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2,168 results for “deletion”
Genome stability of murine cytomegalovirus vectors with large deletions and insertions
<p>We investigated the basic characteristics of a new murine cytomegalovirus (MCMV) vector platform. Using BAC technology, we engineered replication-competent recombinant MCMVs with deletions of up to 26% of the wild type genome. To this end, we targeted five gene blocks (m01-m17, m106-m109, m129-m141, m144-m158, and m159-m170). BACs featuring deletions from 26-18% of the wild type genome exhibited delayed virus reconstitution, while smaller deletions (up to 16%) demonstrated reconstitution kinetics similar to the wild type. Utilizing an innovative methodology, we introduced large genomic DNA segments, up to 35 kbp, along with reporter genes into a newly designed vector with a potential cloning capacity of 46 kbp (Q4). Next, two independent stuffer DNAs were inserted into the Q4 BAC resulting in Q4-LAD and Q4-LRBAs BACs. LAD is an AT-rich DNA sequence based on inactivated human adenovirus genome (34 kbp) and a non-coding portion of human LRBA (LPS responsive beige-like anchor protein) gene a non-coding portion of human LRBA gene which is GC-rich (36 kbp). The Q4-LRBAs BAC was further modified by inserting two different transgene expression cassettes encoding for either Gaussian luciferase (GLuc) resulting in Q4-LRBAs-GLuc. First, we rescued replicating vectors after transfection of MEFs with the above described BACs. Each vector preparation was passaged up to 10 passage on MEFs. Then MEF cells (70% confluence) were infected with Q4, Q4-LAD, and Q4-LRBAs-GLuc at MOI 0.5. derived from passage 1, 5 and 10. As control we used lysates of wild type BAC derived MCMV infected MEFs after passages 1, 5, 10, 15, and 20. After 48 hpi, virus particles were harvested, purified, and DNA was extracted using the NucleoSpin Tissue kit (Macherey-Nagel, Germany). Illumina NGS was performed on 100 ng DNA template for each sample (paired end sequencing, 2×150 bp, 5 Mio reads/sample). This dataset contains the raw sequencing data (individually named .zip files) and a table (an .xlsx file packed into MCMV Vector Stability_VACCINES_2024.zip) with the detailed specifications of the dataset. The reference sequences, which we used for the analysis in our Vaccines paper (Riedl et al. Vaccines, 2024), are provided in a zipped folder in .gb format.</p>
text-fig. 54. Reduced consensus tree of the pruned data matrix after the deletion of Shuvosaurus, Segisaurus, and Poekilopleuron. Named nodes: 1, Saurischia; 4, Herrerasauridae; 5, Neotheropoda; 6, Coelophysoidea; 8, Coelophysidae; 9, Liliensternus', 12, Ceratosauria; 13, Abelisauroidea; 14, etanurae; 16, Camosauria; 17, Spinosauroidea; 20, Allosauroidea; 24, Coelurosauria; 26, Coeluridae; 27, Compsognathinae; 30, Tyrannosauroidea; 34, Maniraptora; 37, Deinonychosauria. in The interrelationships and evolution of basal theropod dinosaurs
text-fig. 54. Reduced consensus tree of the pruned data matrix after the deletion of Shuvosaurus, Segisaurus, and Poekilopleuron. Named nodes: 1, Saurischia; 4, Herrerasauridae; 5, Neotheropoda; 6, Coelophysoidea; 8, Coelophysidae; 9, Liliensternus', 12, Ceratosauria; 13, Abelisauroidea; 14, etanurae; 16, Camosauria; 17, Spinosauroidea; 20, Allosauroidea; 24, Coelurosauria; 26, Coeluridae; 27, Compsognathinae; 30, Tyrannosauroidea; 34, Maniraptora; 37, Deinonychosauria.
text-fig. 52. wo selected reduced consensus trees from the analysis of the complete data set. a, after deletion of 'Chilantaisaurus' maortuensis. B, after deletion of Proceratosaurus and Xuanhanosaurus. in The interrelationships and evolution of basal theropod dinosaurs
text-fig. 52. wo selected reduced consensus trees from the analysis of the complete data set. a, after deletion of 'Chilantaisaurus' maortuensis. B, after deletion of Proceratosaurus and Xuanhanosaurus.
Fig. 3 in An exceptional case of mitochondrial tRNA duplication-deletion events in blood-feeding leeches
Fig. 3 Genetic signature of the trnD1/trnD2 genes of Placobdella species highlighted in an alignment
Fig. 4 in An exceptional case of mitochondrial tRNA duplication-deletion events in blood-feeding leeches
Fig. 4 Position of the conserved nucleotides in the P. parasitica trnD product (highlighted in purple)
Fig. 1 in An exceptional case of mitochondrial tRNA duplication-deletion events in blood-feeding leeches
Fig. 1 Maximum Likelihood tree built based on 4 concatenated molecular markers (cox1, nad1, ITS and 12S). Taxon names in orange correspond to specimens in which trnD2 was found. Taxon names in pink and blue possess, respectively, a trnD3 or trnD4 locus. Taxon names in black possess only trnD1 and the gray taxon names indicate lack of data. Horizontal bars next to taxon names represent the order and relative length of genes between atp8 and cox2. Cox2 segment is 530 bp long and the sizes of the other genes in each diagram are proportional to it. Pie charts in nodes represent the character state predicted for that node by a parsimony approach, where purple indicates presence of additional loci (trnD2–4) and white, absence. Node A represents the last common ancestor of all leeches, node B is the ancestor of all Placobdella species and node C is the first node in Placobdella which represents an ancestor with almost 100% certainty of having multiple trnD copies
Fig. 2 in An exceptional case of mitochondrial tRNA duplication-deletion events in blood-feeding leeches
Fig. 2 Predicted secondary structures of the products of trnD2 in samples that present substitutions in the GUC canonical anticodon. (A) P. rugosa, samples from Ontario, Manitoba, and Nebraska; (B) Placobdella sp. 1 AL; (C) P. kwetlumye
Single cell deletion of the transcription factors Trps1 and Sox9 reveals novel functions in adult cortical astrocytes
Open the record for dataset details and reuse information.
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Event logs containing deletions
<p>Supplemental dataset containing deletions.</p>
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The chicken pan-genome reveals gene content variation and a promoter region deletion in IGF2BP1 affecting body size
<p></p><p>Domestication and breeding have reshaped the genomic architecture of chicken, but the retention and loss of genomic elements during these evolutionary processes remain unclear. We present the first chicken pan-genome constructed using 664 individuals, which identified an additional ∼66.5 Mb sequences that are absent from the reference genome (GRCg6a). The constructed pan-genome encoded 20,491 predicated protein-coding genes, of which higher expression level are observed in conserved genes relative to dispensable genes. Presence/absence variation (PAV) analyses demonstrated that gene PAV in chicken was shaped by selection, genetic drift, and hybridization. PAV-based GWAS identified numerous candidate mutations related to growth, carcass composition, meat quality, or physiological traits. Among them, a deletion in the promoter region of IGF2BP1 affecting chicken body size is reported, which is supported by functional studies and extra samples. This is the first time to report the causal variant of chicken body size QTL located at chromosome 27 which was repeatedly reported. Therefore, the chicken pan-genome is a useful resource for biological discovery and breeding. It improves our understanding of chicken genome diversity and provides materials to unveil the evolution history of chicken domestication.</p><p></p>
Figure 36. Strict consensus trees from the taxon addition–deletion runs. A in Craniodental characters and the relationships of Procyonidae (Mammalia: Carnivora)
Figure 36. Strict consensus trees from the taxon addition–deletion runs. A, consensus tree of the five most parsimonious trees recovered by an exhaustive search of extant taxa only; B, most parsimonious tree recovered by a heuristic search of taxa with more than 50% of the characters scorable; C, consensus tree of the 11 most parsimonious trees recovered by a heuristic search of taxa with more than 25% of the characters scorable; D, consensus tree of the 342 most parsimonious trees recovered by a heuristic search of all taxa scored. Numbers below the nodes indicate node number. †, extinct taxa.
Data_Tab1_Deletion of the transcription factor Prox-1 specifically in the renal distal convoluted tubule causes hypomagnesemia via reduced expression of TRPM6 and NCC
<p>Data of Tab1 from “Deletion of the transcription factor Prox-1 specifically in the renal distal convoluted tubule causes hypomagnesemia via reduced expression of TRPM6 and NCC”</p> <p>Dataset (doi: 10.1007/s00424-020-02491-1) contains the original publication as PDF-format (10.1007_s00424-020-02491-1.pdf). Corresponding raw data obtained from LC-MS/MS analysis provided as one file in CSV format (31003A-179400_10.1007_s00424-020-02491-1_DW_4-1.csv). All further experiment related information provided as two meta-data-files (31003A-179400_10.1007_s00424-020-02491-1_DW _4-1_M_1.PDF, 31003A-179400_10.1007_s00424-020-02491-1_DW _4-1_M_2.pdf) as PDF format.</p>
Ubiquitin Ligase Wwp1 Gene Deletion Attenuates Diastolic Dysfunction in Pressure Overload Hypertrophy
<p><strong><em>Background.</em></strong> Heart failure with a preserved left ventricular (LV) ejection fraction (HFpEF) often arises from a prolonged LV pressure overload (LVPO) and accompanied by abnormal extracellular matrix (ECM) accumulation. The E3 ubiquitin ligase WWP1 is a fundamental determinant ECM turnover. We tested the hypothesis that genetic ablation of<em> Wwp1</em> would alter the progression of LVPO induced HFpEF.</p> <p><strong><em>Methods/Results</em></strong><em>.</em> LV echocardiography in mice with global <em>Wwp1</em> deletion (n=41; <em>Wwp1<sup>-/-</sup></em>) was performed at 12 weeks of age (Baseline) and then at 2 and 4 weeks following LVPO (transverse aortic banding) or surgery without LVPO induction. Age-matched wild type mice (<em>Wwp1<sup>+/+</sup></em>; n=33) underwent identical protocols. LV EF remained constant and unchanged with LVPO and LV mass increased in both groups but was lower in the <em>Wwp1<sup>-/-</sup></em> mice. With LVPO, the E/A ratio, an index of LV filling, was 3.97 + 0.46 in <em>Wwp1<sup>+/+</sup></em> but was 1.73 + 0.19 in the <em>Wwp1<sup>-/-</sup></em> group (p<0.05). At the transcriptional level, mRNA for fibrillar collagens (types I and III) decreased by approximately 50% in <em>Wwp1<sup>-/-</sup></em> compared to the <em>Wwp1<sup>+/+</sup></em> group at 4 weeks post-LVPO (p<0.05) and was paralleled by a similar difference in LV fibrillar collagen content as measured by histochemistry. Moreover, mRNA levels for determinants favoring ECM accumulation, such as transforming growth factor (TGF) increased with LVPO, but were lower in the <em>Wwp1<sup>-/-</sup></em> group.</p> <p><strong><em>Summary.</em></strong> The absence of <em>Wwp1</em> reduced the development of LVH and subsequent progression to HFpEF. Modulating the WWP1 pathway could be a therapeutic target to alter the natural history of HFpEF.</p>
Deletion of the sodium/hydrogen exchanger 6 causes low bone volume in adult mice
<p>The sodium/hydrogen exchanger 6 (NHE6) localizes to recycling endosomes, where it mediates endosomal alkalinization through K<sup>+</sup>/H<sup>+</sup> exchange. Mutations in the SLC9A6 gene encoding NHE6 cause severe X-linked mental retardation, epilepsy, autism and corticobasal degeneration in humans. Patients with SLC9A6 mutations exhibit skeletal malformations, and a previous study suggested a key role of NHE6 in osteoblast-mediated mineralization. The goal of this study was to explore the role of NHE6 in bone homeostasis. To this end, we studied the bone phenotype of NHE6 knock-out mice by microcomputed tomography, quantitative histomorphometry and complementary ex vivo and in vitro studies. We detected NHE6 transcript and protein in both differentiated osteoclasts and mineralizing osteoblasts. In vitro studies with osteoclasts and osteoblasts derived from NHE6 knock-out mice demonstrated normal osteoclast differentiation and osteoblast proliferation without an impairment in mineralization capacity. Microcomputed tomography and bone histomorphometry studies showed a significantly reduced bone volume and trabecular number as well as an increased trabecular space at lumbar vertebrae of 6 months old NHE6 knock-out mice. The bone degradation marker c-terminal telopeptides of type I collagen was unaltered in NHE6 knock-out mice. However, we observed a reduction of the bone formation marker procollagen type 1 N-terminal propeptide, and increased circulating sclerostin levels in NHE6 knock-out mice. Subsequent studies revealed a significant upregulation of sclerostin transcript expression in both primary calvarial cultures and femora derived from NHE6 knock-out mice. Thus, loss of NHE6 in mice causes an increase of sclerostin expression associated with reduced bone formation and low bone volume.</p>
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Allen Brain Atlas
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Annotated Behaviour and Observability Dataset (ABODe)
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