EMBO/sd-character-level-ner huggingface dataset:
d) Schematic representation of the model suggested by our findings. Committed progenitors have similar and low proliferation rates around and away from HF during telogen. However during anagen, proliferation of CPs is increased in a zone of influence around hair follicles. In all cases, CPs divide according to a random fate as proposed by Clayton et al (Clayton et al, 2007). Upon proliferation of CPs around hair follicles, some CPs exit the zone of influence and remain slow-cycling in subsequent anagen phases.
Negative stain 2D class averages of endospore-associated S-Enas show variation in pitch and axial curvature, likely as a result of strain exerted during deposition of spores on the grid surface. The observed range in pitch corresponds to a range in longitudinal spacing of 2.5 to 12 Å between helical turns (labeled red in panel B).
(A and B) Chronological aging in SC 2% glucose medium supplemented with 1 ng/ml doxycycline of wild-type and Δach1 cells combined with or without knockdown of ACS2 (tet-ACS2). Survival (A) was determined by colony-forming capacity (clonogenicity). Age-associated cell death (B) was assessed through propidium iodide (PI) staining analyzed by flow cytometry. Data represent day 1 normalized means ± SEM (n = 4).(C and D) Survival (C) and cell death (D) of chronological aging experiment similar to (A) and (B) but in the background of ATG7-deleted autophagy-incompetent cells (Δatg7). Data represent day 1 normalized means ± SEM (n = 4).
(A) Schematic representation of MS2/PP7 stem-loop repeats at the 5'UTR of GCG1/SUT098 sequence, respectively. Upon transcription, respective coat proteins (dark blue and dark purple) with fluorescent proteins (red and green) bind to the MS2/PP7 repeats at the 5' UTR of GCG1 and SUT098 transcript. The ON and OFF state of transcription versus the time determines the duration and frequency (time between transcription events) of transcription.
Western blot detection of the presence of cGAS and STING in the immunoprecipitates of streptavidin beads. THP-1 cells were stimulated with biotin-ecGAMP (5 μg/ml) or biotin-icGAMP (1 μg/ml) for indicated time and cell lysates were harvested for IP with streptavidin beads. Data (A-B, D-G) are representative of 3 independent experiments.
Histogram of selected differentially expressed genes of LL-37+/+ mouse lung versus wild type FVB mouse lung prior to infection. Blue bars indicated genes up-regulated in wild type FVB mouse lungs, red bars indicated genes up-regulated in LL-37+/+ mouse lungs.
A) Bar graph of number of IBA-1+cells in the retina of IgG control, anti-VEGF-A, anti-ANG-2 (all 5 mg/kg IP), and bispecific anti-VEGF-A/ANG-2 (at 10, 5, and 3 mg/kg)-treated mice in the late interference model at D60.B) IgG control, C) anti-VEGF-A, D) anti-ANG-2, E-G) anti-VEGF-A/ANG-2 low, mid and high: representative micrographs of whole-mount eyecup preparations stained with isolectin-B4-positive (green) to stain vessels and anti-IBA1 (red) to stain for macrophages show a decrease both in absolute numbers and clustering of subretinal IBA-1-expressing cells associated with neovascular complexes in anti-VEGF-A/ANG-2 treatment groups. Error bars show SEM with n = 6 animals per group (Scale bar, 200µm). All significant differences are shown by * after one sided ANOVA (***, P < 0.0008) and Tukey's multiple t-test. IgG control is significant against anti-VEGF-A/ANG-2 low (*, P < 0.0134), -mid (**, P < 0.0078) and -high (**, P < 0.0042); furthermore anti-ANG-2 against anti-VEGF-A/ANG-2 mid (*, P < 0.0353).
H-I. Confocal single plane images of third instar larval wing discs stained with anti-Ct (cyan) showing the lineage of GAL4 (green) and the active GAL4 (red) in (H) E(spl) m3-HLH[GMR10E12]>gTRACE and (I) E(spl) m6-BFM-GAL4>gTRACE.
(e) Co-staining for Atg14 and Cx43 in NRK cells maintained in the presence/absence of serum. Merged channels are shown and single channels and broad-field images are shown in Supplementary Fig. 5d. Insets: higher magnification.
(Top) Schematic representation of the chromosomal location of the CALIC gene locus. Arrows indicate the orientation of transcription. (Bottom) ENCODE ChIP-seq data for H3K4Me3 is displayed in the UCSC browser illustrations. Gray boxes mark locations of exons (Ex1-2) of CALIC.
Representative pictures of H&E staining of small intestine of Casp8WT and Casp8BECko mice (E), enteropathy score (F; n= 5 WT, 6 ECko, two tailed unpaired Student's t-test) Scale bars: 100µm, insets: 50µm. Data information: Data shown as mean ± SEM. ns: not significant.
C Quantification of the time-lapse imaging of the proliferation of NucLight-labeled 1205Lu cells using the IncuCyte ZOOM system. Cells were plated for 48 h on FRC- or MAF-derived ECMs prior a 96 h treatment with vehicle or 5 µM BRAFi in the presence or not of 7 µM Imatinib or 1 µM DDR1-IN-1. The bar plots represent the mean normalized to vehicle of NucLight red nuclear objects per field ± SEM from 3 independent experiments performed in triplicate. ****P<0.0001, two-way ANOVA followed by Sidak's multiple comparison test.
The homology modelling of the STK38L shows a shift from the positively charged arginine to a non-polar and bulky tryptophan pointing inside towards the ATP-binding site, thereby possibly inhibiting the ATP-binding and kinase activity of STK38L
(C) In vitro kinase assays to test the ability of recombinant CHK2 to phosphorylate recombinant GST-Beclin 1-WT, S9093A (AA), S90A and S93A protein. Reactions were analyzed by SDS-PAGE followed by autoradiography. The asterisks in the blot indicate the phosphorylation of Beclin 1 mutants.
(h) The measured lactate secretion flux in synchronized cells shown in red (mean and s.d. of n=5; in Equation 9;); the deconvoluted secretion flux dynamics, in case of no synchronization loss (green; in Equation 10); and the expected secretion flux based on the deconvoluted fluxes and considering the loss in synchronization, matching the measured fluxes (black; Equation 10).
e, Co-immunoprecipitation of beclin 1 with BCL2 in muscle tissue from mice at indicated time points after exercise. IP, immunoprecipitate; WB, western blot; WCL, whole cell lysates.
lymphoma burden as determined by lymph node weight (B), of cohorts of 9-12 mice each (n indicated in figure) of the indicated genotypes.
(B) Representative flow cytometry blots of blood samples from mice of both groups 3 weeks after treatment start showing successful depletion of CD45+CD3+ T cells in the αCD4+αCD8 treatment group.
A) anti-TFEB immunofluorescence on rapamycin- and rilmenidine-treated WT and Cox15sm/sm muscles vs. untreated (UT) samples. CD11C (blue signal) indicates inflammatory cells. Right panel: quantification of n=3 animals/group. The scale bars correspond to 30µm. Error bars represent SEM. The asterisks represent the significance levels calculated by one-way ANOVA with Tukey post-hoc multiple comparison test B) Quantification of the TFEB-positive nuclei (n=3/group). Quantification was performed using Imaris spots surface excluding the CD11C positive nuclei. Error bars represent SEM. The asterisks represent the significance levels calculated by one-way ANOVA with Tukey post-hoc multiple comparison test *p=0.0199 (WT vs. WT+rapamycin), *p=0.0150 (Cox15sm/sm vs. Cox15sm/sm+rapamycin), ***p=0.0001
A) Visualisation of the pathology load at 9M of age of TAUwt, TAUtg and APPtg mice at 9M of age. Immunofluorescent staining for X34 (a fluorescent derivative of Congo Red), Iba1 (microglia) and TO-PRO-3 (nuclei) has been pseudocolored. Scale bar = 100μm.
(A) Experimental design to evaluate the virucide effect of FD20, in the presence or not, of other antibodies. Different concentrations and 20-time dilution were used to achieve 70% inhibition when the antibody is provided alone. The comparisons of neutralization groups (3 to 5) relative to corresponding conditions without antibodies allow evaluating the irreversible effect of FD20 on particles. Group 4 is normalized using Group 1; Group 3 and 5 are normalized using Group 2.
Effect of PP2A knockdown on IL-10 level in Ld-infected cells expressing phosphorylation defective mutant of Ago2. In RAW 264.7 cells, depleted for endogeneous Ago2 (using a specific siRNA against the 3'UTR of Ago2 mRNA), either the wild type or Y529F mutant of FH-Ago2 (without having the 3'UTR of Ago2) was expressed in siCon or siPP2A treated RAW 264.7 cells. IL-10 mRNA level was measured subsequent to Ld infection. Relative IL-10 levels were plotted. Expression levels in non-infected siCon treated cells in each case were designated as unit (mean+/- s.e.m., n=3).
(A) ARPE-19 cells were nucleofected with the indicated Rag-expressing plasmids. 6 h after nucleofection, cells were infected with adenovirus expressing TFEB-FLAG-WT. 12 h later, cells were lysed and subjected to immunoprecipitation with the anti-FLAG antibody. The immunoprecipitates were analyzed by immunoblotting with antibodies against Rag proteins and FLAG (used to detect TFEB-WT).
A. Cellular proliferation analysis of Mettl3 or Mettl14 depleted and control CT26 cells treated with indicated combinations of cytokines for 48h. The mean ± SD of three replicates is shown. * P < 0.05; * * P < 0.01 by Student's t-tests.
BJcl2 cells with or without hTRF2 overexpression were inoculated into the backs of immunodeficient Nude mice and treated with anti-GR1 antibody or isotypic control (200µg/IP) and NK cells recruitment, degranulation and MDSC infiltration were monitored by FACS Density plot of CD11bHi GR1Hi MDSC staining in control or anti-GR1-treated Matrigel plugs (K).
(E) STING-IRF3 interaction in human cells required EGFR: WT and EGFR-/- (KO) HeLa cells were transfected with cGAMP, 2h later cells were lysed, immunoprecipitated with anti-STING antibody and analyzed by Western blot.
Western blot showing levels of GAPDH association with mitochondria in Atg5 KO MEF cells. n = 2. *P = 0.04.
Hypertension did not induce mesangial expansion and activation in wt mice, but led to a significant increase in hypertensive Foxd1Cre::Pdgfrb+/J mice as visualized by α-SMA staining. (H) Histomorphometric analysis of α-SMA positive percentage of the glomerular tuft area.
C. Gene ontology reveals that the MEblue cluster is linked to cognition and synapse organization.
Representative sentinel, axillary and brachial lymph nodes (SLN, ALN and BLN, respectively) of mCherry-SK-Mel-147-driven xenografts in Vegfr3Luc nu/nu mice treated with vehicle (V) or 4 doses of BO-110 (BO, 0.8 mg/kg) and imaged for mCherry fluorescence to assess metastatic potential as a function of treatment. Numbers in parenthesis correspond to mice with positive metastases in at least one LN (lymph node) with respect to the total animals analyzed per condition. Scale, p/s/cm2/sr (x108). See also Fig. EV1D,E for images and quantification of lymphatic vessels in lymph nodes.
(A) Overlay of 15N-1H HSQC spectra of 15N-labeled Ca2+/CaM by itself (red peaks) and after addition of saturating, unlabeled PSD-95 (1-21) (blue peaks) or saturating, unlabeled PSD-95_pT19 (green peaks). All NMR experiments were recorded at 600 MHz 1H frequency.
G Epifluorescence stereo microscopy of mammary glands from 10‐day‐old littermates either MMTV::Cre; mT/mG Wnt4fl/+ or MMTV::Cre; mT/mG; Wnt4fl/fl. Scale bar: 1 mm. Arrowhead marks the main duct originating from the nipple.H Bar plot showing ratio of branching points in prepubertal Cre+;Wnt4fl/fl (n = 12) relative to Cre+;Wnt4fl/+ littermates (n = 10). Two‐tailed, paired Student's t‐test was used to calculate statistical significance.
Evaluation of liver toxicity following glufosinate treatment. Quantification of liver glufosinate (C) in serum of vehicle and glufosinate (10 and 20 mg/kg) treated mice (n=8).
analysis of the most prominent bacterial phyla (B; n= 4 Control, 6-8 Antibiotics; multiple t-tests with Holm-Sidak method) by qPCR analysis, In B, the cycle number of 16S rDNA expression compared to the total number of cycles is shown. Data information: Data shown as mean ± SEM. ** P <0.01, *** P <0.001, **** P <0.0001; ns: not significant. Scale bars: 100μm.
(A) Stacked column depicts proportions of cell types in the TME of 99LN-BrM analyzed by flow cytometry (n=4).
(G) Exceptional growth genes that are associated with between-line size variation (association type 2).
Relative γ-H2AX intensity in cells transfected with either Empty Vector (EV) or HA-E2F1 treated with Chk1i for 20 hours. γ-H2AX fluorescence in HA positive cells was normalized to the empty vector transfected cells and compared to cells not expressing HA.
A Schematic illustration of mutant PLTP (PLTPM159E). The point mutation of PLTP coding sequence by substitution of methionine with glutamate at 159 amino acid position.
HEp-2 cells treated with 20 µg/ml of whole cell extract of Y. pseudotuberculosis expressing indicated CNFY variants for 4 h were lysed and the deamidation of RhoA was analyzed by the mobility shift of the modified RhoA GTPase detected by immunoblotting.
C.) Live epifluorescence microscopy of PfMev parasites that are expressing api-SFG (green) and the P. falciparum DPCK-mCherry protein (red) with DAPI marking the nuclei (blue). The borders of the red blood cell and parasite are marked with dotted blue and white lines, respectively. Microscopy images represent fields that are 10µm long by 10µm wide.
F) Schematic representation of GB-DRP1 mutant variants analyzed for the interaction with RA-BAX. The variants are displayed in the domain distribution of DRP1 (amino acid positions correspond to DRP1 isoform 3).
ChIP analysis of enrichment of HDAC4 (C) on promoters of Acta1 and Nppa in ventricular samples. n=4:4 for (C)
(A) Control HeLa cells and HeLa cells stably expressing GFP‐LC3B or GFP‐GATE‐16 were transfected with HsAtg4AC77A‐Myc‐His6. After 48 h interval, the cells were incubated for 2 h in EBSS, and subjected to immunostaining with anti‐Atg16 and anti‐myc followed by confocal microscopy analysis. Quantification of cells containing Atg16 structures larger than 2 μm from three independent experiments is presented at the right panel. Scale bar: 20 μm.
Cell cycle distribution in representative miRNAs evoking G1 phase accumulation in miRNA mimic transfected Dgcr8-/- ESCs. Error bars indicate s. d. (n=3). Full data are shown in Supplementary Fig S3A, B.
(C) IHC analysis of UHMK1 expression in a GC patient tissue array (n=102). Representative images are shown. Scale bars=100μm.
(A) Immunoblots for ClC-3, ClC-4, VGLUT1, VGLUT2, VGAT, GluR4 and GABAA-R-α1 of whole lysates from brain of Clcn3+/+ and Clcn3-/- mice at 2, 6 and 12 weeks of age.
A) Average read-count normalized MNase signal (RPM) from 2-4 h and 14-17 h embryos are shown at the different effector gene promoter groups. The grey area highlights the changes in nucleosome occupancy, which are prominent at highly paused genes (arrow).
(A) The bur1-∆C mutant, but not bur1-∆C vac17∆ double mutant, shows normal vacuole inheritance. Quantitative analysis of vacuole inheritance in wild-type, vac17∆, bur1-∆C, and bur1-∆C vac17∆ cells. Cells were pulse-chase labeled with FM4-64, and vacuole inheritance was assessed as the percent cells with inherited vacuoles. Error bars; SD calculated from three independent experiments with at least 100 cells counted in each strain/experiment.
C 5hmC MedIP and qPCR for human CD45 exon 5 in siTet1/2 and siNT WT-C and WT-hmC clones, relative to a minigene region lacking CpGs.
(f) Endogenous LC3-II levels in PC12 cells treated with or without 200 μM NF449 for 24 h.
(D) Flow cytometric analysis of T cell subpopulations in 99LN-BrM (n=4 for isotype, n=3 for all other groups).
(F) Representative immunoblots of an endogenous CIP2A protein complex immunoprecipitated from lysates of MCF7 cells left untreated or treated for 4 h with 100 nM rapamycin (Rapa) and 2 nM ConA as indicated. Mouse IgG served as a negative control.
B) Density maps for all DNase-Seq and ChIP-Seq peaks shown in order of increasing DNase-Seq tag count signal for CD4 TB compared to TN. The TN H3K27ac track is from published data (Lara-Astiaso et al, 2014).
(B) mRNA level of TFAM in 50 HCC patients' paired tissues from TCGA database. The relative expression ratio of tumor to non-tumor was log2-transformed.
(b) U2OS cells expressing an ATG7-TALEN (TAL2-ATG7) or control TALEN (TAL2-CTL) were subjected to glutamine starvation for 6 days followed by 6 days recovery in glutamine-replete medium. Cells were then stained with SRB and absorbance was read at 540 nM. Graph shows average results from five clonal sub-lines for each condition. The statistical significance (P value) was determined by a two-tailed, paired Student's t-test. P0.05. (c) Representative images of SRB-stained clones in b
(i) Quantification of normalized RPS3 protein level (black bars) or RPS3 mRNA level (white bars) in U2OS cells after 48 h 5-FU treatment. RPS3 mRNA levels were determined by quantitative real-time reverse transcriptase-PCR.
D Western blot of HA from total cell lysates or biotin pulldowns of cells containing Ice2-TurboID, Pah1-HA and deletions of NEM1 or SPO7 as indicated (SSY2978, 2979, 3117, 3118).
Motor behavioural assays (Rotarod rod test (H) N = 8 animals each group. Bars and error bars represent the mean ± SEM. Statistical significance was determined using a one-way ANOVA followed by post hoc Bonferroni test for multiple group comparison. *P<0.05;**P< 0.01.
(C) Percentage of Listeria‐infected cells displaying mTOR localization to LAMP2+ vesicles. Values are means±s.e.m. n=3. ***P0.001 and **P0.01 over uninfected.
Quantification of telomere sister chromatid exchange events. Cells were transfected with 20nM of siRNA for 48 hours prior to the addition of BrdU/BrdC. Metaphases were imaged by confocal microscopy and each data point represents a metaphase. For each condition, there were 3 biological repeats with a total of at least 1300 chromosome ends quantified. Values shown are mean±sem. Conditions were analyzed using two-way ANOVA followed by Sidak's test.
E Following transfection of control siRNA or siDHX9 into KGN cells, AGO3-mediated RISC-associated RNAs were immunoprecipitated using an anti-AGO3 antibody. IgG was used as a control. Co-immunoprecipitated mRNAs were reverse transcribed using a FOXL2-430-R primer binding downstream of the 402C>G site. The cDNA products were used for FOXL2 allele-specific PCR analysis with a FOXL2-279F primer (Appendix Fig S1A), and a representative result obtained by RT-PCR (top) is shown. Quantitative real-time RT-PCR results (middle) are also presented as fold enrichment of FOXL2 mRNAs normalized using the level of GAPDH mRNA. Western blots of immunoprecipitated AGO3 and the inputs are shown in the bottom panel. The data are presented as the mean ± SEM from three independent experiments. Different letters denote statistically significant differences (p < 0.05; Student-Newman-Keuls test).
Mean current densities of maximally activated ICl,vol at −80 mV. The number of cells is indicated for each column.
(B) Right. In vitro pull-down binding assay and subsequent SDS-PAGE. Amylose beads are used as a bait to demonstrate interaction of purified prApe1 dodecamers with MBP-Atg19 (lane 1) whereas purified mApe1 dodecamers are not capable of interacting with MBP-Atg19 (lane 3). As controls, MBP does not bind prApe1 and mApe1 (lanes 2 and 4). Left. SDS-PAGE showing input of the corresponding pull-down assay.
Schemes summarizing identified phenotypes in in vivo and in vitro model systems upon acute ECE2 KD (E) or chronic inhibition or KO (F) or upon acute ECE2 OX (G) and thus the molecular action of ECE2 (Abbreviations: d = day, pe = post electroporation, VZ = ventricular zone, SVZ = subventricular zone, IZ = intermediate zone, CP = cortical plate, aRG = apical radial glia, bRG = basal radial glia, IP = intermediate progenitor, ECM = extracellular matrix).
Fluorescence images of cells expressing Chs5-GFP and TGN marker Sec7DsRed (C) and binding kinetics of Chs5-GFP at the TGN (D) in WT, or CHS6BCH2 (C, D) strains. The brightness and contrast were adjusted differently in the merged images. Bar, 5 µm. The mean of 20-30 FRAP measurements from different cells is shown. Calculated parameters are shown in Table 2.
(C) Representative immunofluorescent (IF) images of cerebellar molecular layer between the cerebellum lobule V and VI across different genotypes at 36 weeks old, stained with anti-Calbindin 1 antibody. Scale bar = 100 μm.
D. Whole cell lysates from indicated yeast strains carrying a plasmid expressing 3xFlag-Sre2MS were analyzed by western blot with anti-Flag antibody. Two independent isolates, A and B, are shown for each strain. Asterisk denotes non-specific band.
B. Rapamycin suppresses TLR3-stimulated IFNβ mRNA production in cultured macrophages: RAW264.7 macrophages were treated as above but stimulated -/+poly (I:C) [30 μg/ml] for 3 hr. q-RT-PCR measured IFNβ gene expression. Results represent the mean +/- SD of triplicate samples from one experiment. *p=.03 relative to no Poly(I:C) by paired t-test (one-tailed); **p=.04 relative to +Poly (I:C) by paired t-test (one-tailed).
(C) Titration of selected human sera by ELISA using the S1 protein and by flow cytometry with Jurkat-S cells. Samples with antibodies detected by flow cytometry and not by ELISA are indicated (#8, #46, #48, #49). Data represent the mean±SD of duplicates. An unpaired two-tailed t-test was carried out to compare the results of 1:50, 1:150 and 1:450 dilutions of sera #8, #46, #48 and #49 by FC to the pre-COVID-1 sample as a negative control. *, p<0.05; **, p<0.005; ***, p<0.0005.
A. N2a cells were transfected with WT or mutant SOD1 in the presence or absence of IP3R3. Plotted viability of the cells measured by a neurotoxicity assay revealed that IP3R3 is involved in cell vulnerability against mutant SOD1. Data are expressed as mean ± SEM from three independent experiments, triplicated in each experiment. **: p < 0.01, *: p < 0.05.
(A) Schematic showing that DCS directly binds to the GluN1 subunit of NMDARs and activates NMDARs. Note that enhanced expression of SLC6A20 in PtenΔC/ΔC microglia and astrocytes surrounding the indicated synapse may decrease synaptic levels of glycine and suppress NMDAR function.
Effects of DC and Beva treatment in 786-O orthoxenograft. Evaluation of (C) tumor weight at sacrifice, (D) vessel number, Box plots indicate median, Q1/Q3 and max/min value whiskers in Control (black), DC101 (red) and Beva (blue) treatment groups. 5-8 tumors/group were analyzed by Mann-Whitney test, and Mantel-Cox test for survival where *p < 0.05, **p < 0.01 and ***p < 0.001 and DC * p < 0.05 and Beva # p < 0.05 vs Control).
D. Quantification of the average adipocyte size in SubWAT and EpiWAT of male mice of the specified genotypes in normal and high-fat diet.
H&I) Overexpression of the Dicer-binding deficient deletion mutant of TRBP (GFP-TRBP Δ) occludes BDNF-induced dendritogenesis. H) Hippocampal neurons were transfected with 200ng dsRed and either 50ng GFP or 200ng GFP-TRBP Δ, and treated two days later with BDNF or control vehicle. DsRed signal fluorescence was used to set a threshold on images obtained on a confocal microscope (scale bars; 10μm). I) Total number of intersections was quantified in Sholl analysis and values were normalized to control treatment in each experiment (n=5, p<0.02, t-test type 3, error bars; s.d.).
(C) BNGE, Western blot and immunodetection, with anti-NDUFS1 (cI), anti-ATP5A (cV) and anti-SDHB (cII) antibodies, of samples from the WT cybrids and from ∆4-CYB clones E (#17.3E) and B (#17.3B).
(a) Wild-type Gli+/+ or Gli1−/−, Gli2−/− and Gli3−/− MEFs were treated with 100 mM trehalose alone or in combination with 10 μM of Pmph for 24 h, or left untreated. Total cell lysates were subjected to immunoblot with anti-LC3 and anti-actin antibodies.
D MA-plot (log2 fold-change over the average expression level) of all detected introns in HSATIII KD and control cells (n=3). The introns with significant changes in their expression levels (adjusted p-value < 0.01) are shown as green dots. Among these introns, up-regulated (log2 fold-change > 1) and down-regulated (log2 fold-change < -1) introns are shown with magenta and light blue dots, respectively. Genes and introns that were experimentally validated in subsequent experiments are indicated as gene symbol-i (intron) #. Total numbers of introns and genes utilized were 144769 and 32623, respectively.