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Emerging microbes & infections
2021 Nov 16
Frank, C;Wickel, J;Brämer, D;Matschke, J;Ibe, R;Gazivoda, C;Günther, A;Hartmann, C;Rehn, K;Cadar, D;Mayer, TE;Pörtner, K;Wilking, H;Schmidt-Chanasit, J;Tappe, D;
PMID: 34783638 | DOI: 10.1080/22221751.2021.2007737
In 2021, three encephalitis cases due to the Borna disease virus 1 (BoDV-1) were diagnosed in the north and east of Germany. The patients were from the states of Thuringia, Saxony-Anhalt, and Lower Saxony. All were residents of known endemic areas for animal Borna disease but without prior diagnosed human cases. Except for one recently detected case in the state of Brandenburg, all >30 notified cases had occurred in, or were linked to, the southern state of Bavaria. Of the three detected cases described here, two infections were acute, while one infection was diagnosed retrospectively from archived brain autopsy tissue samples. One of the acute cases survived, but is permanently disabled. The cases were diagnosed by various techniques (serology, molecular assays, and immunohistology) following a validated testing scheme and adhering to a proposed case definition. Two cases were classified as confirmed BoDV-1 encephalitis, while one case was a probable infection with positive serology and typical brain magnetic resonance imaging, but without molecular confirmation. Of the three cases, one full virus genome sequence could be recovered. Our report highlights the need for awareness of a BoDV-1 etiology in cryptic encephalitis cases in all areas with known animal Borna disease endemicity in Europe, including virus-endemic regions in Austria, Liechtenstein, and Switzerland. BoDV-1 should be actively tested for in acute encephalitis cases with residence or rural exposure history in known Borna disease-endemic areas.
Emerging infectious diseases
2021 Dec 01
Hierweger, MM;Koch, MC;Rupp, M;Maes, P;Di Paola, N;Bruggmann, R;Kuhn, JH;Schmidt-Posthaus, H;Seuberlich, T;
PMID: 34808081 | DOI: 10.3201/eid2712.210491
European perch (Perca fluviatilis) are increasingly farmed as a human food source. Viral infections of European perch remain largely unexplored, thereby putting farm populations at incalculable risk for devastating fish epizootics and presenting a potential hazard to consumers. To address these concerns, we applied metatranscriptomics to identify disease-associated viruses in European perch farmed in Switzerland. Unexpectedly, in clinically diseased fish we detected novel freshwater fish filoviruses, a novel freshwater fish hantavirus, and a previously unknown rhabdovirus. Hantavirus titers were high, and we demonstrated virus in macrophages and gill endothelial cells by using in situ hybridization. Rhabdovirus titers in organ samples were low, but virus could be isolated on cell culture. Our data add to the hypothesis that filoviruses, hantaviruses, and rhabdoviruses are globally distributed common fish commensals, pathogens, or both. Our findings shed new light on negative-sense RNA virus diversity and evolution.
Development
2021 Nov 15
Morrison, J;McLennan, R;Teddy, J;Scott, A;Kasemeier-Kulesa, J;Gogol, M;Kulesa, P;
| DOI: 10.1242/dev.199468
The dynamics of multipotent neural crest cell differentiation and invasion as cells travel throughout the vertebrate embryo remain unclear. Here, we preserve spatial information to derive the transcriptional states of migrating neural crest cells and the cellular landscape of the first four chick cranial to cardiac branchial arches (BA1-4) using label-free, unsorted single-cell RNA sequencing. The faithful capture of branchial arch-specific genes led to identification of novel markers of migrating neural crest cells and 266 invasion genes common to all BA1-4 streams. Perturbation analysis of a small subset of invasion genes and time-lapse imaging identified their functional role to regulate neural crest cell behaviors. Comparison of the neural crest invasion signature to other cell invasion phenomena revealed a shared set of 45 genes, a subset of which showed direct relevance to human neuroblastoma cell lines analyzed after exposure to the in vivo chick embryonic neural crest microenvironment. Our data define an important spatio-temporal reference resource to address patterning of the vertebrate head and neck, and previously unidentified cell invasion genes with the potential for broad impact.
Development
2021 Nov 15
Kelsh, R;Camargo Sosa, K;Farjami, S;Makeev, V;Dawes, J;Rocco, A;
| DOI: 10.1242/dev.176057
Neural crest cells are crucial in development, not least because of their remarkable multipotency. Early findings stimulated two hypotheses for how fate specification and commitment from fully multipotent neural crest cells might occur, progressive fate restriction (PFR) and direct fate restriction, differing in whether partially restricted intermediates were involved. Initially hotly debated, they remain unreconciled, although PFR has become favoured. However, testing of a PFR hypothesis of zebrafish pigment cell development refutes this view. We propose a novel ‘cyclical fate restriction’ hypothesis, based upon a more dynamic view of transcriptional states, reconciling the experimental evidence underpinning the traditional hypotheses.
PLoS pathogens
2021 Nov 22
Braspenning, SE;Verjans, GMGM;Mehraban, T;Messaoudi, I;Depledge, DP;Ouwendijk, WJD;
PMID: 34807956 | DOI: 10.1371/journal.ppat.1010084
Primary infection with varicella-zoster virus (VZV) causes varicella and the establishment of lifelong latency in sensory ganglion neurons. In one-third of infected individuals VZV reactivates from latency to cause herpes zoster, often complicated by difficult-to-treat chronic pain. Experimental infection of non-human primates with simian varicella virus (SVV) recapitulates most features of human VZV disease, thereby providing the opportunity to study the pathogenesis of varicella and herpes zoster in vivo. However, compared to VZV, the transcriptome and the full coding potential of SVV remains incompletely understood. Here, we performed direct long-read RNA sequencing to annotate the SVV transcriptome in lytically SVV-infected African green monkey (AGM) and rhesus macaque (RM) kidney epithelial cells. We refined structures of canonical SVV transcripts and uncovered numerous RNA isoforms, splicing events, fusion transcripts and non-coding RNAs, mostly unique to SVV. We verified the expression of canonical and newly identified SVV transcripts in vivo, using lung samples from acutely SVV-infected cynomolgus macaques. Expression of selected transcript isoforms, including those located in the unique left-end of the SVV genome, was confirmed by reverse transcription PCR. Finally, we performed detailed characterization of the SVV homologue of the VZV latency-associated transcript (VLT), located antisense to ORF61. Analogous to VZV VLT, SVV VLT is multiply spliced and numerous isoforms are generated using alternative transcription start sites and extensive splicing. Conversely, low level expression of a single spliced SVV VLT isoform defines in vivo latency. Notably, the genomic location of VLT core exons is highly conserved between SVV and VZV. This work thus highlights the complexity of lytic SVV gene expression and provides new insights into the molecular biology underlying lytic and latent SVV infection. The identification of the SVV VLT homolog further underlines the value of the SVV non-human primate model to develop new strategies for prevention of herpes zoster.
Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research
2021 Nov 16
Lavicky, J;Kolouskova, M;Prochazka, D;Rakultsev, V;Gonzalez-Lopez, M;Steklikova, K;Bartos, M;Vijaykumar, A;Kaiser, J;Porizka, P;Hovorakova, M;Mina, M;Krivanek, J;
PMID: 34783080 | DOI: 10.1002/jbmr.4471
Considerable amount of research has been focused on dentin mineralization, odontoblast differentiation, and their application in dental tissue engineering. However, very little is known about the differential role of functionally and spatially distinct types of dental epithelium during odontoblast development. Here we show morphological and functional differences in dentin located in crown and roots of mouse molar and analogous parts of continuously growing incisors. Using a reporter (DSPP-cerulean/DMP1-cherry) mouse strain and knockout mice with ectopic enamel (Spry2+/- ;Spry4-/- ) we show that the different microstructure of dentin is initiated in the very beginning of dentin matrix production and is maintained throughout the whole duration of dentin growth. This phenomenon is regulated by the different inductive role of adjacent epithelium. Thus, based on the type of interacting epithelium we introduce more generalized terms for two distinct types of dentins: cementum vs. enamel-facing dentin. In the odontoblasts which produce enamel-facing dentin we identified uniquely expressed genes (Dkk1, Wisp1 and Sall1) which were either absent or downregulated in odontoblasts which form cementum-facing dentin. This suggests the potential role of Wnt signalling on the dentin structure patterning. Finally, we show the distribution of calcium and magnesium composition in the two developmentally different types of dentins by utilizing spatial element composition analysis (LIBS). Therefore, variations in dentin inner structure and element composition are the outcome of different developmental history initiated from the very beginning of tooth development. Taken together, our results elucidate different effect of two main types of dental epithelium, important for either crown or root formation, on adjacent odontoblasts which give rise to dentin of different quality. This article is protected by
Communications biology
2021 Nov 12
McKellar, DW;Walter, LD;Song, LT;Mantri, M;Wang, MFZ;De Vlaminck, I;Cosgrove, BD;
PMID: 34773081 | DOI: 10.1038/s42003-021-02810-x
Skeletal muscle repair is driven by the coordinated self-renewal and fusion of myogenic stem and progenitor cells. Single-cell gene expression analyses of myogenesis have been hampered by the poor sampling of rare and transient cell states that are critical for muscle repair, and do not inform the spatial context that is important for myogenic differentiation. Here, we demonstrate how large-scale integration of single-cell and spatial transcriptomic data can overcome these limitations. We created a single-cell transcriptomic dataset of mouse skeletal muscle by integration, consensus annotation, and analysis of 23 newly collected scRNAseq datasets and 88 publicly available single-cell (scRNAseq) and single-nucleus (snRNAseq) RNA-sequencing datasets. The resulting dataset includes more than 365,000 cells and spans a wide range of ages, injury, and repair conditions. Together, these data enabled identification of the predominant cell types in skeletal muscle, and resolved cell subtypes, including endothelial subtypes distinguished by vessel-type of origin, fibro-adipogenic progenitors defined by functional roles, and many distinct immune populations. The representation of different experimental conditions and the depth of transcriptome coverage enabled robust profiling of sparsely expressed genes. We built a densely sampled transcriptomic model of myogenesis, from stem cell quiescence to myofiber maturation, and identified rare, transitional states of progenitor commitment and fusion that are poorly represented in individual datasets. We performed spatial RNA sequencing of mouse muscle at three time points after injury and used the integrated dataset as a reference to achieve a high-resolution, local deconvolution of cell subtypes. We also used the integrated dataset to explore ligand-receptor co-expression patterns and identify dynamic cell-cell interactions in muscle injury response. We provide a public web tool to enable interactive exploration and visualization of the data. Our work supports the utility of large-scale integration of single-cell transcriptomic data as a tool for biological discovery.
The Journal of neuroscience : the official journal of the Society for Neuroscience
2021 Aug 18
Lamtahri, R;Hazime, M;Gowing, EK;Nagaraja, RY;Maucotel, J;Alasoadura, M;Quilichini, PP;Lehongre, K;Lefranc, B;Gach-Janczak, K;Marcher, AB;Mandrup, S;Vaudry, D;Clarkson, AN;Leprince, J;Chuquet, J;
PMID: 34210784 | DOI: 10.1523/JNEUROSCI.2255-20.2021
Following stroke, the survival of neurons and their ability to reestablish connections is critical to functional recovery. This is strongly influenced by the balance between neuronal excitation and inhibition. In the acute phase of experimental stroke, lethal hyperexcitability can be attenuated by positive allosteric modulation of GABAA receptors (GABAARs). Conversely, in the late phase, negative allosteric modulation of GABAAR can correct the suboptimal excitability and improves both sensory and motor recovery. Here, we hypothesized that octadecaneuropeptide (ODN), an endogenous allosteric modulator of the GABAAR synthesized by astrocytes, influences the outcome of ischemic brain tissue and subsequent functional recovery. We show that ODN boosts the excitability of cortical neurons, which makes it deleterious in the acute phase of stroke. However, if delivered after day 3, ODN is safe and improves motor recovery over the following month in two different paradigms of experimental stroke in mice. Furthermore, we bring evidence that, during the subacute period after stroke, the repairing cortex can be treated with ODN by means of a single hydrogel deposit into the stroke cavity.SIGNIFICANCE STATEMENT Stroke remains a devastating clinical challenge because there is no efficient therapy to either minimize neuronal death with neuroprotective drugs or to enhance spontaneous recovery with neurorepair drugs. Around the brain damage, the peri-infarct cortex can be viewed as a reservoir of plasticity. However, the potential of wiring new circuits in these areas is restrained by a chronic excess of GABAergic inhibition. Here we show that an astrocyte-derived peptide, can be used as a delayed treatment, to safely correct cortical excitability and facilitate sensorimotor recovery after stroke.
Acta pharmacologica Sinica
2021 Nov 22
Zhang, YM;Ye, LY;Li, TY;Guo, F;Guo, F;Li, Y;Li, YF;
PMID: 34811511 | DOI: 10.1038/s41401-021-00807-0
Hypidone hydrochloride (YL-0919) is a novel antidepressant in clinical phase II trial. Previous studies show that YL-0919 is a selective 5-HT (serotonin) reuptake inhibitor, 5-HT1A receptor partial agonist, and 5-HT6 receptor agonist, which exerts antidepressant effects in various animal models, but its effects on neural function remain unclear. Medial prefrontal cortex (mPFC), a highly evolved brain region, controls highest order cognitive functions and emotion regulation. In this study we investigated the effects of YL-0919 on the mPFC function, including the changes in neuronal activities using electrophysiological recordings. Extracellular recording (in vivo) showed that chronic administration of YL-0919 significantly increased the spontaneous discharges of mPFC neurons. In mouse mPFC slices, whole-cell recording revealed that perfusion of YL-0919 significantly increased the frequency of sEPSCs, but decreased the frequency of sIPSCs. Then we conducted whole-cell recording in mPFC slices of GAD67-GFP transgenic mice, and demonstrated that YL-0919 significantly inhibited the excitability of GABAergic neurons. In contrast, it did not alter the excitability of pyramidal neurons in mPFC slices of normal mice. Moreover, the inhibition of GABAergic neurons by YL-0919 was prevented by pre-treatment with 5-HT1A receptor antagonist WAY 100635. Finally, chronic administration of YL-0919 significantly increased the phosphorylation levels of mTOR and GSK-3β in the mPFC as compared with vehicle. Taken together, our results demonstrate that YL-0919 enhances the excitability of mPFC via a disinhibition mechanism to fulfill its rapid antidepressant neural mechanism, which was accomplished by 5-HT1A receptor-mediated inhibition of inhibitory GABAergic interneurons.
Frontiers in Molecular Neuroscience
2021 Nov 18
Roa, J;Ma, Y;Mikulski, Z;Xu, Q;Ilouz, R;Taylor, S;Skowronska-Krawczyk, D;
| DOI: 10.3389/fnmol.2021.782041
Protein kinase A (PKA) signaling is essential for numerous processes but the subcellular localization of specific PKA regulatory (R) and catalytic (C) subunits has yet to be explored comprehensively. Additionally, the localization of the Cβ subunit has never been spatially mapped in any tissue even though ∼50% of PKA signaling in neuronal tissues is thought to be mediated by Cβ. Here we used human retina with its highly specialized neurons as a window into PKA signaling in the brain and characterized localization of PKA Cα, Cβ, RIIα, and RIIβ subunits. We found that each subunit presented a distinct localization pattern. Cα and Cβ were localized in all cell layers (photoreceptors, interneurons, retinal ganglion cells), while RIIα and RIIβ were selectively enriched in photoreceptor cells where both showed distinct patterns of co-localization with Cα but not Cβ. Only Cα was observed in photoreceptor outer segments and at the base of the connecting cilium. Cβ in turn, was highly enriched in mitochondria and was especially prominent in the ellipsoid of cone cells. Further investigation of Cβ using RNA BaseScope technology showed that two Cβ splice variants (Cβ4 and Cβ4ab) likely code for the mitochondrial Cβ proteins. Overall, our data indicates that PKA Cα, Cβ, RIIα, and RIIβ subunits are differentially localized and are likely functionally non-redundant in the human retina. Furthermore, Cβ is potentially important for mitochondrial-associated neurodegenerative diseases previously linked to PKA dysfunction.
The Journal of molecular diagnostics : JMD
2021 Nov 18
Petrova-Drus, K;Quesada, AE;Bowman, AS;Ptashkin, R;Yao, J;Arcila, ME;Ho, C;Moung, C;Regalado, J;Benayed, R;Benhamida, JK;Galera, PK;Dogan, A;Vanderbilt, C;
PMID: 34801704 | DOI: 10.1016/j.jmoldx.2021.10.009
Epstein-Barr virus (EBV) is associated with hematologic and solid tumors. In this study, we utilized a hybridization capture-based next-generation sequencing (NGS) platform that targets 400 genes associated with hematological malignancies to detect and quantify nontargeted viral-derived EBV reads that aligned to the EBV reference contig (NC_007605). We evaluated 5234 samples from 3636 unique patients with hematological neoplasms and found that 100 samples (1.9%) in 93 unique patients had ≥6 EBV reads (range, 6 to 32,325; mean, 827.5; median, 54). Most (n = 73, 73%) represented known EBV-associated conditions, and the most common was post-transplant lymphoproliferative disorders (n = 21, 29%). Documented EBV viremia accounted for a moderate quantity of EBV reads in 4 of 27 samples corresponding to conditions not known to be EBV associated, whereas suspected viremia or low-level activation was likely the etiology in the remaining 23 samples. A good correlation (Spearman r = 0.8; 95% CI, 0.74-0.85) was found between EBV reads by NGS and systematic semiquantitative EBER in situ hybridization assessment in 162 available samples, particularly at higher level of EBV involvement. An optimal threshold for significant morphologic EBV involvement was found to be ≥10 reads by the receiver operating characteristic analysis (area under the curve, 0.990; 95% CI, 0.9974%-1.000%). Thus, in addition to mutational analysis, hybrid-capture-based NGS panels can be used to detect and quantitate off-target EBV-derived viral DNA, which correlates well with morphology.
Journal of Cystic Fibrosis
2021 Nov 01
Bedwell, D;Sharma, J;Du, M;Wong, E;Mutyam, V;Li, Y;Chen, J;Wangen, J;Thrasher, K;Fu, L;Peng, N;Tang, L;Liu, K;Mathew, B;Bostwick, B;Augelli-Szafran, C;Bihler, H;Liang, F;Mahiou, J;Saltz, J;Rab, A;Hong, J;Sorscher, E;Mendenhall, E;Coppola, C;Keeling, K;Green, R;Mense, M;Suto, M;Rowe, S;
| DOI: 10.1016/S1569-1993(21)01955-X
Background: Although recently developed CFTR modulator drugs can alleviate cystic fibrosis (CF) in the majority of patients, CF patients with mutations that form premature termination codons (PTCs) cannot benefit from modulator therapies. PTCs terminate translation before a full-length CF transmembrane regulator (CFTR) protein can be generated. In addition, a PTC can trigger nonsense-mediated mRNA decay of the CFTR transcript, further reducing expression of CFTR protein. Together, these 2 PTCmediated events result in negligible CFTR protein, abrogating the usefulness of CFTR modulators, whose action requires CFTR expression. Nonsense suppression therapy uses small molecules to suppress translation termination at in-frame PTCs (nonsense mutations) to restore partial levels of full-length, functional CFTR protein. Methods: Although some compounds have been identified that can suppress translation termination at PTCs (also called readthrough), poor efficacy of current readthrough agents prompted us to search for more effective compounds. To this end, we developed a NanoLuc reporter system in Fischer rat thyroid cells that responds to readthrough and nonsensemediated mRNA decay. This assay was used to screen 771 345 lowmolecular-weight compounds. Results: Of the 180 compounds identified with readthrough activity, SRI37240 and its more potent derivative SRI-41315 suppressed multiple CFassociated PTCs in immortalized and primary human bronchial epithelial cells, restoring partial CFTR expression and function. Mechanistically, we found that these compounds induce a prolonged pause at stop codons and suppress PTCs by targeting the termination factor eRF1 to the proteasome and thus reducing its abundance. Moreover, SRI-41315 enhances aminoglycoside-mediated readthrough, leading to synergistic increases in CFTR activity. Conclusion: SRI-37240 and SRI-41315 are the first pharmacological agents known to alter eRF1 levels and thus represent a new class of readthrough compounds that could potentially be used as part of a nonsense suppression therapy to treat genetic diseases in patients who carry PTCs
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| Description | ||
|---|---|---|
| sense Example: Hs-LAG3-sense | Standard probes for RNA detection are in antisense. Sense probe is reverse complent to the corresponding antisense probe. | |
| Intron# Example: Mm-Htt-intron2 | Probe targets the indicated intron in the target gene, commonly used for pre-mRNA detection | |
| Pool/Pan Example: Hs-CD3-pool (Hs-CD3D, Hs-CD3E, Hs-CD3G) | A mixture of multiple probe sets targeting multiple genes or transcripts | |
| No-XSp Example: Hs-PDGFB-No-XMm | Does not cross detect with the species (Sp) | |
| XSp Example: Rn-Pde9a-XMm | designed to cross detect with the species (Sp) | |
| O# Example: Mm-Islr-O1 | Alternative design targeting different regions of the same transcript or isoforms | |
| CDS Example: Hs-SLC31A-CDS | Probe targets the protein-coding sequence only | |
| EnEm | Probe targets exons n and m | |
| En-Em | Probe targets region from exon n to exon m | |
| Retired Nomenclature | ||
| tvn Example: Hs-LEPR-tv1 | Designed to target transcript variant n | |
| ORF Example: Hs-ACVRL1-ORF | Probe targets open reading frame | |
| UTR Example: Hs-HTT-UTR-C3 | Probe targets the untranslated region (non-protein-coding region) only | |
| 5UTR Example: Hs-GNRHR-5UTR | Probe targets the 5' untranslated region only | |
| 3UTR Example: Rn-Npy1r-3UTR | Probe targets the 3' untranslated region only | |
| Pan Example: Pool | A mixture of multiple probe sets targeting multiple genes or transcripts | |
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