EMBO/sd-character-level-ner huggingface dataset:
(A) Chromosomal positions of various histone H3 genes, ash1 and marker transgenes. 23 histone gene repeat units, each containing single His1, His2B, His2A, His4, and His3.2 gene, are clustered near the centromere (black circle) of chromosome 2. These histone genes are removed by the ∆HisC deletion. To select the animals homozygous for the deletion, the ∆HisC chromosomes are marked with insertions of either Elav-Gal4 or UAS-2xYFP transgenes (black triangles on chromosome 2L). The His3.3A and His3.3B genes encode the same protein, but reside on chromosomes 2L and X. The transgenes carrying twelve copies of either the wild-type histone repeat unit (12xWT) or the unit in which H3 gene is altered to have K36 replaced with arginine (12xH3K36R) are inserted in the same attP site (black triangle on chromosome 3L) [47]. The ash1 gene is located on the same chromosome arm.
D. A schema for the changes in lamin B1 levels during adult hippocampal neurogenesis.
A. Macrophages play a role in mediating shrinkage of lung cancer by Carfilzomib. TetO‐EGFR (T790M/Del19)/CC10-rtTA (TD) mice were fed with doxycycline for 3 months to induce lung cancer. Tumor burdens were then documented through computed tomography (CT) imaging before treatment (PreRx). After two-week treatment with saline (iv), Clodrosome (iv), Carfilzomib (iv), or Carfilzomib plus Clodrosome, mice were CT-scanned again (PstRx). Treatment effect was determined by comparing tumor-areas of PreRx and PstRx through ImagJ analysis. B. Statistics of the tumor burden in lung tissue. Data are means ± SD of three independent experiments. *p < 0.05, **p < 0.01 (student's t-test).
Scheme illustrating the Nsmce2 conditional allele (Nsmce2lox) used in this study. A cross with Flp recombinase‐expressing mice eliminated the FRT‐PGK‐neo‐FRT cassette present on the initial allele (Nsmce2lox‐neo) (see ). In the conditional allele, exon 3 is flanked by loxP sites allowing for its deletion in the presence of Cre recombinase.
(G) Shh levels assayed by ELISA from mouse cortex and hippocampus at the indicated time after the initiation of status epilepticus (SE) induced by pilocarpine (n=7-10).
F. Venn diagram showing overlapping differentially expressed genes (FDR≤0.05, |log2Ratio|≥1) in different genotype comparisons.
F. Diagram illustrating the catalytic pocket of HAT1 bound to succinyl-CoA. Structures of HAT1 (PDB ID 2P0W) and succinyl-CoA (PDB ID 5TRL) were used for the modeling by Discovery Studio.
MRI analysis of ejection fraction (EF%) in 24 month-old mice treated or not with navitoclax. Data are mean±S.E.M of n=6 mice per treatment group.
G, H Quantitative analyses of the ALP activity and calcium mineralization of MSCs. Results are shown as mean ± SEM; n=6; *: p<0.05 by t test
E RT-qPCR analysis of relative mRNA expression of thermogenic genes in SAT, VAT and BAT after treatment of lean mice treated with MP-10 (30 mg/kg) (n=7) or vehicle control (n = 6). **** P < 0.0001 (Pgc1alpha in VAT), ** P = 0.0012 (Ucp1 in VAT), ** P = 0.0071 (Pgc1alpha in BAT) and * P = 0.0486 (Ucp1 in BAT) using unpaired 2-tailed Student's t tests.
Regulaton of autophagy and lysosome pathway by TFEB silencing. qPCR showing the differentially expressed autophagy and lysosome related genes between human scr-shRNA and sh-TFEB ECs. Data are expressed as relative fold-change compared with the expression in control cells after normalization to the housekeeping gene TBP
The T6SS assembly begins first with the recruitment of the membrane complex (MC) in its resting state (1). The MC recruits the baseplate (BP) and the tail tip complex (TTC) is assembled (2). The recently solved structures of the BP (Cherrak et al, 2018) and MC (this paper) in the membrane context are shown in the inset. A conformational change leads to the channel opening (3) and release of the toxin onto the VgrG spike by contraction of the TTC (4). Once the secretion has occurred, the TTC is recycled (5) and the MC can return to its resting state (6).
a-c, RFA1::FLAG DDC2::MYC cells were arrested in G2 and released in YP galactose to induce HO endonuclease. After 30 min, the culture was split in two: +VPA and -VPA. c, Fold enrichment of the 0.2-kb fragment was calculated after ChIP of Rfa1-Flag, Ddc2-Myc.
(A) Schemes of Far1(1-150)-GFP constructs, either wild-type or mutant where NLxxxL motif is replaced with RxL motif (VKRTLF), that are used in time-lapse microscopy experiments in panel 'C'.
Analysis of Tfh cell development in the spleen (SPL), mesenteric lymph nodes (MLN), and Peyer´s patches (PP) of Pou2af1-/- and Pou2af1+/- mice following immunization with sheep red blood cells. (E) Coexpression of ICOS, PD1, and BTLA on Tfh cells. CD4+CXCR5hi T cells were analyzed for the simultaneous expression of these costimulatory molecules. Venn diagrams illustrate the overlap of ICOS, PD1 and BTLA expression on CD4+ICOShi T cells. Data represent mean values from 4 independent experiments. *, P < 0.05; **, P < 0.01; ***, P < 0.001; P < 0.0001; unpaired Mann Whitney test.
(B) Phosphoproteomics workflow. Protein extracts were prepared from the indicated cells, digested with trypsin and labelled with 6-plex TMT reagents. The TMT-labelled peptides were then mixed and subjected to fractionation by high pH reverse phase into 24 fractions. From each fraction, 95% was taken for phospho-enrichment and 5% retained for analysis of unmodified peptides. For phospho-enrichment, the 24 fractions were combined into a total of 16 fractions. Samples (unmodified and phospho-enriched) were then analysed by LC-MS/MS on an Orbitrap Fusion instrument using synchronous precursor selection (SPS). This analysis resulted in detection of 11,234 phosphorylation sites, of which 5,670 were quantitated. The number of class I sites are indicated in brackets (site localisation probability > 0.75).
RT-qPCR and western blot analyses of S100A9 expression in MoLC from the two donors treated as above. RT-qPCR data were represented as means ± SD.
(D) Graph relative to Notch1 expression in MuSCs isolated from 1.5 month old mdx mice treated either with vehicle (CTR) or TSA (TSA), and in EVs derived from FAPs (EVs-FAPs) isolated from 1.5 month old mdx mice treated either with vehicle (CTR) or TSA (TSA) n=3. Star (*) indicates statistical analysis by Tukey test relative to mdx vehicle treated mdx mice (CTR); *p<0,05;. hash (#) means significance compared to EVs-FAPs CTR; *p < 0.05. § indicates significance by Anova test; §§ p>0,01.
(C) τdecay of the STC evoked by single pulse stimulation in layer 1 astrocytes in acute cortical slices from P22-23 WT mice before (Ctr WT) and after application of 1.5 µM DL-TBOA (TBOA 1.5) (n = 4; N=4). The STC τdecay in TBOA 1.5 is 22 ± 3 % higher than in Ctr WT (paired t-test: P = 0.004).
Relative mRNA expression in the spleen of B mice 6 h after i.p. injection of PBS (black, n = 10) or DEX (grey, n = 10). Significant up-regulation of Tsc22d3, Sgk, Tat and Mrc1. DEX had no effect on TNFR1 mRNA levels. Significant up-regulation of miR-511 by DEX.
(I) Average plot (top) and heatmap (bottom) of H3K27ac reads in the cis-regulatory regions of genes having the GO term "fatty acid biosynthetic process" in HSCs in the steady state or early phase.
F. Confocal single plane image of third instar larval wing disc and orthogonal views of the disc stained with anti-Zfh1 (red) and anti-Fas3 (green).
(A-D) 25HC inhibits entry of SARS-CoV-2 pseudovirus (A and B), SARS-CoV pseudovirus (C), and MERS-CoV pseudovirus (D). Calu-3 cells were treated with EtOH or indicated concentrations of 25HC for 16h. Cells were then challenged with FLuc-expressing pseudovirus (A, C and D) and EGFP-expressing pseudovirus (B, C and D) at MOI=0.2, with EtOH or 25HC. After 2 h of infection, virus was removed and pseudovirus infection was quantified by luciferase assay at 24 h post infection (A, C and D) or visualized by fluorescence microscopy (B, C and D). IC50 was calculated by Graphpad using non-linear regression analysis.
E, F Salt-resistance assay of two PIM accessions (TS-21 and TS-422) and two BIG (TS-577 and TS-670). 20-day-old seedlings grown in soil were treated with 200 mM NaCl for 3 weeks (E). The survival rates were obtained from at least 12 plants in three repeated experiments (F).
In C endogenous CALCOCO1 is analysed and the bars represent the mean±sd of band intensities relative to the actin loading control, as quantified using ImageJ of three independent experiments. Statistical comparison was analyzed by one-way ANOVA followed by Tukey multiple comparison test and significance displayed as ***p ˂ 0.001, **p ˂ 0.005, *p ˂ 0.01; ns is not significant.
C The expression of endogenous CXCR4 in lentivirally-transduced MCF-7 ENTREP-KO cells. CXCL12 (+) and (-) indicate the presence and absence of CXCL12 treatment. In CXCL12-treated ENTREP-EGFP expressing cells, a non-negligible amount of CXCR4 was observed in the cytoplasm, in which CXCR4 was overlapped with ENTREP-EGFP. CXCR4 expression on the cell surface still remained (arrows). Scale bar 10 mm. The images are representative of at least three independet experiments.
Alignment of the sequences in the first intron of mDia2 (Diap3) genes of different species that harbor a SMAD2/3 binding element (SBE) (consensus sequence highlighted in red and italics) (top). Chromatin-immunoprecipitation of lysates from activin A- or TGF-β1-treated fibroblasts using a SMAD2/3 antibody and amplification of the bound DNA with mDia2 primers (bottom). Pre-immune serum (IgG) was used as negative control, and the input chromatin is shown. N=3.
(A) Images of matrigel collagen gels previously remodelled by PSCs, second harmonic generation signal for fibrillar collagen (green) and F-actin (red), scale bar 100 μm. (B) Fiber thickness colour-code map in a represented through the BoneJ plugin where larger spheres fit along fibers represent greater thickness, scale bar 100 μm. (C) SHG fibrillar collagen images used for calculation of alignment through the FFT algorithm. Insets show FFTs of fibrillar collagen-I images, representing alignment with respect to the elliptical distribution of the FFT central maxima. Circular behaviour (values approaching 1) represent no aligned orientation and lower values represent fiber orientation as alignment is displayed as a power distribution orthogonal to the orientation direction. Scale bar 20 μm (D-F) Quantification of fiber thickness, length, and alignment for images in A-C. (G) Quantification of collagen fiber thickness using the BoneJ algorithm for images in B,H. n≥6 matrices per condition. In the scattered plots each point represents a section. In the box-and-whisker plot, the central box represents values from the lower to upper quartile. The middle line represents the mean. The vertical line extends from the minimum to the maximum value. Histogram bars represent mean±s.e.m. ***P<0.001 (t-test for D, E, F and ; Anova and Tukey"s post hoc test for G). Three experimental replicates for all p
Quantification at 3 dpe, counting the proportion of brains with reduced density of Pax6 in the VZ, ectopic progenitors or neurons, and changes in apico-basal polarity (including ectopic apical surface formation and reduction in apically localised apical markers; n=6 brains per condition; Exact binomial test: ****P < 0.0001). Scalebars in A, B, D, E, H, I=100 µm; in C, F, G Scalebar = 50 µm. V marks the position of the ventricle.
A Density plot showing the measured fluorescence intensity distribution of individual cells for each timepoint after HPG addition. Time is represented on the y-axis with the bottom of the distribution plot aligning to the corresponding timepoint.
G. Balance beam test of NEX-Cre, FBXO7fl/fl or NEX-Cre;fl/fl mice. Coordination score and time to cross were measured. n=11, 14, and 15, respectively (ANOVA (time), Kruskal-Wallis test, Dunn's multiple comparison (coordination score), * p<0.05, ** p<0.01, *** p<0.001, mean +s.e.m.).
(A) Representative electron micrographs of Brucella-infected control (left-hand panel) and Yip1A-knockdown (right-hand panel) cells at 24 hr p.i. Insets are magnifications of the boxed areas on the main image, showing the typical forms of BCVs. In control cells, BCVs can be seen in the form of ER-derived membrane-bound compartments (inset in left-hand panel, defined as 'I'). Note the presence of ribosomes on the membrane (arrowheads). In Yip1A-knockdown cells, the bacteria were not sequestered into such compartments (inset in right-hand panel, defined as 'II'). Scale bars are 2 μm.
H Absence of correlation between mitotic index and epithelial H2AX Hscore, in LumA HER2 and TN BC.
Mettl5 partners identified as significantly-enriched candidates in mass spectrometric analysis of Mettl5-FLAG-Myc affinity purifications (ribosomal proteins not listed for simplicity). Measurements of 2 biological replicates.
Top left: Scheme for the chimera contribution assay. Bottom left: Representative brightfield/mCherry images from chimeras at E7.5. Scale bar: 100um. Right: Percentage of mCherry-positive cells in chimeric embryos measured by FACS. Blue circles and red circles represent the percentage of mCherry-positive cells derived from control and T-induced PSCs (GOF-positive E3 EpiSCs [E3G], reverted E3 EpiSCs [rE3], and 2iLIF ESCs), respectively.
C) Average DNase I and H3K27ac profiles of the 1049 dDHSs in TN and TB (+/-PMA/I) which are 4 fold diminished after stimulation.
B Venn diagrams showing overlap between genes up-regulated (1.5 fold) in abo1Δ mutants with genes up-regulated under the indicated condition, along with the significance of the overlaps (based on hypergeometric distribution).
(C) The upper panel of bar charts show the percentage of CD11ahi IFN-γ+ CD8+ T cells and the lower panel the absolute cell counts. Bar charts show mean values (±SEM) from representative experiments (***, p<0.001; one-way ANOVA with Tukey's multiple comparison test). See Appendix Table S4 for exact p-values.
C57BL/6 mice were treated with G-CSF, CoPP or solvent controls (NaCl, DMSO) for 5 consecutive days. Samples were collected 6 hours after the last injection. Relative abundance of different granulocyte phenotypes in BM (C) of mice treated with G-CSF and CoPP. Mice treated with CoPP have higher proportion of granulocytes with mature phenotype, than mice treated with G-CSF.
A Representative images of NHF, Lowe 1676 and Lowe 3265 cells immunostained with anti-α-tubulin (red) and anti-γ-tubulin (green) antibodies. Scale bar, 10 μm. B Quantitative analyses of focused microtubule arrays numbers at γ-tubulin (microtubule organizing center MTOC) measured in the experiments shown in A. n = 3 cells per group, three independent experiments. C Data information: data are presented as mean ± SEM. * ≤ 0.05, ** ≤ 0.01, calculated by two-way ANOVA, multiple comparisons.
Thymocytes isolated from Ifih1-/- and Cd4cre A1fl/fl Ifih1-/- mice were stained with anti-CD4, anti-CD8, anti-CD25 and anti-Foxp3 antibodies and were gated on 4SP thymocytes. Representative images are shown (upper panel). The percentages of CD25+Foxp3+ 4SP thymocytes (thymic Treg cells) were compared among Ifih1-/-, Cd4cre A1fl/fl Ifih1-/- and Cd4cre A1fl/fl mice (lower panel). The same data shown in Fig 2H was used for Cd4cre A1fl/fl mice.
(E) Western Blot analysis to check expression of HA-HuR in liver samples of injected mice. β-Actin was used as loading control. HA-HuR expressing Huh7 cells lysate was used as positive control.
(D) Western blot analysis of total and active form of Rsk3 and Msk1 in the cerebella and brainstem of 12 weeks old WT and SCA1 mice (n = 4). Relative Rsk3 and Msk1 levels were represented into log2 scale. The protein levels of the two kinases are significantly different between the two brain regions. Mean ± SD, *P<0.05, **P<0.01, ****P <0.0001, two-way ANOVA. Data information: BS: brainstem, CBM: cerebellum
e) Western blots showing absence of LC3-II accumulation in U2OS cells transfected with siRNA against MSH-2. The same blot probed with anti-MSH-2 antibodies confirm efficient knockdown. (f) Quantification of LC3-II levels in cells transfected with control or MSH-2 siRNA with or without FU treatment for 24 h.
(C) Wt macrophages (Atg16L1flox/flox; Cre-) and autophagy-deficient macrophages (Atg16L1flox/flox Lyz-cre; Cre+) were activated with IFN-γ or not, followed by infection with the live/dead Mtb reporter strain. % viable was quantified after addition of AnTc. **P<0.005, ***P<0.0001, Fisher's exact test (in which the proportions of viable to non-viable Mtb was compared).
A Comparison of the cryo-EM structure of H2A.B-NCP with the structure of canonical nucleosome (PDB: 3LZ0) in disc view. Histone octamers containing H2A.B and canonical H2A were superimposed for comparison. The ~103 bp DNA of H2A.B-NCP in green color is shown in surface mode. The 145 bp DNA of canonical nucleosome is colored in grey. Histones H2A.B, H2B, H3 and DNA at SHL 5 through SHL 7 are highlighted to show the structural differences between two nucleosomes. Histones H2A.B, H2B and H3 in H2A.B-NCP are colored in orange, warmpink, and cyan. Their counterparts in canonical nucleosome are colored in yellow, red, and blue. Histone H4 is colored in grey. B Close-up view of the structures of H2A.B C-terminal regions (top) and H2A C-terminal regions (bottom). Black and white arrows indicate the last residue at the C-terminus of H2A.B (V109) and H2A (K118) that are observable in the structures.
Representative photographs of coronal brain sections and graph quantification of infarct volume (dashed white line) measurements in bone marrow (BM) chimeric mice 24 hours after tMCAO. WT>WT: transplantation of WT BM into WT hosts; C2βD1212A>WT: transplantation of C2βD1212A/D1212A BM into WT hosts; C2βD1212A>C2βD1212A: transplantation of C2βD1212A/D1212A BM into C2βD1212A/D1212A hosts; WT> C2βD1212A transplantation of WT BM into kinase-dead hosts. Data represent mean ± SEM; n=13-16 mice per group; *p<0.05 **p<0.01; ***p<0.001 vs WT>WT, Mann-Whitney test or unpaired t-test, as accordance.
m6A-related proteins identified by HSATIIII-ChIRP-MS (cf. Table EV3 in Ninomiya et al., 2020).
YUMM1.7 Ctrl or STING KO cells were injected into mice. 5-FU and DTIC responses were followed according to the schematics in (A). (F) Mean tumor volumes of Ctrl or STING KO YUMM1.7 with DMSO, DTIC or 5-FU treatment were followed during the experiment. N=3 to N=5, as shown in (E).
F PhosphoUb competition assays for UBE2N/UBE2V1‐mediated Lys63 diUb formation. Time course with K63R Ub (donor) and Ub ΔGG (acceptor) generates Lys63 diUb and is not inhibited upon increasing concentrations of phosphoUb, revealing phosphoUb does not compete with Ub for UBE2N/UBE2V1‐mediated Lys63 diUb formation.
C. Multiple-sequence alignment of the pre-stem hairpin (the putative transmembrane region) from different aerolysin members. The members include Dln1, the earthworm Eisenia foetida lysenin, the mushroom Laetiporus sulphureus lectin (LSL) and Aeromonas hydrophila aerolysin. The alignment is generated according to the alternating pattern of hydrophilic and hydrophobic residues by GeneDoc. The hydrophilic and hydrophobic residues are marked in hot pink and gray, respectively.
Compared Hallmarks for upregulated and downregulated genes in the transcriptome of E16.5 Lgr5 KOs vs E16.5 HEs, adult HEs vs E18.5 HE embryos and adult Lgr5-Cre cKO vs HEs. * Asterisks refer to given pathways for which differentially modulated genes were found upregulated and downregulated. Right panels: GSEA showing enrichment of the epithelial to mesenchymal transition (EMT) data set in E16.5 Lgr5 KOs vs E16.5 HEs, adult HEs vs E18.5 HE embryos, and adult Lgr5 cKO vs adult HE modulated genes. NES: Normalized Enrichment Score. Biological replicates for RNAseq experiments on ISC Lgr5-DTReGFP E16.5 independent embryonic pools, each obtained from independent litters (n= 2 HE, 2 KO); Lgr5-DTReGFP E18.5 individual embryos (n=2 HE) and Lgr5-DTReGFP adult individual animals (n=2 HE); Lgr5-Cre/flox adult individual animals (n= 2 HE, 3 cKO).
(E) THP-1 control and knockout cells for NLRP3 were mock treated or infected with the VN Wt and ΔF2 strains for 24 h at MOI 10 and IL-1β levels were assessed by ELISA from the supernatants. The mean ± standard deviation of five independent experiments is shown. Statistical analysis was performed by one-way ANOVA, p-values are indicated.
G. Co-immunoprecipitation between Sae2-GFP and Sir3 from untagged, Sae2-GFP WT cells, and Sae2-GFP cells overexpressing WT Sir3 (oeSir3, WT), Sae2-GFP sir3Δ or Sae2-GFP overexpressing the sir3-T557I mutant (oeSir3, T557I) using antibodies against Sae2-GFP, analysed by Western blot with anti-GFP and anti-Sir3 antibodies.
(A) Serum NfL levels in preataxic SCA3 subjects (cross-sectional data) were plotted over the time from the individually estimated ataxia onset. NfL levels increased significantly with proximity to the estimated onset (F(1,21)=39.68, p<.001, R2=0.64). For benchmarking the levels of preataxic subjects, the blue dashed line visualises the optimal cut-off for differentiating ataxic SCA3 subjects from controls in the pooled cohort (20.3 pg/ml, 99.0% sensitivity, 95.2% specificity).
VDAC1-specific siRNA abrogates Parkin translocation to mitochondria after 2 h, and mitochondrial clearance after 24 h, of CCCP treatment. Both effects can be rescued by re-transfection with wild-type VDAC1. (a) Immunofluorescence and (b) western blot of siRNA-transfected HeLa cells used in c-g demonstrate partial silencing of endogenous VDAC1. (a) Silenced cells were stained with anti-HtrA2/Omi, a mitochondrial marker (pseudo coloured; blue), and anti-VDAC1 (red) antibodies. (b) Lysates from silenced cells were subjected to western blot analysis and probed with an anti-VDAC1 antibody, while TOM20 and β-actin probing served as loading controls.
C Co-IP and western blot results showing the interaction of βTrCP1 with BTG4 in the presence or absence of PABPN1L.
B Inhibition of Tsc2-deficient 105K tumor growth with different monotherapies, as indicated in the inset. Asterisks indicate significant reductions relative to vehicle (two-way ANOVA; clorgyline P = 0.015, loratadine P = 0.018, and rasagiline P = 0.049). Each data point represents the mean and SEM.
A A section of a UMOD filament is shown that consists of 5 consecutive subunits (UMOD 1-5) related by the helical symmetry operation indicated in the top panel. In the middle panel, where the helical axis is represented by a large black arrow, subunits are depicted in cartoon (UMOD 1, 3 and 5) and surface (UMOD 2, 3 and 4) representation to highlight protein-protein interfaces (with UMOD 1 ZP-N and UMOD 5 ZP-C omitted for clarity). In the filament, the ZP-N/ZP-C linker of each molecule (for example, UMOD 3) wraps around the ZP-C domain of the subunit that precedes it (UMOD 2) and the ZP-N domain of the subunit that follows it (UMOD 4); additionally, the ZP-N and ZP-C domains of the same molecule are engaged in interactions with the ZP-C domain of the subunit that in turn precedes UMOD 2 (UMOD 1) and the ZP-N domain of the subunit that follows UMOD 4 (UMOD 5), respectively. As summarized in the bottom panel, every UMOD subunit is thus interacting with another four by being engaged in six interfaces that belong to three different types (ZP-N/ZP-C, black arrow; ZP-N/β1, dark red arrow; E'FG,α1β/ZP-C, light red arrow). Subunits 3, 2 and 4 in this figure correspond to Fig 3 chains A, B and C, respectively. B Path of the interdomain linkers of UMOD1-5, whose domains are outlined in the background. The view is rotated by ~40° around the Y axis, compared to panel A.
B. A mutant of Rab18 unable to bind nucleotide, N122I, was co-immunoprecipitated with Myc-TRAPPC9 by anti-Myc antibody.
E Kaplan-Meier survival curves of mice treated with vehicle, Imatinib, BRAFi or BRAFi plus Imatinib. Median time to progression was 18, 20, 36 and 48 days, respectively. Log rank (Mantel-Cox) for BRAFi vs BRAFi/Imatinib mesylate. ****P<0.0001 and hazard ratio (log rank): 0.2403 (95% CI of ratio, 0.08123 to 0.7106).
E. Measured angles of c-ring rotation between states 1-3 of yeast V-ATPase. The measured rotation angles deviate slightly from the predicted angles due to a small "over rotation" of state 2, which brings the three c-ring angles even closer to the 120º steps of the DF central rotor.