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  1. Detailansicht für Treffer 1 öffnen
    Figure 4—figure supplement 2. Lateral positioning of ROBO1-expressing longitudinal axons in Nova1/2 dKO embryos. ; (A) Anti-ROBO1 staining of transverse sections of E12.5 lumbar spinal cords. The antibodies do not distinguish between isoforms. ROBO1 was expressed at a low level on precrossing axons and was highly upregulated on postcrossing axons in both WT and Nova1/2 dKO embryos. ROBO1-expressing axons displayed the same lateral positioning defect as anti-L1 labeled axons (compare with Figure 4B). Reducing Robo1(e6b+) partially rescued the lateral positioning defect in Nova1/2 dKO embryos, while reducing Robo2(e6b+) alone did not rescue. Reducing Robo1/2(e6b+) together further rescued the defect. Arrows indicate the lateral funiculus (LF) and ventral funiculus (VF). Scale bar, 50 μm. (B) Quantification of the lateral positioning of ROBO1-expressing axons in A. Data are represented as the mean ± SD (one-way ANOVA and Bonferroni post test; animal numbers and p values are indicated; ns, not significant). (C) Anti-ROBO2 staining of transverse sections of E12.5 lumbar spinal cords. The antibodies do not distinguish between isoforms. ROBO2 was primarily expressed by axons in the lateral funiculi, and the overall patterns were comparable between the WT and Nova1/2 dKO embryos. (D) Anti-ROBO1 and anti-ROBO2 staining in the corresponding KO embryos, showing the specificity of the antibodies. The Robo1 KO was generated by trapping the protein product in intracellular compartments (Friedel et al., 2005). ROBO1 expression was seen in neuronal cell bodies but not in axons in Robo1 KO spinal cords, as previously reported (Long et al., 2004).
    2019
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  2. Detailansicht für Treffer 2 öffnen
    Figure 8. Bim CTS binds with non-transmembrane topology to cellular membranes. ; (A) Selected images for sub-cellular localization of VBimEL and BimELV in BMK-DKO cells compared to MitoTracker. The scale bar represents 10 µm. (B) In live cells CBcl-XL binding to BimELV is resistant to ABT-263. FLIM-FRET binding curves for the interactions between CBcl-XL and BimELV in ABT-263 (blue) or DMSO (green) treated BMK-DKO cells expressing CBcl-XL. Binding of CBcl-XL to VBimEL (black) measured in the same three experiments is shown for comparison. Data from ROIs from three independent experiments were combined and used to generate binding curves with 95% confidence intervals as in Figures 1 and 2. (C) Sub-cellular localization of BimELV is impaired compared to VBimEL but ABT-263 resistant binding to CBcl-XL (RABT-263) is unchanged. Colocalization for Venus and MitoTracker-Red was measured in this experiment for manually selected regions of interest from transiently transfected cells expressing VBimEL or BimELV (Pearson’s r, red); Error bars, SEM, n > 30 cells. RABT-263 of CBcl-XL:VBimEL or CBcl-XL:BimELV complexes, black dots. Data are mean ±95% confidence intervals calculated from FLIM-FRET binding curves shown in panel b.
    2019
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  3. Detailansicht für Treffer 3 öffnen
    Figure 3—figure supplement 1. Placentas lacking Firre and Dxz4 on Xaor Xi show a similar methylation levels as in wildtype. ; (A) Scatter plot illustrating the relationship between mean CpG islands methylation as measured by reduced representation bisulfite sequencing (RRBS) for wildtype placenta (x axis, n = 3) versus DKO deletion on Xa or Xi (y axis, n = 2). (B) Boxplot showing CpG islands methylation levels on autosomes and on the X chromosome between wildtype and DKO deletion on Xa and Xi.
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  4. Detailansicht für Treffer 4 öffnen
    Figure 4—figure supplement 1. Analyzing adult female organs carrying a homozygous deletion of Firre and Dxz4. ; (A) Heatmap showing unsupervised clustering of a Pearson correlation matrix (48 samples, DKO bodymap) from expression data (TPM), confirming the expected developmental relationship. The DKO bodymap includes spleen, brain, kidney, heart, lung and liver from 6 weeks old females (4 WT and 4 DKO replicates). (B) Firre, Dxz4 (4933407K13Rik) and Xist expression abundance in the bodymap organs. One of the replicates is shown.
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  5. Detailansicht für Treffer 5 öffnen
    Figure 2. Chicken ANP32B is not functional for IAV polymerase. ; Cells were transfected with avian H5N1 50–92 polymerase (PB2 627E or 627K) together with NP, firefly minigenome reporter, Renilla expression control, either Empty vector (control) or ANP32 expression plasmid and incubated at 37°C for 24 hr. (a) Minigenome assay in human eHAP1 cells with co-expressed Empty vector, FLAG-tagged chANP32A or chANP32B. (b) Minigenome assay in double knockout (dKO) eHAP1 cells. (c) Western blot analysis of dKO eHAP1 cell minigenome assay confirming expression of PB2 and FLAG-tagged chANP32A and B. (d) Minigenome assay in WT DF-1 cells with either co-expressed Empty vector or chANP32B. (e) Minigenome assay in DF-1 ANP32B knockout (bKO) cells with either co-expressed Empty vector or chANP32B. Data shown are firefly activity normalised to Renilla, plotted as mean ± SEM (n = 3 biological replicates). Two-way ANOVA with Dunnet’s multiple comparisons to Empty vector. ns = not significant, ****p
    2019
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  6. Detailansicht für Treffer 6 öffnen
    Figure 3—figure supplement 1. Alternative splicing of Robo1/2. ; (A) Quantitative RT-PCR of a constitutive exon in Robo1/2 showing the total Robo mRNA levels in Nova1/2 dKO dorsal spinal cord at E11.5. (B) Western blotting analysis of ROBO1/2 protein levels in E11.5 spinal cords. The antibodies do not distinguish between the alternative isoforms. (C) Quantitative RT-PCR analysis of Robo1 and Dutt1 levels in Nova1/2 dKO dorsal spinal cord, which are two alternative mRNAs produced from two different promoters (Nural et al., 2007),. Other alternative 5’ sequences of Robo1 and Robo2 were also tested and no significant difference was observed between WT and Nova1/2 dKO spinal cords. (D) Quantification of Robo1 exon 6b expression in nine different genotype combinations of Nova1 and Nova2. Robo1 exon 6b level was sensitive to Nova1/2 gene copy number. Robo2 exon 6b level was regulated in a similar dose-sensitive manner. Data are normalized to the WT and are represented as the mean ± SD (Student’s t-test in A,C; one-way ANOVA and Bonferroni post test in D; n = 3 for all genotypes; p value are indicated; ns, not significant). (E) Genomic DNA included in exon 6b splicing reporters. Exon 6b sequences are capitalized and in bold. Potential NOVA-binding sites (YCAY repeats; Y = C/U) that were mutated in the splicing assays are in bold and in red. Two additional candidate NOVA-binding sites (in black, bold, and lower case) are present in Robo1 intron 6b but were not mutated, as the mutations themselves constitutively repressed exon 6b inclusion. (F) Splicing assays of Robo2 exon 21. Schematic shows the Robo2 exon 21 splicing reporter, which contains the complete genomic sequences between exons 20 and 22 (5.8 kb). Candidate NOVA-binding sites (7 YCAY repeats) are located in intron 20. Expression of e21- and e21+ isoforms was detected by semi-quantitative RT-PCR. NOVAs had no direct effect on Robo2 exon21 alternative splicing.
    2019
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  7. Detailansicht für Treffer 7 öffnen
    Figure 7. The β2AR mutant selectively supports carvedilol-induced augmentation of LTCC activity in neurons. ; (A–B) β1AR/β2AR double knockout (DKO) mouse hippocampal neurons on 7–10 days in vitro (DIV) were cotransfected with FLAG-tagged β2AR WT (A) or mutant (B) and HA-tagged LTCC α11.2 subunit, 24 hr later cells were either mock treated (NT), or treated for 5 min with 10 nM isoproterenol (ISO) or carvedilol (CAR), fixed and labeled with anti-FLAG and a phospho-specific antibody for S1928 phosphorylated α11.2. Confocal images show mutant β2AR losts the ability of promoting LTCC phosphorylation upon ISO stimulation but remained the ability upon CAR stimulation in neurons. Scale bar, 10 μm. Representative of 6 images for each condition, three experiments. (C) Representative single channel recordings of LTCC CaV1.2 currents using 110 mM Ba2+ as charge carrier in DKO neurons on 7–10.days DIV expressing mutant β2AR after depolarization from −80 to 0 mV in in control patches (mutant) and patches containing 1 μM isoproterenol (ISO) or 1 μM carvedilol (CAR) in the patch pipette. Shown are 20 consecutive sweeps from representative experiments. Arrows throughout the figure indicate the 0-current level (closed channel). Scale bar denotes 2 pA and 200 ms. (D) Ensemble average currents as determined from all sweeps recorded for all the experimental conditions. Scale bar denotes 50 fA and 400 ms. (E–G) Mean ± s.e.m. for (E) Po (%), (F) availability (i.e. likelihood that a sweep had at least one event) (%) and (G) the mean ensemble average current (fA) for each experimental condition. *p
    2019
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  9. Detailansicht für Treffer 9 öffnen
    Figure 4. Homozygous deletion of Firre and Dxz4 loci results in organ-specific expression changes on autosomes. ; (A) Cartoon illustrating the structural differences of the X chromosome between wildtype and DKO female mice (left), and the organs collected from 4 WT and 4 DKO six-weeks old adult females to generate the transcriptomic bodymap (right). (B) Overview of the differentially expressed genes in the female bodymap and their overlap across the six organs (DEseq2: FDR ≤ 0.1, |log2FC| ≥ 1). The bar plot shows the proportion of differentially expressed genes between autosomes and the X chromosome. Genes that are directly affected by the deletion are underlined (Firre, Dxz4 transcript (4933407K13Rik) and crossFirre (Gm35612, antisense to Firre). (C) Cartoon illustrating the structural differences of the X chromosome between WT and each of the KO strains (left), and the SKO organs collected from six-weeks old adult females (Firre = 3, Dxz4 = 2) (right). (D) Heatmap showing the fold changes of megadomain, superloop and Firre locus dependent gene sets in the spleen. (E) MA plot for all KO strains of the genes extracted from the top five gene sets (GSEA analysis) identified in the DKO and Firre SKO spleen (more details in the Materials and methods section and Supplementary file 1 sheet I). The black dot indicates significant differentially expressed genes (DEseq2: FDR ≤ 0.1).
    2019
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  11. Detailansicht für Treffer 11 öffnen
    Figure 1. Functional effects caused by deleting the Munc13-1 C2C domain. ; (A) Cartoon depicting the domain structure of Munc13-1 and Munc13-1 ∆C2C. (B), Example EPSC traces recorded from Munc13-1/2 DKO autaptic hippocampal neurons expressing either Munc13-1 WT (black) or Munc13-1 ∆C2C (burgundy red). (C) Plot showing the average EPSC amplitudes obtained from the DKO neurons rescued with Munc13-1 WT or Munc13-1 ∆C2C. (D) Example traces of synaptic current responses induced by 5 s application of 500 mM sucrose from DKO neurons rescued with the WT and the C2C truncated mutant indicated above. (E) Plot of the average RRP charge for both groups. (F) Plot of the calculated Pvr in % for Munc13-1 WT and C2C truncated mutant. (G) Graph showing the absolute EPSC amplitudes in response to a train of 50 action potentials (APs) with an inter-stimulus interval (ISI) of 100 ms (10 Hz) for the WT and truncated C2C domain mutant. Numbers at the top of the bars represent the number of neurons pooled together for each group. Numbers in parentheses represent the number of cultures or replicates used. All data are mean ± SEM. Significance and p values were determined by Mann-Whitney test. ****p
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  12. Detailansicht für Treffer 12 öffnen
    Figure 6—figure supplement 1. Extended characterization of HMOX1; SLC48A1 mice. ; (A) Representative images of WT and KO BMDMs post-EP. (B) Representative images of intracellular reactive oxygen species (ROS) in WT and KO BMDMs at the indicated timepoints post-treatments. (C) Observed and expected numbers of pups born of the indicated genotypes for HMOX1 HET intercrosses, either on a WT or KO background. Quantification of splenic RPMs (D) and bone marrow macrophages (BMMs) (E) in HMOX1 KO and DKO mice by flow cytometry. (F) Quantification of total Ter-119+ cells in the bone marrows of HMOX1 KO and DKO mice. (G) Quantification of subpopulations of Ter-119+ cells represented as a percentage of total Ter-119+ cells in the bone marrow. (H) Quantification of total Ter-119+ cells in the spleen. The %single cells* on the y-axis denote single cells that are negative for CD4/8/41, B220 and Gr-1. (I) Quantification of populations II and III of Ter-119+ cells represented as a percentage of total Ter-119+ cells in the spleen. At least 100,000 single cells were analyzed per sample. Each dot represents one mouse. (J) LDH content in cells and media of HMOX1 KO and DKO BMDMs post-erythrophagocytosis (EP), represented as percentage of total LDH in cells and media. (K) Representative images of HMOX1 KO and DKO BMDMs post-EP.
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  13. Detailansicht für Treffer 13 öffnen
    Figure 2. Midline crossing defect in Nova1/2 dKO embryos results from elevated ROBO repulsion. ; (A) Anti-ROBO3 staining of commissural axons in transverse sections of E11.5 spinal cords. The bottom panel shows closeup images of the floorplate. Nova1/2 dKO and Dcc KO embryos had reduced ventral commissures. Dcc; Nova1; Nova2 triple KO mutants had even thinner commissures than Dcc KO embryos, and some axons appeared to remain on the ipsilateral side without entering the midline (arrow) in the triple KO mutants. In contrast, Nova1; Nova2; Robo1 triple KO mutants had a slightly increased ventral commissure size compared to Nova1/2 dKO embryos. Scale bars, 50 μm. (B) Quantification of the ventral commissure size in A. Data are normalized to the WT and are represented as the mean ± SD (one-way ANOVA and Bonferroni post test; animal numbers and p values are indicated). (C) DiI labeling of E12.5 mouse spinal cords in openbook preparations. In Nova1/2 dKO embryos, about half of the axons arriving at the midline did not project across. This defect was alleviated by Robo1 KO. Nova1/2 dHet and Robo3 Het, which were phenotypically normal on their own, synergistically blocked midline crossing. Brackets indicate the midline. Scale bar, 50 μm. (D) Quantification of midline crossing in C. Data are normalized to the WT and are represented as the mean ± SD (one-way ANOVA and Bonferroni post test; animal numbers and p values are indicated).
    2019
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  14. Detailansicht für Treffer 14 öffnen
    Supplementary file 1. RNA and reduced representation bisulfite sequencing analysis. ; (A) Log2FC (lfcMLE) and adjusted p-values (padj) from DEseq2 differential expression analysis, computed by comparing female WT placentas of the forward cross (n = 8) with each of the deletion strains (deletion on Xa, n = 3–4) and female WT placentas of the reverse cross (n = 9) with each of the deletion strains (deletion on Xi, n = 3–4). (B) Log2FC (lfcMLE) and adjusted p-values (padj) from DEseq2 differential expression analysis, computed by comparing male WT placentas of the forward cross (n = 9) with each of the KO strains (n = 3). (C) Methylation levels as measured by reduced representation bisulfite sequencing (RRBS) for WT placenta and DKO deletion on Xa or Xi. (D) Imprinted ratios of X-linked placenta genes for WT and each of the deletion strains (deletions on Xa or Xi, 0.5 = 100% maternal, −0.5 = 100% paternal). The allelic ratios for each replicate per genotype was combined by using the median. (E) Imprinted ratios of X-linked visceral yolk sac genes for WT and DKO (deletions on Xa or Xi, 0.5 = 100% maternal, −0.5 = 100% paternal). The allelic ratios for each replicate per genotype was combined by using the median. (F) Differentially expressed genes (DEseq2 differential expression analysis) in all tissues (bodymap) of DKO female and liver and spleen of SKO female. (G-H) Log2FC of megadomain, superloop and Firre locus dependent gene sets in the liver and spleen. (I) Top enriched gene sets identified in the DKO and Firre SKO spleen. (J) Information of every analyzed sample in this study.
    2019
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  16. Detailansicht für Treffer 16 öffnen
    Figure 6. HCT116 cells treated with the apoptotic drug ABT-737 contain inner membrane compartments that are lacking the enclosing outer membranes. ; (A) FM of a section of resin-embedded Bax/Bak DKO HCT116 cells stably expressing GFP-Bax, treated with ABT-737 for 3 hr. GFP-Bax (green), MitoTracker Deep Red (magenta). Yellow square indicates the field of view imaged by ET, white circles indicate fluorescent signals of interest localized in electron tomograms. (B) Virtual slice through an electron tomogram acquired at area indicated by the yellow square in A. Green and magenta crosses indicate predicted position of GFP-Bax and MitoTracker Deep Red signal centroids, respectively, indicated by white circles in fluorescence micrographs. Black square indicates area magnified in C. (C) Magnified area of the virtual slice shown in B, corresponding to the black square. The image shows an accumulation of single membrane compartments near the GFP-Bax clusters. (D) 3D segmentation model of mitochondria and single-membrane compartments seen in B. Outer membranes are in dark blue, inner membranes in light blue. (E) Virtual slice through an electron cryo-tomogram of a cryo-FIB milled Bax/Bak DKO HCT116 cell stably expressing GFP-Bax treated with ABT-737 for 3 hr. Arrows indicate compartments reminiscent of mitochondrial inner membranes that appear to have no outer membrane.Arrowhead indicates an inner membrane within an intact mitochondrion. (F, G) Magnified areas of the virtual slice shown in E, corresponding to the black squares. White arrowheads indicate putative ATP synthase heads. (H) 3D segmentation model of compartments seen in E. Membranes are in light blue, putative ATP synthase heads in red. White box indicates magnified area in I. (I) Magnified area from white box in H, depicting the arrangement of putative ATP synthase heads. (J) Measured distances between head and membrane. Comparison between ATP synthases identified in mitochondria in HeLa cells, and putative ATP synthases in the compartments without outer membrane in HCT116 cells. The red lines indicate the mean and the standard deviation. For numerical data see Figure 6—source data 1. Scale bars: 500 nm (A), 100 nm (B–E, H), 20 nm (F, G, I).
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  18. Detailansicht für Treffer 18 öffnen
    Figure 2—figure supplement 2. Drug-induced GFP-Bax recruitment to mitochondria in HCT116 cells causes outer membrane ruptures and inner membrane rearrangement similar to those induced in HeLa cells upon GFP-Bax overexpression. ; Live confocal FM of Bax/Bak DKO HCT116 cells stably expressing GFP-Bax (green), treated with ABT-737 and Q-VD-OPh for 3 hr. Cells were stained with MitoTracker Deep Red (magenta) prior to treatment. Cells were imaged every 30 min for 3 hr after treatment. FM images shown are from (A) 30 min, (B) 1 hr, and (C) 2 hr 30 min following treatment. White squares indicate areas shown magnified below A-C. The three magnified images correspond to: GFP-Bax channel (left), MitoTracker Deep Red channel (middle), and merge (right). (D–F) Correlative microscopy: FM image of section of resin-embedded Bax/Bak DKO HCT116 cells stably expressing GFP-Bax (green) that were treated with ABT-737 and Q-VD-OPh for 3 hr. GFP-Bax (green), MitoTracker Deep Red (magenta). Yellow squares indicate the field of view imaged by ET. White circles indicate GFP-Bax signals localized in electron tomograms. (G–I) Virtual slices from electron tomograms acquired at areas indicated by yellow square in FM images. White arrowheads indicate ruptured membranes. Green crosses indicate predicted positions of GFP-Bax signal centroids indicated by white circles in fluorescence micrographs. (J–L) 3D segmentation model of mitochondria in G-I, respectively. Outer membranes in dark blue, inner membranes in light blue. Scale bars: 10 µm (A-C, upper panels), 2 µm (A-C, lower panels), 500 nm (D–F), 100 nm (G–L).
    2019
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  19. Detailansicht für Treffer 19 öffnen
    Figure 4. Restoring Robo1/2 exon 6b levels rescues axon guidance defects in Nova1/2 dKO embryos. ; (A) Alternative splicing of exon 6b in animals with or without the exon 6b deletion allele. Semi-quantitative RT-PCR was performed using RNA from E11.5 dorsal spinal cord. Deleting one copy of exon 6b from Robo1/2 genomic DNA in Nova1/2 dKO embryos restored e6b+ expression to a comparable level as in the WT. (B) DiI labeling of spinal cord openbooks (top panel) and anti-L1 staining of transverse spinal cord sections (bottom panel) in E12.5 animals with or without exon 6b deletion. As it is difficult to obtain a large number of compound mutants, the rostral half of the spinal cord was used for DiI labeling and the lumbar level was used for anti-L1 staining. Brackets indicate the midline. Arrows indicate the lateral funiculus (LF) and ventral funiculus (VF). Reducing Robo1(e6b+) partially rescued both midline crossing and lateral positioning defects in Nova1/2 dKO embryos, while reducing Robo2(e6b+) alone did not rescue. Reducing Robo1/2(e6b+) together further rescued both defects. Scale bars, 50 μm. (C) Quantification of axon midline crossing and lateral positioning in B. As Nova deficiency reduces the number of postcrossing axons due to fewer axons reaching the midline, we compared the ratio between the thickness of the lateral and ventral funiculi within the same section. Data are represented as the mean ± SD (one-way ANOVA and Bonferroni post test; animal numbers and p values are indicated; ns, not significant).
    2019
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xs 0 - 576
sm 576 - 768
md 768 - 992
lg 992 - 1200
xl 1200 - 1366
xxl 1366 -