@ -9605,6 +9687,20 @@ @article{schule_eomes_2023 year = {2023} } +@article{schult_viral_2024, + abstract = {Viral genomes are enriched with G-quadruplexes (G4s), non-canonical structures formed in DNA or RNA upon assembly of four guanine stretches into stacked quartets. Because of their critical roles, G4s are potential antiviral targets, yet their function remains largely unknown. Here, we characterize the formation and functions of a conserved G4 within the polymerase coding region of orthoflaviviruses of the Flaviviridae family. Using yellow fever virus, we determine that this G4 promotes viral replication and suppresses host stress responses via interactions with hnRNPH1, a host nuclear protein involved in RNA processing. G4 binding to hnRNPH1 causes its cytoplasmic retention with subsequent impacts on G4-containing tRNA fragments (tiRNAs) involved in stress-mediated reductions in translation. As a result, these host stress responses and associated antiviral effects are impaired. These data reveal that the interplay between hnRNPH1 and both host and viral G4 targets controls the integrated stress response and viral replication.}, + author = {Schult, Philipp and Kümmerer, Beate Mareike and Hafner, Markus and Paeschke, Katrin}, + doi = {10.1016/j.chom.2024.07.006}, + issn = {1931-3128}, + journal = {Cell Host \& Microbe}, + keywords = {{\textgreater}UseGalaxy.eu, G-quadruplex, antiviral stress response, hnRNPH1, host factor, orthoflavivirus, tiRNA}, + month = {August}, + title = {Viral hijacking of {hnRNPH1} unveils a {G}-quadruplex-driven mechanism of stress control}, + url = {https://www.sciencedirect.com/science/article/pii/S1931312824002658}, + urldate = {2024-08-04}, + year = {2024} +} + @article{schwabenland_neonatal_2023, abstract = {While the precise processes underlying a sex bias in the development of central nervous system (CNS) disorders are unknown, there is growing evidence that an early life immune activation can contribute to the disease pathogenesis. When we mimicked an early systemic viral infection or applied murine cytomegalovirus (MCMV) systemically in neonatal female and male mice, only male adolescent mice presented behavioral deficits, including reduced social behavior and cognition. This was paralleled by an increased amount of infiltrating T cells in the brain parenchyma, enhanced interferon-γ (IFNγ) signaling, and epigenetic reprogramming of microglial cells. These microglial cells showed increased phagocytic activity, which resulted in abnormal loss of excitatory synapses within the hippocampal brain region. None of these alterations were seen in female adolescent mice. Our findings underscore the early postnatal period’s susceptibility to cause sex-dependent long-term CNS deficiencies following infections.}, author = {Schwabenland, Marius and Mossad, Omar and Sievert, Annika and Peres, Adam G. and Ringel, Elena and Baasch, Sebastian and Kolter, Julia and Cascone, Giulia and Dokalis, Nikolaos and Vlachos, Andreas and Ruzsics, Zsolt and Henneke, Philipp and Prinz, Marco and Blank, Thomas}, @@ -10430,6 +10526,22 @@ @article{tangaro_laniakea_2020 year = {2020} } +@article{tapia_nanopore_2024, + author = {Tapia, Stephanie and Orellana, Joseph and Duran, Yerson and Rodriguez, Jose and Angulo, Derly and Dominguez-Mendoza, Luz and Grabiel, Sandra and Silva, Jose and Caballero, Romina and Zapata, Katherine and Gómez, Muriel and Tataje-Lavanda, Luis and Velazco, Rodolfo}, + doi = {10.1128/mra.00190-24}, + journal = {Microbiology Resource Announcements}, + keywords = {{\textgreater}NanoGalaxy, {\textgreater}UseGalaxy.eu}, + month = {August}, + note = {Publisher: American Society for Microbiology}, + number = {0}, + pages = {e00190--24}, + title = {Nanopore sequencing of {IPNV} vp2 gene in {Peruvian} {Andean} trout ({Oncorhynchus} mykiss) cultures}, + url = {https://journals.asm.org/doi/full/10.1128/mra.00190-24}, + urldate = {2024-08-24}, + volume = {0}, + year = {2024} +} + @article{tari_u2af65_2019, abstract = {Abstract The essential splicing factor U2AF65 is known to help anchoring U2 snRNP at the branch site. Its C-terminal UHM domain interacts with ULM motifs of SF3b155, an U2 snRNP protein. Here, we report a cooperative binding of U2AF65 and the related protein CAPERα to the multi-ULM domain of SF3b155. In addition, we show that the RS domain of U2AF65 drives a liquid?liquid phase separation that is amplified by intronic RNA with repeated pyrimidine tracts. In cells, knockdown of either U2AF65 or CAPERα improves the inclusion of cassette exons that are preceded by such repeated pyrimidine-rich motifs. These results support a model in which liquid-like assemblies of U2AF65 and CAPERα on repetitive pyrimidine-rich RNA sequences are driven by their RS domains, and facilitate the recruitment of the multi-ULM domain of SF3b155. We anticipate that posttranslational modifications and proteins recruited in dynamical U2AF65 and CAPERα condensates may further contribute to the complex mechanisms leading to specific splice site choice that occurs in cells.}, author = {Tari, Manel and Manceau, Valérie and de Matha Salone, Jean and Kobayashi, Asaki and Pastré, David and Maucuer, Alexandre}, @@ -10559,7 +10671,7 @@ @article{thompson_draft_2023 year = {2023} } -@article{thompson_draft_2023, +@article{thompson_draft_2023-1, author = {Thompson, Ryan Michael and Fox, Edward M. and Montero-Calasanz, Maria del Carmen}, doi = {10.1128/mra.00486-23}, journal = {Microbiology Resource Announcements}, @@ -10680,6 +10792,24 @@ @article{toth_genomic_2024 year = {2024} } +@article{tregear_micro-rna-regulated_2022, + abstract = {Sexual differentiation of inflorescences and flowers is important for reproduction and affects crop plant productivity. We report here on a molecular study of the process of sexual differentiation in the immature inflorescence of oil palm (Elaeis guineensis). This species is monoecious and exhibits gender diphasy, producing male and female inflorescences separately on the same plant in alternation. Three main approaches were used: small RNA-seq to characterise and study the expression of miRNA genes; RNA-seq to monitor mRNA accumulation patterns; hormone quantification to assess the role of cytokinins and auxins in inflorescence differentiation. Our study allowed the characterisation of 30 previously unreported palm MIRNA genes. In differential gene and miRNA expression studies, we identified a number of key developmental genes and miRNA-mRNA target modules previously described in relation to their developmental regulatory role in the cereal panicle, notably the miR156/529/535-SQUAMOSA PROMOTER-BINDING PROTEIN-LIKE (SPL) gene regulatory module. Gene enrichment analysis highlighted the importance of hormone-related genes, and this observation was corroborated by the detection of much higher levels of cytokinins in the female inflorescence. Our data illustrate the importance of branching regulation within the developmental window studied, during which the female inflorescence, unlike its male counterpart, produces flower clusters on new successive axes by sympodial growth.}, + author = {Tregear, James W. and Richaud, Frédérique and Collin, Myriam and Esbelin, Jennifer and Parrinello, Hugues and Cochard, Benoît and Nodichao, Leifi and Morcillo, Fabienne and Adam, Hélène and Jouannic, Stefan}, + doi = {10.3390/plants11050685}, + issn = {2223-7747}, + journal = {Plants (Basel, Switzerland)}, + keywords = {{\textgreater}RNA Workbench, SQUAMOSA PROMOTER-BINDING PROTEIN, branching, inflorescence, miRNA, oil palm, sexual differentiation}, + language = {eng}, + month = {March}, + number = {5}, + pages = {685}, + pmcid = {PMC8912876}, + pmid = {35270155}, + title = {Micro-{RNA}-{Regulated} {SQUAMOSA}-{PROMOTER} {BINDING} {PROTEIN}-{LIKE} ({SPL}) {Gene} {Expression} and {Cytokinin} {Accumulation} {Distinguish} {Early}-{Developing} {Male} and {Female} {Inflorescences} in {Oil} {Palm} ({Elaeis} guineensis)}, + volume = {11}, + year = {2022} +} + @article{trifonova_combination_2023, abstract = {Background The SARS-CoV-2 virus significantly changed our knowledge about coronaviruses. The interplay between SARS-CoV-2 and the human host, the infection ranges from asymptomatic to lethal, and differences in the degree of disease severity are important examples.Methods In this retrospective study, 24 nasopharyngeal swabs from 21 out of 457 patients with SARS-CoV-2 infection were analysed by whole-genome sequencing. The principal selection criteria were the duration of infection and disease severity.Results Two co-occurring rare mutations in the SARS-CoV-2 M gene were detected in six samples. Three of these samples were collected from an immunocompromised patient with fatal outcome, two from an immunocompetent patient, and one from a patient with severe disease and fatal outcome, all with a prolonged course of infection.Conclusions Although this interesting finding was demonstrated in a small number of patients, the results increase the knowledge regarding the significance of mutations in the M gene of SARS-CoV-2 in the context of persistent infection and viral escape mechanisms.}, author = {Trifonova, Angelina and Syarov, Atanas and Takov, Svetlomir and Angelov, Krassimir and Vazharova, Radoslava and Terzieva, Velislava}, @@ -11547,6 +11677,21 @@ @article{wirth_chlorella_2020 year = {2020} } +@article{wirth_gene_2024, + abstract = {IntroductionChronic heart failure is associated with adverse remodeling of the heart that is typically characterized by cardiomyocyte hypertrophy. This requires the formation of new capillaries to maintain oxygen supply. Insufficient angiogenesis promotes the transition from compensated hypertrophy into heart failure. The aim of the present study was to identify angiogenesis-related gene networks and corresponding regulatory hubs in endothelial cells from failing human hearts.Methods and resultsWe isolated left ventricular endothelial cells from patients with advanced heart failure undergoing left ventricular assist device surgery (n = 15) and healthy organ donors (n = 2) and performed RNA sequencing. Subgroup analysis revealed no impact of co-morbidities on gene expression. In a weighted coexpression network analysis, we found 26 gene clusters, of which nine clusters showed a significant positive or negative correlation with the presence of heart failure. We identified the transcription factors CASZ1 (castor zinc finger 1), ZNF523 (zinc finger protein 523), and NFE2L1 (nuclear factor erythroid 2-related factor 1) as hub genes of a cluster related to angiogenesis. Knock-down of CASZ1, ZNF523, or NFE2L1 in human umbilical vein endothelial cells led to a downregulation of genes from the respective cluster, including CD34 and platelet derived growth factor β, confirming their regulatory function.ConclusionIn conclusion, we assessed gene networks in endothelial cells and identified transcription factors CASZ1, ZNF532, and NFE2L1 as potential regulators of angiogenesis in failing human hearts. Our study provides insights into the transcriptional regulation of angiogenesis beyond the classical vascular endothelial growth factor signaling pathway.}, + author = {Wirth, Luisa and Erny, Elias and Krane, Markus and Lahm, Harald and Hein, Lutz and Gilsbach, Ralf and Lother, Achim}, + doi = {10.1152/ajpheart.00425.2024}, + issn = {0363-6135}, + journal = {American Journal of Physiology-Heart and Circulatory Physiology}, + keywords = {{\textgreater}UseGalaxy.eu, endothelial cells, heart, heart failure, transcription factor, transcriptome}, + month = {July}, + note = {Publisher: American Physiological Society}, + title = {Gene expression networks in endothelial cellsfrom failing human hearts}, + url = {https://journals.physiology.org/doi/abs/10.1152/ajpheart.00425.2024}, + urldate = {2024-07-21}, + year = {2024} +} + @article{witmer_epigenetic_2020, abstract = {The malaria parasite replicates asexually in the red blood cells of its vertebrate host employing epigenetic mechanisms to regulate gene expression in response to changes in its environment. We used chromatin immunoprecipitation followed by sequencing in conjunction with RNA sequencing to create an epigenomic and transcriptomic map of the developmental transition from asexual blood stages to male and female gametocytes and to ookinetes in the rodent malaria parasite Plasmodium berghei. Across the developmental stages examined, heterochromatin protein 1 associates with variantly expressed gene families localised at subtelomeric regions and variant gene expression based on heterochromatic silencing is observed only in some genes. Conversely, the euchromatin mark histone 3 lysine 9 acetylation (H3K9ac) is abundant in non-heterochromatic regions across all developmental stages. H3K9ac presents a distinct pattern of enrichment around the start codon of ribosomal protein genes in all stages but male gametocytes. Additionally, H3K9ac occupancy positively correlates with transcript abundance in all stages but female gametocytes suggesting that transcription in this stage is independent of H3K9ac levels. This finding together with known mRNA repression in female gametocytes suggests a multilayered mechanism operating in female gametocytes in preparation for fertilization and zygote development, coinciding with parasite transition from host to vector.}, author = {Witmer, Kathrin and Fraschka, Sabine A. and Vlachou, Dina and Bártfai, Richárd and Christophides, George K.}, @@ -11873,6 +12018,24 @@ @article{wylie_whole-genome_2019 year = {2019} } +@article{wynne_apoe_2023, + abstract = {Mitochondria influence cellular function through both cell-autonomous and non-cell autonomous mechanisms, such as production of paracrine and endocrine factors. Here, we demonstrate that mitochondrial regulation of the secretome is more extensive than previously appreciated, as both genetic and pharmacological disruption of the electron transport chain caused upregulation of the Alzheimer’s disease risk factor apolipoprotein E (APOE) and other secretome components. Indirect disruption of the electron transport chain by gene editing of SLC25A mitochondrial membrane transporters as well as direct genetic and pharmacological disruption of either complexes I, III, or the copper-containing complex IV of the electron transport chain elicited upregulation of APOE transcript, protein, and secretion, up to 49-fold. These APOE phenotypes were robustly expressed in diverse cell types and iPSC-derived human astrocytes as part of an inflammatory gene expression program. Moreover, age- and genotype-dependent decline in brain levels of respiratory complex I preceded an increase in APOE in the 5xFAD mouse model. We propose that mitochondria act as novel upstream regulators of APOE-dependent cellular processes in health and disease.}, + author = {Wynne, Meghan E and Ogunbona, Oluwaseun and Lane, Alicia R and Gokhale, Avanti and Zlatic, Stephanie A and Xu, Chongchong and Wen, Zhexing and Duong, Duc M and Rayaprolu, Sruti and Ivanova, Anna and Ortlund, Eric A and Dammer, Eric B and Seyfried, Nicholas T and Roberts, Blaine R and Crocker, Amanda and Shanbhag, Vinit and Petris, Michael and Senoo, Nanami and Kandasamy, Selvaraju and Claypool, Steven Michael and Barrientos, Antoni and Wingo, Aliza and Wingo, Thomas S and Rangaraju, Srikant and Levey, Allan I and Werner, Erica and Faundez, Victor}, + doi = {10.7554/eLife.85779}, + editor = {Chacinska, Agnieszka and Pfeffer, Suzanne R and Chacinska, Agnieszka}, + issn = {2050-084X}, + journal = {eLife}, + keywords = {{\textgreater}UseGalaxy.eu, APOE, alzheimer's disease, mitochondria}, + month = {May}, + note = {Publisher: eLife Sciences Publications, Ltd}, + pages = {e85779}, + title = {{APOE} expression and secretion are modulated by mitochondrial dysfunction}, + url = {https://doi.org/10.7554/eLife.85779}, + urldate = {2024-07-22}, + volume = {12}, + year = {2023} +} + @article{xu_reprogramming_2023, abstract = {Xu and colleagues report that the poly-U-specific endoribonuclease ENDU-2/ENDOU activates a transcriptional reprogramming after a brief heat shock and this has a long-term beneficial effect in the model organism C. elegans.}, author = {Xu, Fan and Li, Ruoyao and von Gromoff, Erika D. and Drepper, Friedel and Knapp, Bettina and Warscheid, Bettina and Baumeister, Ralf and Qi, Wenjing},