EMBO/sd-character-level-ner huggingface dataset:
(E) Western blot analysis of the protein level of HIF1A in differentiated beige adipocytes described in (D).
E Human motoneurons were differentiated from the human embryonic stem cell (ESC) HuESC 3 Hb9::GFP line. Differentiated neurons were transduced with lentivirus expressing GFP alone or together with PDIs-expressing plasmids. Transduced cells were cultured for another 10 days. To identify motoneurons after lentiviral transduction, immunocytochemistry analyses were performed. Quantification of neurite outgrowth in the different experimental conditions of GFP and HB9 positive neurons were obtained. Neurite number and assessment of the length of each neurite was performed in a similar manner as for primary rat motoneurons (see methods). Four independent experiments were performed.
(F) The total GDH1 protein in 786-0 and 769-P cells with or without aa starvation for 12 hours was measured by WB.
Schematic Representation of CRISPR/Cas9-based Genome-Wide Screen under Doxorubicin treatment.
(B-D) TLN localizes to autophagic vacuoles of catD−/−hippocampal neurons. Lysotracker staining revealed sparsely distributed small-sized organelles in wild-type and PS1−/− neurons in contrast to catD−/−neurons where high numbers of large Lysotracker-positive organelles were found (B, arrowheads). Although TLN accumulations in PS1−/− were fully negative for Lysotracker, some acidic organelles tended to closely associate (C, arrowheads, middle). In catD−/− neurons, TLN was clearly detected in the large acidic organelles (C, bottom). Bars, 20 μm. (D) At the immuno-EM level, the large acidic organelles seen in catD−/−neurons represent dense autophagic vacuole-like structures (star) that label positive for TLN (10-nm gold). M, mitochondrion. Bars, 200 nm.
(B) Western blotting of the anti-AXL immunoprecipitation in SKOV3-Empty "E" and OPCML "O" cells for AXL and PTPRG. Input: 1/100 of SKOV3-Empty or SKOV3-OPCML whole cell lysate. IP: Immunoprecipitated protein, IB: Immunoblotted protein
ChIP analysis of enrichment of HDAC5 (D) on promoters of Acta1 and Nppa in ventricular samples. n=3:3 for (D
D-H GlaB inhibits Gli1‐dependent BCC tumor growth in ASZ001 BCC allografts in vivo. (H) qRT-PCR of Hh and proliferation target mRNA expression levels. Results were normalized to endogenous control (β2‐microglobulin and HPRT). Shown is the mean ± SD of tumor (n = 6) for each treatment. *P 0.05 versus Ctr.
(g) CCCP-induced recruitment of Parkin and expression of Mfn1 and Drp1 in DOX-treated WT, p53−/− and p21−/− mice were determined by immunoblotting of the heartmitochondria-rich fraction. Representative immunoblots are shown from four independent experiments. Data are shown as the means±s.d. *P0.05; **P0.01 (two-tailed unpaired Student's t-test).
Figure 1: Endothelial Ang-2 upregulation correlates with WHO grading in human gliomas. ELISA displaying human Ang-2 (A) and Ang-1 (B) level in serum of healthy patients (Ang-2 n=4; Ang-1 n=21) or patients with low grade glioma (WHOII) (n=5), anaplastic astrocytoma (WHOIII) (n=7) or glioblastoma (WHOIV) (n=39) are shown.
B) Western Blot analysis of selected glycoproteins in mouse tissues from two wildtype C57BL/6J (Black6) mice. Endogenous Nicastrin (NCT) and SPPL2a were analysed in membrane preparations from testis, kidney, brain, spleen and liver in littermate male mice. Note that immature proteins (im) accumulate in testis compared to other tissues. SPPL2c protein is only detected in testis tissue.
(A) Streptozotocin-induced diabetic DEREG C57BL/6 mice were treated with mouse recombinant IL-33 daily for 5 consecutive days, as well as diphtheria toxin (DT), PC61 or DT+PC61 on days -4 and -1 prior to and on day 2 post islet transplantation. Mice were sacrificed at day 80 post-islet transplantation or at the day when grafts were considered rejected.
A, Parental HEK293T, HET and HOM1 cells were treated with Activin A or Activin B for the indicated times. Quantifications are shown on the right. Data information: quantifications are the average normalized intensities ± SEM of between 3 and 10 In A, quantifications are the levels of pSMAD1/5 normalized to Actin ns, not significant; *, p<0.05; **, p<0.01; ***, p<0.001; ****, p<0.0001. The p-values are from two-way ANOVA with Dunnett's post-hoc test. In all panels, Western blots of whole cell lysates were probed with the antibodies indicated.
F) In vitro lipid kinase activities of WT-, 6SA- or 6SE-reconstituted VPS34 complex I on GUVs (giant unilamellar vesicles) were assessed. Representative images show GUV membranes (Lissamine Rhodamine-PE, green) and PI3P (AlexaFluor647-PX, red). Bottom left: VPS34 complex activities over time measured by recruitment of AlexaFluor647-PX to GUVs are shown. Bottom right: kinase reaction rates for GUVs phosphorylated with WT, 6SA or 6SE complexes, taken from linear portion of reactions. Representative data from 1 of 4 independent repeats are shown, with mean +/-SD. In this experiment, 67 GUVs were analysed in total (15 from WT, 17 from 6SA and 35 from 6SE).
Rescue of the subcellular localization of UNC-18 in worms expressing G544D UNC-18. C. elegans expressing WT::GFP or G544D::GFP were immobilized, and the ventral nerve cord was imaged. Solid arrowheads point to pairs of bigger puncta, broken arrowheads to single, smaller puncta (N, O). Scale bar in (N) and (O) = 10 µm. 4-PBA = 4-phenylbutyrate.
(C) Cell proliferation. shCTR (n=3) and shCxcr4 MM cells (pools1+2, n=6)) were plated (4.4x104 at the start of the experiment, t-16h), treated or not with 800 nM BoxA for 24 hours and counted. Statistics: t-test.
(a) Representative merged images using GFP-LC3 MCF-7 cells expressing Flag-TSC1, Flag-TSC2 or both Flag-TSC1 and Flag-TSC2 showing GFP-LC3 (green) puncta. Scale bars, 10 μm. (b) Quantification of GFP-LC3 puncta was performed and the results are represented as the average puncta fluorescence per cell (±s.e.m., n = 3 independent experiments) from 100 cells per experiment as shown in a. ***P0.001; NS, not significant.
b Paired-pulse facilitation at CA3-to-CA1 synapses excluded strong alterations of presynaptic function in mutant mice. The stimulation strengths (in nC) necessary to elicit a pre-volley of 1.0 and 1.5 mV and the resulting fEPSP amplitudes were comparable in all genotypes but showed only a trend towards lower fEPSP amplitudes recorded at 1.5 mV pre-volley amplitudes in Grin2aS/S mice. The fEPSP amplitudes necessary to elicit a just detectable population spike (1) and a population spike of 2 mV amplitude (2) and the paired-pulse facilitation ratio (PPF) at an interstimulus interval of 50 ms did not indicate any synaptic impairments in Grin2aS/S and Grin2a+/S mice compared to WT littermates. The number of slices is indicated in the bar graphs or in brackets.
Lethally irradiated WT mice were reconstituted with BM from Lyzs-Cre (Cx BMLyzs-Cre) or p38γ/δLyzs-KOmice (Cx BMp38γ/δLyzs-KO). Two months after the transplant, mice were fed the HFD for 10 weeks. (A) Freshly prepared CD45.2 whole BM mononuclear cells (2 × 107) were transplanted into lethally irradiated B6.SJL (CD45.1) mice, and engraftment by CD45.2 cells (%) was analyzed by antibody staining and FACS of peripheral blood and liverCD45+ cells. Charts show CD45.1 and CD45.2 expression in blood cells (left) and liver cells (right) isolated from transplanted mice (n = 3). Representative FACS dot plots of CD45.1 and CD45.2 expression are shown beneath the charts.
Two-tailed Spearman correlation test between PAR and γH2AX (% positive with a median intensity cut-off). Exact p values are indicated when available
D The sucrose preference of susceptible mice with intracerebroventricular infusion of ARL67156 (n = 12, 10, 10, 10 mice. Interaction F1, 38 = 5.352, P = 0.0262; Group F1, 38 = 5.711, P = 0.0219; Drug F1, 38 = 9.703, P = 0.0035; CSDS - ACSF vs Ctrl - ACSF, P = 0.0083; Ctrl - ARL67156 vs CSDS - ACSF, P = 0.0027; CSDS - ARL67156 vs CSDS - ACSF, P = 0.0031. Two-way ANOVA with Tukey's post-test).
(E) Amplification of the cDNA fragment between exons 9-10 and 11 of PSMC3 showing the abnormally spliced RNA fragment. One band at 180bp representing the normal allele is seen for the control and two bands for the individual II.4 (pathologic allele at 300bp).
(B). The schematic diagram shows key residues of PTP-MEG2 defining the substrate specificity adjacent to the pY83 site of NSF. (D). Statistical diagram of the quantal size in Fig. 5A and Appendix Figure S6A-D. The secretion amount of each group was standardized with respect to the control group. Data information: (B Green color represents the amino acids which are found to modulate foot probability based on structure analysis, and red color means amino acids which does not regulate foot probability. , * indicates PTP-MEG2 mutants overexpression group compared with the WT overexpression group. # indicates the overexpression group compared with the control group. **, P<0.01; *** P<0.001 and #, P<0.05; ##, P<0.01; ### P<0.001. N.S. means no significant difference. Data were from 6 independent experiments. All the data were analyzed using one-way ANOVA and showed as the mean ± s.e.m.
A Example of the mapping results. Wild allele frequency in progeny of a cross of the gab1-1 temperature sensitive allele to the YJM975 strain (y-axis) along the yeast genome (x-axis) at the permissive 26°C (blue) and restrictive 34°C (TS allele loss-of-function, cyan). The allele frequency change between the two temperatures is used in mapping. Labels: selected loci in the cross. Blue regions: called suppressor loci. B
Figure 3. Computing stability in multistability regimes. A. Two plots that show the non-degeneracy of even and odd modes in an elliptical geometry for varying cell geometry and MinD recruitment rate. The degeneracy (light blue area) increases with the MinD recruitment rate.
HeLa cells were transfected with an empty vector or plasmids expressing aluRNA or L1‐repeat RNA and GFP from a separate promoter. Transfected cells were identified by GFP fluorescence, and nucleoli volumes were evaluated based on the immunofluorescence signal of the nucleolar marker NPM. The graphs show that the volume of nucleoli is increased by 30% in the presence of ectopic aluRNA (± 95% CI, n = 20). **P‐value 0.01, t‐test. Scale bar, 10 μm.
(a,b) Subcellular fractionation of HepG2 (b) cells demonstrated the localization of TSC2, TSC1, Rheb, TBC1D7 (FAO, a) and AKT in various subcellular compartments. Catalase, PMP70 and lamin A/C were used as subcellular markers for the peroxisome (P) and nuclear (N) fractions, respectively. EEA1, LAMP1 and VDAC were used as markers for endosomes, lysosomes and mitochondria, respectively. WCE, whole-cell extracts; M, membrane; C, cytosol.
D Quantified epoxomicin-sensitive proteasome activity (as measured through the turnover of fluorescent chymotrypsin substrate) from lysates of the indicated genotype and time point. *P<0.001, ANOVA with Dunnett's posthoc comparison to the wild-type control equivalent time point. N=3 trials. Error bars indicate SEM.
C) Cell monolayers two days post infection in Vero E6 (top) and Vero CCL81 (bottom row) at multiple dilutions.
(E) Percentage of eosinophils (Siglec-F+CD11b+ cells) among CD45+ cells was measured after acute or chronic papain-induced lung inflammation (T test, **p=0.0038). Bars represent mean ± SEM. Data information: are representative of 2 independent experiments.
(C) Still images of A549 cells showing the live recruitment of hPARP-mCherry and hXRCC4-GFP, at the site of laser-induced DNA-DSBs from the cells pre-treated with the indicated reducing sugars as described in methods.
Western blot of NIH-3T3 cells expressing sgCtrl, sgSlc25a1-1 or sgSlc25a1-2 and treated with TGFβ or mock for 48h.
B. Genome-wide occupancy profiles (top) and heatmaps (bottom) of IN5, WT, and indicated mutants, +/- 1kb upstream and downstream of all tDNAs.
B Percent of tissue‐specific enhancers validated by LacZ reporter mice (Vista enhancer browser) that overlap with SclMES binding sites shows that Scl binds to experimentally verified heart enhancers more often compared to enhancers from other tissues.
a, List of synaptic targets among DEG containing conserved binding sites (human and mouse) for indicated miRNAs based on TargetScan v7.1. Category of binding site from TargetScan (v7.1) is shown in brackets.
A. Cryo-EM structure of PC2. Left: bottom view of PC2 homomeric tetramer showing the pore-lining S5-S6 from each subunit assemble into the channel pore. Right: side view of S5-S6 from two subunits showing the L677 and N681 (in red) contribute to the restriction at the lower gate. F604P (in cyan) on S5 and the three residues (in green) forming the selectivity filter are also indicated. The structure shown here is previously reported with Protein Data Bank (PDB) code 5T4D [20]. A grey dashed line indicates the path of the ion flow.
A-F) The indicated yeast strains were transformed with expression plasmids for FYVE2-GFP and their vacuolar membranes were labeled with FM4-64. FRAP was performed using a spinning disk microscope equipped with an emission beam splitter and two synchronized cameras, allowing to simultaneously analyze FM4-64 and GFP fluorescence. The histograms show the kinetics of signal recovery for (A) wildtype (WT), (B) vam3tsf, (C) ypt7T22N, (D) vma16F190Y, (E) vps33P184L, and (F) nyv1∆ cells. Scale bar: 2 µm. Arrows indicate the bleaching area. Means and s.d. are shown for 20 stained vacuoles from 3 independent experiments.
Immunofluorescence analysis of Myc-Egg WT (red) in OSCs upon Flag-Wde WT and ∆CC mutant (green) co-expression. Anti-Myc and anti-Flag antibodies were used. DAPI (blue) shows the nuclei. Scale bar: 10 μm.
(d) qRT-PCR assays of Miz1 target genes in control and Miz1ΔPOZ MEFs after incubation in DMEM or in EBSS. Error bars depict s.d. of technical triplicates from one experiment.
A) Alignment and conservation of residues encoded by TUBB1 orthologues and genes encoding for other β-tubulins (TUBB2A, TUBB2B, TUBB3, TUBB4A, TUBB4B, TUBB5, TUBB6, and TUBB8)
Diagram illustrating relocation of piRNA-target TE coding chromosome regions away from the nuclear periphery.
H) Quantification graph of PH3-positive NSCs (Dpn+, Mira+) per brain lobe for wild-type control (yw), klp64Dk5h klp64Dk5h/Df, kap3V5, kap3V6 and kap3V6; g-kap3#11, and kap3V6; g-kap3#31 larval brains. n=26 BL for control; n=16 BL for klp64Dk5h; n=7 BL for klp64Dk5h/Df; n=20 BL for kap3V5; n=7 BL for kap3V6; n=6 BL for kap3V6; g-kap3#11; n=6 BL for kap3V6; g-kap3#31. ****p<0.0001; control vs. kap3V6; g-kap3#11, p=0.0977 (ns); control vs. kap3V6; g-kap3#31, p=0.1658 (ns)
G. Representative images showing 2i-specific BAZ2A-bound regions and H3K27ac and H3K27me3 in ESC+2i and ESC+serum. The grey box highlights strong TIP5-bound regions and corresponding histone modifications.
(M) Representative control (of 5) and SHP099-treated (of 5) B16F10 tumor sections through the maximum diameter; H&E staining (scale bar: 10mm). (N) Cleaved caspase-3+ fluorescence intensity in SHP099 and control tumors (n=3/group). Data information: Error bars: ± S.D.; P values from two-tailed Student's t-test; *P<0.05, **P<0.01 and ***P<0.001.
(C) Repetitive jumping behavior in open field test. n = 8 for WT mice, n = 7 for KO mice. *, p<0.05, One-way ANOVA with Bonferroni's post hoc test (F(1, 13) = 5.09). Data are presented as mean ± SEM.
G Metabolic characterization of untreated and MARS-over-expressing NE4C cells based on pathway analysis of significantly changed metabolites. Columns show significantly enriched pathways, and yellow columns indicate oxidative stress-associated pathways.
(C) Fluorescent microscopy demonstrates that downregulating ERMES contacts (by growing GALp-MDM34 strains in glucose) indeed caused expansion of vCLAMP (GFP-Vps39). However, this expansion was diminished in a Δlam6 background. Scale bar represents 5 μm (see also Figure S4).
Co‐localization of Hsp70 with Siglec‐5 and Siglec‐14 ligands in lung bronchiolesImmunofluorescence of human lung and prostate sections probed with Siglec‐5 R119A Fc or Siglec‐14 R119A Fc (red) with an anti‐Hsp70 antibody (green). The co‐localized signals for the Siglec‐Fc probes with an anti‐Hsp70 antibody suggest that Hsp70 is one of the possible sialic acid‐independent ligands of Siglec‐5 and Siglec‐14 in the lung bronchiole. White dashes mark the lung bronchiole epithelium. All images are representative of at least 2-3 replicates.
C) Analysis of Tbk1-/- MEFs stably expressing the indicated TBK1 alleles and infected with S. Typhimurium. Percentage of S. Typhimurium coated with ubiquitin (detected by FK2 antibody) at 1 or 4 h p.i. Western blot for Flag-tagged TBK1 variants in post nuclear cell lysates.
D HeLa cells were incubated in EBSS medium for 1 h after co-transfection eGFP-USP19 and dsRed-Beclin-1 for 48 h. Cells were imaged for eGFP and dsRed. Scale bar, 200 μm.E Quantitative data are mean ± SEM of triplicate samples (20 cells per sample). *p < 0.05, **p < 0.01 and ***p < 0.001.
PEA1 (B) (EMPTY and OPCML transduced) cell lines were serum starved and stimulated with Gas6 over a 24 hour time course. GAPDH was used as a loading control Data in (A, B, D, F) are representative blots of at least three experiments. RPPA analysis was performed in triplicate
(i) Real-time PCR assessing the expression of cell cycle inhibitors and proinflammatory cytokines (n=8 per group).
(F) IPA analysis of TMT/iTRAQ scan results and prediction of downstream effects. Legend indicates color-coding of molecules and connections. Shades of red and green are proportional to fold change, whereas shades of blue and orange are proportional to the strength of the prediction, as calculated by IPA.
F Snapshots of representative IGV tracks displaying RNA-Seq data from WT whole muscle (WM), single myofibers (SF) and satellite cells (SC) showing the expression of EGF, EGFR and VEGFA. Ckm and Myf6 are used as positive controls for whole muscle and single fibers. PDGFRA, a marker of fibro/adipogenic progenitor cells, is used as a control to show the lack of niche cells in the single myofiber samples.
D) Dephosphorylation by the PP2A-B56α holoenzyme complex of the indicated phosphorylated GST-ADAM17 (V724-C827) fragments. The GST-ADAM17 (V724-C827) substrates was phosphorylated with radioactive ATP using Protein Kinase A and incubated with the PP2A-B56α holoenzyme. Removal of radioactive phosphate was monitored over time. The mean and Standard deviation of 4 independent experiments are shown.
C) MEF cells transduced with AdV-ACE2/GFP were mock treated (- IFN) or treated with mouse IFNβ (+ IFN) for 24 h followed by infection with SARS-CoV-2 (MOI 1) for 24 h. Representative example flow cytometry plots measuring percent infection are shown for each cell line and treatment condition.
miR-181-mimic transfection specifically inhibits Luciferase activity of constructs containing WT 3'-UTR predicted target sequences. Point mutations (mut) in miR-181a/b binding sites abolish Luciferase repression in all cases apart from PPARGC1A. Data are normalized to negative mimic transfection (dashed line). N=6 independent experiments.
D) Proline biosynthesis protein levels in breast cancer subtypes (Log2 ratios of light vs. SILAC standard). The upper and lower limits of the box show values from the first to the third quartile, with the horizontal line indicating the median. The whiskers extend 1.5 times the interquartile range from the edges of the box. Outlier values were plotted outside the whiskers. Significance was determined using paired Student's t-test and p values were corrected using permutation based FDR . *p < 0.05 and *** p < 0.001.
Quantification of differentially expressed genes (false discovery rate (FDR) ≤ 0.01, Log2FC ≥ 1/≤-1 and maximal transcripts per million (maxTPM) ≥ 1) detected by RNA-seq in each cellular state upon EZH2i treatment. UT: untransformed, PN: pre-neoplastic, TR: transformed.
qRT-PCR gene expression analysis showing the fold change of Pi3K/mTOR associated gene panel in KSL cells sorted from: (A) Molm-14-xenografted mice
Immunolocalization of Aβ in AVs from L/APP cells and PS1/APPbrains and γ-secretase components (PS1 and nicastrin) in L/APP cells. Immunogold localization of Aβ40 (A), Aβ42 (B), PS1 (C), nicastrin (D), and in the absence of primary antibody (E) in L/APP cells grown for 6 h in the absence of Leu and His. (F) Quantification of gold particle frequency in AV or tubulovesicular compartments (TBV), which comprise 27.0 ± 11.0 and 19.2 ± 7.2%, respectively, of the total cell area. Error bars represent SEM.
Proliferation assay examining the effect of EMX2 ectopic expression in U-87 MG and DBTRG-05MG GBM cells, RFP is used as a control. Values represent mean ± SEM from three biological replicates. The fold change in cell number after eight days of proliferation whilst expressing the exogenous protein is shown relative to an uninduced control. Two asterisks indicate p-value < 0.01 (one-tailed unpaired Student's t-test). Similar results were reported in [103] using other GBM cell lines.
Hemizygous K18-hACE2 mice were treated intranasally with 20 µg of NM1251 (n = 15) or NM1267 (n = 12) seven hours prior to infection with 3*103 PFU SARS-CoV-2 B.1. Weight loss were monitored for 14 days. Dashed line indicates humane endpoint and symbols represent mean ± SEM ****P < 0.0001, by two-way ANOVA with Sidak's multiple comparison test in
E COS‐1 cells were treated with EHD1 siRNA1 for 72 h and stained for TfnR. The image represents the maximum intensity z‐projection of four confocal slices. Scale bar, 10 μm.
B Interactions between LSD1 and CARM1 were detected by co-immunoprecipitation (Co-IP) assay with anti-Flag in HEK-293T cells transfected with Flag-LSD1 or Flag-CARM1, respectively.
RT-qPCR data of Mlkl , in ileum biopsy samples of C57BL/6J mice treated with normal drinking water or 25 mM ZnSO4 in the drinking water for 1 week, either or not pretreated with antibiotics (AB) for three weeks. (N=5 per group)
D. Representative Per2::Luciferase traces before and after administration (arrow) of vehicle (black), Prok2 (red) or VIP (blue) within CT9-12.
E. TBK1 is not required for insulin-stimulated mTORC1 signaling: TBK1+/+ and TBK1-/- MEFs were stimulated with insulin as in C.
Samples were prepared as described in Fig. 6E but, after trypsin treatment, infected cells were subjected to buffers at the indicated pH for 5 min at 37°C and left to recover for an additional hour at 37°C. Images of microscope fields (50 < n < 120) were quantified, and fusion index was calculated as in Fig. 6F. n > 50 microscope fields were analyzed.
F RNA pulldown assays using biotin-labeled RNA probes. The cell lysates with RBM47-flag were immunoprecipitated with biotin-conjugated RNA probes, and the elution was blotted with an anti-Flag antibody. Data information: Data are representative of n = 3 independent experiments. NS, non-significant; **P ≤ 0.01, and ***P ≤ 0.001 (Student's t-test).
F. Assessment of Hh pathway activation using Gli1-luciferase reporter assay in MEFs Sufu-/- upon reintroduction of HA-tagged Sufu WT or Sufu mutant S352F using a retroviral system. (mean ± SEM from 3 independent experiments, **p<0.005; ***p<0.0005).
Representative images showing YAP protein expression in the 13th passage hOSE Cells with or without LATS2 knockout. YAP protein was examined by fluorescent immunohistochemistry and visualized using an Alexa-488 (Green) conjugated secondary antibody. Nuclei were stained with DAPI (blue).
Western blot for p53 pS15, p53, and vinculin (vinc) in HCT116 treated with 300 μM 5-FU upon silencing of PHD1 and p38α, alone or in combination. Vinculin (vinc) is used as a loading control.
(G) mTOR inhibition with rapamycin results in reduced USP1 protein content and enhanced Akt phosphorylation at T308. However, a simultaneous downregulation of USP1 is required to promote TSC1 accumulation. Soluble fraction of muscles expressing shLacz or gUSP1 (in vivo CRISPR) from fed and fasted mice injected i.p. with rapamycin (6mg/kg body weight) or saline were analyzed by SDS-PAGE and immunoblot.
Unsupervised hierarchical clustering (correlation-based distance) obtained from RNA-seq in T-induced PGCLCs (T-PGCLCs), in vivo PGCs, and FACS-sorted cell fractions as indicated in Fig 2A-C.