EMBO/sd-character-level-ner huggingface dataset:
D HCT binds to the open (AB) 1 pair. View of ScV1 looking along the central rotor subunit D towards the cytoplasm, showing the position of the H subunit binding at the interface of the open A/B pair (AB) 1. The catalytic hexamer is shown in surface representation and the central rotor, peripheral stalks and subunit H are shown as ribbons.
A-C The RPE cells as described in Fig 3 were stained for paxillin (as a marker for focal adhesion; green), F-actin (red) and DNA (blue). The representative images are shown (A). Scale bars, 20 μm or 5 μm (insets). The cell spreading area of the cells (B, n ≥ 108) and the number of focal adhesions per cell (C, n ≥ 30) were measured.
Representative western blot showing level of IKKε in IKBKE (IKKε)-silenced (B) MDA-MB-468 breast cancer cell lines.
B Analysis of the methylation status at nephrin gene promoter in podocytes cultured in normal, high glucose or high mannitol at the indicated time points. U, unmethylated-specific primers; M, methylated-specific primers.
(A) Schematic of the screening procedure. Compounds were dispensed in matrigel coated 384 well plates prior to seeding of murine myoblasts. Myoblasts were incubated for 24 h with 10 µM of the individual compounds, 5 µM of the positive control Trichostatin A or with the negative control DMSO. After fixation and staining with the IIH6 antibody, detecting glycosylated α-dystroglycan, the cells were imaged using the confocal PE Opera LX high-throughput microscope. The intensity of the α-dystroglycan glycosylation staining was determined, values normalized and a hit list generated. Scale bar, 20 µm.
F T6P inhibits PIF4 phosphorylation by KIN10. This assay was performed with 1 μg of each protein at 30 °C for 30 min in the presence of 1 mM T6P or sucrose (Suc).
(D) Quantification of clonal survival assay relative total cell numbers (top panel) or normalized to DMSO controls (lower panel).
C. wt and mdi1 egg chambers stained for Larp (green) and ATP-S (red) to reveal mitochondria. Larp closely associates with mitochondria in wt egg chambers. Mitochondria in mdi1 flies are clumped together, and completely lack Larp staining. Bars in (B) (C): 10 m.
F. Translocation efficiency of the unmodified peptide AS_67, triplicate AS3_67 and charge optimized peptide AS_M67 is classified as % of cells that show no translocation '-' to very good '++++' translocation with EGFP-LC3C; n = total number of analyzed cells. Data are presented as mean of three biological replicates ±SD.
(I, J) Immunoprecipitation and immunoblotting (I) and quantification (J, n = 3 independent experiments) showing the interaction of HA-CP110 with Flag-CEP97 in HEK293T cells transfected with the indicated plasmids. The intensity of each Flag-CEP97 band was normalized to that of the β-actin band.
A, B ATAC-seq analyses revealed progressive increased telomeric DNA accessibilities in sgA#10 transduced IMR90 cells. (A) The graph plots show the cumulative percentage of total reads that contained at least indicated number of TTAGGG (or CCCTAA) tandem repeats. (B) The percentage of total reads that contains > 3 tandem telomeric repeats are expressed as means ± s.d., N = 2, unpaired t test.
H. Kaplan-Meier survival curve of the BT12 xenografted animals treated with vehicle (green line, n = 15) and clemastine (black line, n = 12). Survival of the animals has been measured and pooled from two independent experiments. P = 0.044, Mantel-Cox Log-rank test.
RT-qPCR assay showing the expression of HES1 mRNA in the GFP+ cells on day 5 of differentiation with 1.25 nM PLB supplementation alone or in combination with NUMB_S ectopic expression from day 2.5.
(C) The plaque-reduction neutralization assay using two authentic SARS-CoV-2 strains: the Germany isolate (BetaCoV/Munich/BavPat1/2020) and UK/B1.1.7. Mean ± s.d. are plotted (n = 3 biological replicates). Numbers in brackets indicate IC50 values in nM.
qPCR quantification of retinal gene expression under the effect of WNT agonist CHIR99021 and WNT antagonist IWR1 on retinal differentiation (n=3 biological replicates for each group).
(A) Co-visualization of pCASP1::SGN1-mCherry and pCASP1::SGN3-GFP. Note that their respective localization at the PM has only restricted overlap at the cortical side of the CS domain (Arrow). Representative picture is shown, 3-6 roots in 4 different transgenic lines were inspected. Scale bar = 10 µm. "inner" designates the stele-facing endodermal surface, "outer", the cortex-facing surface.
F Verification of Scl‐dependent gene expression using qRT-PCR. Average of three biological replicates with SD are shown.
(c) p85β(ΔSH2C) is more stable than wild-type p85β. RPE1-hTERT cells were infected with either a retrovirus expressing wild-type p85β or p85β (ΔSH2C). Cells were incubated with cycloheximide (CHX) for the indicated times, collected and analysed by immunoblotting as indicated. In the graph, the amount of p85β (wild-type or mutant) is represented relative to the amount at time 0. (
Comparison of SWATH-MS-based quantification to DDA-MS-based strategies (MS1 XIC and spectral counting) with regard to consistency (as judged based upon protein-level SEC chromatogram robustness towards increasing requirements on the number of consecutive detections) and precision (judged based on the correlation between sibling peptide SEC chromatograms) of quantification and overall performance in error-controlled complex-centric query of CORUM complexes in the respective protein level chromatogram sets (also see Appendix Figure S3C). TP, true positive assignments according to error model, P, all positives.
C. Volcano plot presentation of the differently expressed transcripts in FCRLS- and CD11b-positive Trem2-/- (n=5) in comparison to WT (n=6) microglia isolated from 6-month-old male mice. 17 out of 65 analyzed genes are significantly changed more than 20%, with 7 genes upregulated (purple) and 10 genes downregulated (blue). Data information: For statistical analysis the unpaired, two-tailed student`s t-test was performed Statistical significance was set at **, p < 0.01; ***, p < 0.001; ****, p < 0.000; ns, not significant.
(f) Colony formation assay demonstrating that the ferroptosis inhibitor Ferrostatin-1 (Fer) reversed Sorafenib-induced cell death in ATF4-deficient HCC cells. HLE cells transfected with siCtrl or siATF4 were treated with Sorafenib (8μM) or DMSO plus either DMSO or Ferrostatin-1 (Fer; 5μM) for 2 weeks. Results represent three independent experiments.
F) Effect of motor speed on fiber diameter: interestingly, the experimental values are lower than the theoretical ones due to the shrinking of the alginate-based bioink upon exposure to divalent calcium ions.
H,I Levels of ADPR (H), cADPR (I) expressed as nmol/mg protein in diaphragm of WT (n=6), mdx (n=5) and mdx/CD38-/- (n=5) mice. Data information: Each dot of the graphs represents a mouse and measured in duplicate After normality and variance comparison tests, significance was assessed using: ANOVA followed by Fisher's LSD test; ; I: Welch's ANOVA followed by Welch's t-tests Values are expressed as means ± SEM. Significance: *p<0.05, **p<0.01, ***p<0.001.
Fold enrichment of γH2AX at telomere repeats by real-time PCR. Graph represents fold enrichment of γH2AX at telomeric repeats between IgG control, 3 and 30 month old whole mouse hearts. Data are mean ± SEM of n=3 mice per age group.
E, CpGs that gained methylation during neuronal differentiation (Fig. 1), were hypomethylated in KO neurons compared to WT neurons. Depicted are the 441 CpGs covered by RRBS in both datasets.
Xenogeneic inoculation of 786-0 cells lacking GDH1 with restored expression of WT, ED or 3KR mutant GDH1 into the left groin of nude mice. The solid tumor formed by the indicated 786-0 cells is shown (B).
G. Representative images of co-electroporated axons. Dashed white lines delineate axons. White arrows indicate colocalized puncta. Colored arrows represent non-colocalized signal as follows: magenta for CD63, cyan for pre-miR-181a-1, yellow for Rab7a and blue for LysoTracker. Abbreviations: CD63, CD63-eGFP or CD63-mRFP; Rab7a, Rab7a-eGFP or Rab7a-mRFP; pre-miR-181a-1, cy3-pre-miR-181a-1 or cy5-pre-miR-181a-1. Scale bar: 5μm.
M, N Sustained mDA neuroprotective effects. Shown in (M) is a confocal image of TH/HA-stained cells 6 months after NF-AAV injection (Foxa2 gene tagged with HA). Inset, z-stacked image of the boxed area along the y-axis (right) and x-axis (lower). TH+ cells in the right (NF-AAV) and left (C-AAV injected) midbrains were counted 6 and 12 months after AAV injection (N). *P = 0.000019 (6M), 0.000066 (12M), n = 6-7, paired Student's t-test.
Cell cycle analysis of INK128 (200 nM) treated mESCs in 2iL (mean values ± SD). n = 3 biological replicates.
(c) Representative TEM micrographs of nonspecific- or Cltc-RNAi-transfected NRK cells after 12 h of serum starvation. Scale bar, 5 μm.
D, E, F, and G. 3D electron microscopy of thalamus in 12-month-old Ifnb+/+ and Ifnb-/- mice. D. Volume rendering of mitochondria (left panel) and corresponding mitochondria in 2D electron microscopy image (right panel) in cell bodies. Each individual mitochondrion is colored differently. Scale bars equal 2 microns. Voxel size equals 0.00878908x0.00878908x0.03 microns for the Ifnb+/+ neuron and 0.00439453x0.00438453x0.04 microns for Ifnb-/-. Nuclei are in grey and marked with 'N.' E. Reconstituted axonal mitochondria. Images extracted from Movies EV1 and 2. F. Size of individual mitochondria in cell bodies and non-myelinated and myelinated axons. N>30; error bars are SD. G. Number of branches per mitochondrion. N>30; error bars are SD.
ChIP‐qPCR analysis of H3K27Ac and H3K4me3 occupancy on the reporter gene upon transfection of λN-Nxf2 expression vector or control EGFP expression vector. Bar graph shows the occupancy relative to that of the sample transfected with a control plasmid. Error bars indicate SD (n = 3), * = p-value<0.01 (t-test)..
(A) Exponentially growing ypt7Δ cells were starved in SD‐N medium for 4 h, lysed and the extract separated into a cytoplasmic (S) and a 5000 g membrane pellet fraction. The pellet was treated with (+) or without (−) TX‐100, centrifuged and the supernatant (S) and pellet (P) fractions analysed by western blotting with anti‐Atg1, anti‐Pep12 and anti‐Pgk1 antibodies.
(G) Time-lapse 2D-SIM imaging of TssA and sheath dynamics. Imaging was performed on cells of the double-tagged strain (tssB-mCherry2 mNeonGreen-tssA) by 2D-SIM. White arrow indicates an example of paired T6SS assembly.
A) Ratiometric imaging of pH in living HeLa cells at different OXPHOS complexes and in the matrix. WT matrix: MPP-sEcGFP; WT SU γ: SU γ fused to sEcGFP; WT SU e: SU e fused to sEcGFP; WT CoxVIIIa: subunit CoxVIIIa fused to sEcGFP (all C-terminally). HGlc: high glucose; Gal: galactose. Ratio-images for IF1-H49K OE cells are displayed in Figure EV4. Scale bars: 10 µm.
(A) Schematic illustration of proteins involved in TGFβ storage in the extracellular matrix. The Small Latent Complex (SLC) is a non-covalently linked tetramer of 2 LAP (Latency Associated Peptide) (40 kDa) and 2 TGFβ1 (12 kDa). LTBP1 + SLC together form the Large Latent Complex (LLC) through covalent bonds between LAP and LTBP1. LLC interacts with the ECM through non-covalent interactions of LTBP with fibrillins and fibronectin.
(A) Z-Projection of confocal image stacks spanning 5 μm of a control embryo (left) co-expressing endogenously tagged mVenus::βH-spectrin (green) and the plasma membrane marker GAP43::mCherry (magenta) and of an embryo additionally expressing a maternally driven anti-GFP nanobody KD module to knock-down βH-spectrin (right). Co-expression of the anti-GFP nanobody KD system resulted in a drastic decrease of βH-spectrin protein levels as assessed by the fluorescent signal intensity which dropped below the detection limit.
F FRAP analysis of DNA-induced droplets of cGAS (1 μM dsDNA, 10 μM cGAS-mCherry), the yellow dotted circle indicated the region of photobleaching. G FRAP curve of (F). n = 3 biological replicates. H FRAP analysis of cGAS-G3BP1 droplets. 10 μM cGAS-mCherry and 5 μM G3BP1 were used. The yellow dotted circle indicated the region of photobleaching. I FRAP curve of (H). n = 3 biological replicates. Data information: Representative images are shown (A, Error bars, mean with s.d. , *P < 0.05, ****P < 0.0001, two-tailed t-test. NS, non-significant. FRAP, Fluorescence recovery after photobleaching. Scale bars, 2 μm (F and H).
B. Fraction of proteins (in percent) having at least one functional disordered domain (>30 consecutive amino acids) for the mitotic chromosome proteins compared to the cytosolic proteome. More than 81% of the mitotic chromosome proteins have at least one long disordered domain.
(A) ) After 24 h treatment with either EBV or CpG, pDCs were co‐cultured with cord blood‐derived allogeneic CD4+ T cells. The proliferative response was evaluated by measuring ( thymidine and is expressed as cpm. Data are shown as mean + SD of triplicate cultures. One representative experiment out of two performed is shown.
HeLa cell lines were treated with the small-molecule Bcl-2/Bcl-XL-inhibitor ABT-737 for 72 h. Cytokines were measured by ELISA. (A) Concentrations of IL-6 were determined (CTRL, n=9; Bax/Bak, n=6; Bcl-XL, n=3; STING, n=3).
C. Correlation coefficients were also high (i.e., 0.98-0.99), indicating that the obtained sequence data was sufficient for further analysis of age-specific methylation changes.
(a) Schematic representations of all constructs tested. R, mRFP; RH, mRFP fused to HSC70bm (VKKDQ and KFERQ); RS, mRFP fused to scrambled QBP1 (Online Methods); RHS, mRFP fused to HSC70bm and scrambled QBP1; RQ, mRFP fused to QBP1; RHQ, mRFP fused to HSC70bm and QBP1 (Sc, scrambled).
A Confocal microscopy image of endogenous SIRT5 co-localized with endogenous MAVS in H1299 cells detected by immunofluorescence staining using anti-SIRT5 and anti-MAVS antibodies. Mito, Mitotracker; Scale bar = 8 µm.
E TAT-2031 treatment increased lysosomal mobility. Neurons were infected with shLAMTOR1 or shSc AAV; they were treated with TAT or TAT-2031 (10 µM) and imaged with LysoTracker to visualize lysosomal trafficking in dendrites. N = 17-22 neurons from 3 independent experiments. Data information: Data with error bars are represented as means ± SEM. Statistical significance was assessed by two-way ANOVA with Tukey's post-test **P < 0.01, ***P < 0.001.
d & e, Representative Dynamic Light Scatter (DLS) plot of 100K EV sample (N = 13 samples), showing (d) average intensity and (e) volume against diameter (13 DLS measurements per sample);
Measurements (Total epidermis skin thickness, Keratin layer thickness and Squamous cell layer thickness) of dorsal skin sections obtained from male mice of the indicated genotypes. Each dot on the scatter dot plot represents one focus point of the measurement. (N=20, 20, 30, 40, 40 for Hoip+/+; Sharpin+/+, HoipK778R/K778R; Sharpin+/+ , Hoip+/K778R; Sharpin+/cpdm, Hoip+/+; Sharpincpdm/cpdm, Hoip+/K778R; Sharpincpdm/cpdm, respectively.) F
C-F. MDM we treated with 5μM ETO for 18h and co‐infected in the presence of ETO with HIV-1 BaL and SIV VLP Q76A. DNA was isolated 18 h post‐infection for qPCR quantification of D. Late RT products; E. 2LTR circles; F. integrated viral DNA.Integrated copies of viral DNA, Alu-Gag qPCR. (n = 3, mean ± s.e.m.; *P‐value ≤ 0.05; **P‐value ≤ 0.01, paired t‐test).
(A) Growth curves of MCF10A cells exposed to oxidative stress (200μM H2O2) relative to control cells (n=3). Two-way ANOVA was used to test for significance.
(B) The extent of Ubqln4 co‐immunoprecipitation with Ubqln1 was measured and the ratio of Ubqln4 to Ubqln1 was calculated for WT Ubqln1, Ubqln1ΔUBL and Ubqln1ΔUBA. The numbers represent the ratio of Ubqln4 to Ubqln1 relative to WT. Each bar represents the average and s.e.m. of four independent experiments. *P‐value=0.0041.
(e) After labelling SK-Hep1 cells with C14-leucine, cells were treated with FFAs (600 μM PA or 1,200 μM OA). Percent release of radioactivity was measured for 3-6 h as described in the Methods. The difference between the percent proteolysis without E64d/pepstatin A/NH4Cl and that with E64d/pepstatin A/NH4Cl was regarded as lysosomal proteolysis. *P0.05, **P0.01; one-way ANOVA, n=3.
Mammary organoids were isolated from 19-20 weeks old C57Bl/6 mice on normal (ND) Organoids isolated from ND mice were cultured in matrigel/collagen mix for 2 days followed by macrophage-conditioned or control medium stimulation for 24­h. 3D structure of organoids stained for DNA (Hoechst 33342 in blue), F-actin (Phalloidin in red) and α-SMA (green). Bi-layered structure of internal luminal cells and external basal myoepithelial cells is established for non-invasive organoids.
(G) Venn diagram showing the number of proteins significantly altered upon Apamin and XE991 treatment in ALSC9orf72 MN. The lines ALSC9orf72 II and ALSC9orf72 III were used as representative of the ALS genotype.
(c) Plasma from malaria patients induce macrophages to secrete cytokines, which are inhibited by a XO specific inhibitor. Plasma from a healthy control (HP) and from three patients: P1 (with cerebral malaria), P2 and P3 (both with uncomplicated malaria) was pre-incubated for 30 min with febuxostat (Feb) or alone at 37ºC before addition to macrophages at 1:2 dilution in media for 30 min. Cells were washed and cytokine secretion measured in triplicates after 24 h of incubation. unpaired t-tests (c) were performed to determine statistical significance (*p<0.05, **p<0.01).
(C-D) Immunostaining for YFP and Tunel assay (C) and immunohistochemistry for YAP and TAZ (D) in K14CREER/YAP TAZ DKO/Rosa-YFP mice and K14CREER/Rosa-YFP control mice
B) Schematic representation of the MhsT structure (LeuT fold). L-4-Fluoro-phenylalanine shown as gray sticks. Remaining color coding same as in panel A.
D. Size-exclusion chromatography revealing that the N-terminus-truncated version of Mdm12 (residues 11-271) retains the ability to interact with Mmm1. The experiment was performed as in Figure 1B. Eluted fractions indicated by shading were subjected to SDS-PAGE followed by Coomassie Blue staining.
B A cell line derived from the BRAF-V600E-positive human melanoma line WM1158 was generated to carry inducible GFP-Usp27x. GFP-Usp27x was induced, and Bim was detected as in A. Similar results were obtained in n=3 separate experiments.
Schematic view of the experimental setting for the HU-synchronized live cell imaging. 48 hours before imaging, RPE-FUCCI cells were transfected with siRNA against scramble or cyclin F. 16 hours before imaging, cells were synchronized at the G1/S border by HU (2 mM) treatment. Representative images from different channels are shown, and white arrows in Differential Interference Contrast DIC channel indicate the traced cell. Scale bar: 10µm.
D The result of real-time quantitative PCR analysis for UCP1 in brown adipose tissue from HFD-fed control and ad-FADDmice is shown in the bar graph. Data are expressed as mean ± SEM from two independent experiments (n = 4 total for each genotype). *P = 0.0172 (Student's t-test).
(g-i) In situ structures of singlet microtubules from pig (g), horse (h), and mouse (i) sperm endpieces. Note how the MIP binds to two tubulin monomers (white arrowheads).
(A) Axotomised DIV 14-16 rat cortical neurons expressing p110δ and GFP or GFP alone. Axons were cut >1000 μm from the soma imaged for 14 h. Black arrows mark the cut site, white arrows marks the axon tip. See also Movies EV7 and EV8. (B) Percentage of regenerating axons 14 h after laser axotomy. Numbers on bars are injured axons per group, from 4 experiments. (C) Quantification of axon regeneration length 14 h post-axotomy. n=9 axons for GFP, 9 for p110α, 25 for p110αH1047R and 27 for p110δ from 4 experiments. (D) Quantification of time to start of regeneration. n=9 axons for GFP, 9 for p110α, 25 for p110αH1047R and 27 for p110δ from 4 experiments.
F. RT-PCR analysis of RNA isolated from mouse liver for Birc5, FoxM1B and cyclin B1. Data are presented as log2 fold change and were calculated using non-operated mouse liver tissue as a control. Unpaired, two-tailed Student t-test was used to determine the significance between the log2 values of livers 6, 24 and 48 h post PH compared to the sham operated controls. Log2 values are plotted on a linear scale as mean ± SD.
(G). Myelin basic protein (MBP) staining of corpus callosum in P28 controls, Gpr56 null and Gpr56 S4 mice.
Literature analysis of 210 publications using MS-based plasma proteomics to identify new biomarkers. The number of quality markers reported as biomarker candidates in these studies is indicated. Distribution of the reported quality markers according to the three types of likely contaminations. The distribution is shown across studies that report one, two or three proteins of the same quality marker panel.
(A and B) Levels of IL-1β in supernatants from THP-1 cells that were subjected to knockdown as indicated and were treated with LPS, and then (A) treated with LLOMe or (B) starved in EBSS.
H Expression and palmitoylation of ISP1 in ∆isp1/3 parasites complemented with the 3V5 tagged WT ISP1 or C7AC8A mutant.
Fis1 knockdown abolishes DFP-induced LC3-II. Fis1 siRNA was introduced into HeLa cells for 48 h, and the cells were treated with DFP for further 24 h (Nsi, non-specific siRNA; Fis1i, Fis1 siRNA; siRNA concentration, 20nM; DFP, 1mM). Whole cell lysate samples were blotted as indicated. Values are presented as mean ± SEM and are normalized to the control value (n=3, biological replicates; **, p<0.01; paired t-test).
B Site mutation of S947 or all 12 serine and threonine residues in the ATX1 SET domain inhibited the activation of ATX1 by SEC; moreover, mutation of five conserved amino acids in the SEC functional domain inhibited SEC activity.
(D) Cells were fixed and permeabilized then stained with antibody to LC3B. Bar charts represent the percentage of cells with LC3B puncta and are presented as the means ± s.e.m., n = 4.
(D) Pep2 induces PEPR1-FLAG association with SERK1-, SERK2-, BKK1-, and BAK1-HA in N. benthamiana. Experiments were repeated at least three times, with the same conclusions. IP and IB denote imunoprecipitation and immunoblotting with the indicated antibodies, respectively. NT indicates non-transformed plants. (*, p < 0.05 in two-tailed tests compared to the differences (± Pep2) from the corresponding values of WT plants.)
investigating the role of nuclear calcium signaling in mRNA induction of Arc, Fosb and Npas4. j, nuclear calcium imaging of MSN cultures after application of different stimuli. HiK (55 mM), glutamate (Glu, 1 µM), SKF-38393 (SKF, 10 µM) or dopamine (DA, 20 µM) were applied after ~10min of baseline imaging (arrowheads). Grey traces indicate individual cells, black traces indicate mean of all imaged cells (~30) for one stimulation run. inset: y-axis: 100% ∆F/F, x-axis: 10min, n = 3 independent cultures.
(B) Immunoblot analysis of BAT from AdRiKO and control mice treated with either norepinephrine (NE) or vehicle for 30 minutes for the indicated proteins (n=3/group).
C Simulated integrated pS6 response versus simulated cell-cycle indicator of mCFU-E, BaF3-EpoR and 32D-EpoR cells upon 5 U/ml Epo stimulation and single inhibitor treatment at indicated doses
In MM.1S cells treated with mycolactone and/or BZ at the indicated concentrations, or vehicle as control for 6 h: (D) CHOP and GADD34 mRNA levels were quantified by qPCR Data information: Shown mRNA data are Mean fold changes (2-∆∆CT) ± SD, relative to untreated controls (cumulative data of at least 2 independent experiments with technical duplicates or triplicates), pairwise compared by nested one-Way ANOVA with Tukey's multiple comparison test, exact p-values indicated. Thapsigargin (Tg, 2 µM, 6 h), Tunicamycin (Tu, 2 µM, 6 h) were used as positive controls.
H Box plot showing the difference between percentage of reconstitution between WT and MT contralateral grafts in each transplant generation. P values were determined by Mann-Whitney U‐test.
B: Top: Basal area (black line) and limE fluorescent intensity (green line) as a function of time, for the same cell as in A. Inset: Temporal CF of the area and the limE fluorescent intensity (blue) and of the area change rate and the limE fluorescent intensity (magenta). Bottom: Kymograph of the LimE-GFP intensity along the cell outline.