EMBO/sd-character-level-ner huggingface dataset:
HuH-7 (A) and Hep3B (B) hepatocytes were loaded with 150 µM oleate overnight and starved for 48 h in medium containing 0.1% FBS in the presence of Dyn2 inhibitors or DMSO as indicated. Representative images of inhibitor-treated and control cells (stained with Oil Red O) are shown in A and B together with the quantitation of the average LD area per cell from three independent experiments. Pharmacological inhibitors used were: Dynasore (inhibits Dyn2 GTPase activity), MiTMAB (targets PH domain and interferes with membrane binding), Dynole 34-2 (allosteric GTPase inhibitor), and Dynole 31-2 (negative control for Dynole 34-2). Bars, 20 µM.
C Representative western blot images of OXPHOS protein levels of RKO cells at increasing concentrations of IMT1. ACTINB is showed as loading control.
F p97 is essential for cell survival after lysosome rupture. Cells were transfected with control (Ctrl), p97 or SEL1L siRNA oligos and treated with indicated concentrations of LLOMe for 12 h. Cell viability was measured using the MTS assay. Data represent mean ± SD of three independent experiments.
C. HumanHEK293T cells were transfected with plasmids expressing the GFP-TatA-Flag substrate and the indicated rhomboid proteases. Whole cell lysates were analyzed by western blot. P, CN, CC denote precursor, N-terminal cleaved and C-terminal cleaved products, respectively.
B) Real-time PCR. Total RNAs were prepared from primary hepatocytes described in (A). Values were normalized against the amount of mRNA in the Nbr1f/f hepatocytes expressing GFP under normal culture conditions. The experiments were performed at least three times. Data are shown as means ± s.e. *P < 0.05 as determined by Welch's t-test.
H) Cells were treated and analyzed as in 2E. Induction of FLAG-Asf1A-4D was induced using doxycycline. Error bars represent SD, n=5. Statistical significance was tested using a paired two-tailed t-test (NS for P>0.05, * for P≤0.05).
(B-F) Suppression of X-ray-induced autophagy in PPM1D−/−thymocytes. (B, C) The indicated thymocytes were X-rayirradiated (5 Gy), and 3 hr later, thymocytes were immunostained with an anti-LC3 antibody. Nuclei were stained with Hoechst 33342. Representative images are shown in (B). LC3 puncta can be seen in irradiatedPPM1D+/+thymocytes (arrowheads). In (C), the proportion of cells with LC3 puncta was calculated (n > 100 cells in each experiment). Data are shown as the mean  ± SD (n = 3 experiments). *p < 0.05.
Heat map (left) and tSNE plot (right) of the comparative analysis of digested day 23 BALO cultures with (+) and without (-) microinjected TR‑Mac depicting six distinct clusters (C1, club/secretory cells, red; C2, basal cells, yellow; C3, rMC, green; C4, AEC II, blue; C5, AEC I, purple; and C6, ciliated cells, pink)
B DNA-damage induced by 2 Gy ionizing radiation as measured by γ-H2AX foci at 1hr (n=53-77 cell nuclei/condition scored; mean shown); statistical analyses performed using two-tailed Mann-Whitney U test.
(F) HeLa cells were transfected with the indicated siRNAs. Cell lysates were subjected to immunoblot analysis using anti-TDP-43, TFEB, LAMP1 and GAPDH antibodies.
SARS-CoV-2 was subjected to pretreatment with trypsin and furin for 15 min at 37°C prior to infection of Caco-2 and Vero cells (MOIs of 0.4 and 0.3, respectively). Infected cells were quantified by flow cytometry as described in Fig. 1D. Data were normalized to samples not pretreated with trypsin. n = 4-6 biological replicates.
a, Immunoblot of primary intestinal epithelial cell scrapings from mice treated with or without rapamycin for 14 consecutive days (n = 3). b, Enteritis histology score for experiment as in a (n = 4; median shown; Mann-Whitney U-test).
Topical rapamycin treatment twice daily for 4 weeks showed an obvious therapeutic effect in rosacea patients. (C) The change of patients' CEA score showed in scatter histogram at 0 week and 4th week. (D) The change of patients' IGA score showed in scatter histogram at 0 week and 4th week. "The Change value < 0" indicates that skin lesions show positive improvement after treatment; "The Change value > 0" indicates skin lesions show exacerbation after treatment; "The Change value = 0" indicates that skin lesions show no change after treatment; Data represent the mean ± SEM, and two-tailed unpaired Student's t-test was used (C, D).
C) Cellular oxygen consumption rates (OCR) in senescent (10 days after 20Gy X-ray) Control and Parkin-expressing MRC5 fibroblasts. Data were obtained using Seahorse XF24 analyzer and shows mean±S.D. n=4 technical repeats (representative of 2 independent experiments);
D. TBK1 is required for EGF stimulated mTOR auto-phosphorylation within mTORC1: TBK1+/+ and TBK1-/- MEFS were serum starved, pre-treated with Ku-0063794 [1 μM], and EGF stimulated as in A. Raptor was immunoprecipitated, and IPs and WCL were analyzed.
(I) RNA was isolated from vehicle or nutlin-3a (1 μM for 8 times 24 hours) treated BJ cells at 8 dpt and quantified by qRT-PCR for p53 target cell cycle genes, SASP genes (n=3 independent experiments). Data information: Data are means ±SD. Two-way ANOVA *p<0.05, **p<0.01, ***p<0.001.
(A) AUT7 is identical to YBL078c. Genomic fragments isolated from an overexpression library and leading to suppression of the autophagic defects in aut2‐1 mutant cells are illustrated. A complementing StuI-SnaBI subclone carrying only AUT7 as a complete ORF was constructed.
e, Fitted rate parameter, λ, representing the progression rate of each step within a cell cycle phase. Error bars represent std from 1000 bootstraps.
(B) Quantification of LC3‐II levels relative to Hsp90 expression was performed in several experiments performed as presented in (A).
Analysis of the percentage of infolded nuclei in DIV10 hippocampal neurons upon SATB2 overexpression and Vps4a/ Vps4b knockdown. AAV-SATB2-transduced neurons (non-transfected or scrambled siRNA (Scr)-transfected) exhibited higher percentage of infolded nuclei compared to AAV-EGFP-transduced neurons. In contrast, VPS4-depleted AAV-SATB2-transduced cultures showed similar number of infolded nuclei to AAV-EGFP-transduced neurons (n = 4 independent primary cultures, one-way ANOVA followed by Tuckey post hoc test, F3,11 =15.866, p = 0.00026, AAV-EGFP vs. AAV-SATB2 p = 0.0104, AAV-EGFP vs. AAV-SATB2 + Scr p = 0.0028, AAV-EGFP vs. AAV-SATB2 + siVps4 p = 0.605, AAV-SATB2 + Scr vs. AAV-SATB2 + siVps4 p = 0.0007). Number of nuclei analyzed: 594 (AAV-EGFP), 657 (AAV-SATB2), 612 (AAV-SATB2 + Scr), 428 (AAV-SATB2 + siVps4). Data are presented as mean ± SEM, **p < 0.01 compared with AAV-EGFP; ###p < 0.001 compared with AAV-SATB2 + Scr.
(J) Immunohistochemical staining showing that over-expression of circLMP2A could lead to increased expression of TRIM59 and ERG but decreased expression of p53.
(P) The effect of overexpression of consitutively active CDC42 on ABCA1 abundance in MIN6 cells with ABCA12-deficiency. Treatments are defined in the table below.
A Domain architecture of S. pombe bromodomain AAA-ATPases. The D1 and D2 ATPase domains (AAA) are shaded blue and orange, respectively, and the bromodomain (BD) is grey. The percentage similarity to each other and the indicated proteins was determined by FASTA sequence comparison [74] using the scoring matrix BLOSUM50.
(C) Activity of NHE9* co-reconstituted with ATPase into liposomes to mimic the in vivo situation (schematic). Representative ACMA fluorescence traces of liposome reconstituted NHE9* (blue), NHE9* double-mutant N243A-D244A (red), and rat fructose transporter GLUT5 (black). ATP-driven H+ pumping establishes a ΔpH (0-3 min). H+ efflux is initiated by the addition of 40 mM NaCl, and subsequent addition of NH4Cl (4 min) collapses the proton gradient.
Ribbon diagram of the lower subdomain of the shoulder showing the path of p50-A (B) and p50-B (C), colored as in A.
A, B WT THP-1macrophages were treated with GBS WT, ΔcylE, ΔcovR, or ΔcovRΔcylE at an MOI of 1 and incubated for 4 h. Cytotoxicity was measured by LDH release (A), and IL1β release in supernatants was measured by Luminex assay (B).Data information: Data from three independent experiments performed in triplicate are shown, error bars ± SEM. Significance was determined using Bonferroni's multiple comparison test following ANOVA. (A) n = 3, **P = 0.0080 for WT versus ΔcovR; **P = 0.0016 for ΔcovR versus ΔcovRΔcylE. (B) n = 3, *P = 0.03 for WT versus ΔcovR; *P = 0.02 for ΔcovR versus ΔcovRΔcylE. (C) n = 3, ****P < 0.0001. (D) n = 3, *P = 0.01.
D HEK-293T cells were transfected with USP7 WT or USP7 C223S, then treated with MG132 for 10 h. Cell lysates were immunoprecipitated using anti-LSD1 antibody followed by immunoblotting analysis.
Figure 9: VEGF-A-induced non-exudative AMD-like pathologies can be prevented by targeting NLRP3, IL1R1 or caspase-1/caspase-11.A. No significant abnormalities of the choroid, RPE or retina are seen in control wild-type littermate mice. Representative image of a 28-months old control eye is shown. White arrow indicates normal Bruch's membrane. Chor: choroid; RPE; PR: photoreceptor; ONL: outer nuclear layer.B. Aged VEGF-Ahypermice develop a progressive age-dependent degeneration of the RPE (red arrow) and the photoreceptors (yellow arrow) with accumulation of thick sub-RPE basal laminar deposits (black arrow). These non-exudative AMD-like pathologies occur also at sites devoid of CNV lesions.C.-E. Genetic inactivation of CASP1/CASP11, NLRP3, or IL1R1 strongly inhibits the manifestation of RPE and photoreceptor degeneration in aged VEGF-Ahypermice.F.-G. VEGF-Ahyper/IL18-/-mice show significant RPE and photoreceptor degeneration, with shortened and irregular photoreceptor outer segments (white arrows). Thick sub-RPE deposits that protrude into the RPE plane are observed as well (black arrows).H. VEGF-Ahyper/Becn1+/-mice show significant RPE and photoreceptor degeneration.I. In contrast, age-matched VEGF-Ahypomice that are hypomorphic for VEGF-A and express β-galactosidase from the endogenous VEGF-A locus (as do VEGF-Ahypermice) do not show these eye pathologies.B-I. 21-months old mice. Scale bars 20 μm.
a. Schematic representation of experimental set-up for genome-wide fibroblast expression profiling.
Figure 7: PLCβ1 and PTPRN2 promote metastatic breast cancer cell migration as targets of miR-335.(A) Model of PTPRN2 and PLCβ1-mediated regulation of plasma membrane PI(4,5) P2 levels to promote metastatic migration through CFL1. In poorly metastatic breast cancer cells, levels of PLCβ1 and PTPRN2 are low. In highly metastatic breast cancer cells, miR-335 is silenced and PTPRN2 and PLCβ1 levels increase. PTPRN2 and PLCβ1 reduce plasma membrane PI(4,5) P2, releasing CFL1 from its inactive state in the plasma membrane to the cytoplasm where it increases actin remodeling.
d, Representative histogram overlay of PD-1 expression among total CD8 T cells in spleen of 45-wk-old mice (left panel) and percentages of PD-1+ cells among total CD8 T cells (right panel).
Insulin tolerance test (ITT) after 25 weeks on NC or HFD. , ITT following a three hour fast (males, n=6). Data information: values shown are mean ±SD. * = p < 0.05; ** = p < 0.01; *** = p < 0.001; **** = p < 0.0001 (two-way ANOVA with multiple comparisons).
Sequence conservation of sarbecovirus S glycoproteins plotted on the SARS-CoV-2 S structure.
(E) PGC1α OE significantly increased expression of Cpt1 and PDK4, both are involved in key steps of FAO. However, overexpression of PGC1α did not abrogate the TGFβ1 up-regulated genes in glycolysis and αSMA (n=6). *p<0.05; **p<0.01; ****p<0.0001 by one-way ANOVA, mean ± SD.
(B) Survival analysis for Cx3cr1-Rheb1Δ/Δ (n=7) and Rheb1fl/fl (n=7) mice. Chi square test.
Schematic diagram of the in vitro CDC50A-mCherry expression experiment. After 6 days in vitro (DIV), cortical neurons were transfected with CAG-GFP and CAG-mCherry or CAG-GFP and CAG-Cdc50a-mCherry. Representative confocal z-stack images of the rER (Nissl staining, cyan) with GFP (green) and mCherry/CDC50A-mCherry (red). The dashed line represents where the high magnified insert was taken from. Scale bars, 50 (left), 20 (middle), and 5 μm (right). Schematic diagram of in vivo CDC50A-mCherry expression experiment. Neonatal (P0) wild-type mice were injected with AAV9-CAG-Cdc50a-mCherry. Representative confocal z-stack images of the rER (Nissl staining, green) and CDC50A-mCherry (red) in the CTX (cortex). The dashed line represents where the high magnified insert was taken from. Scale bars, 20 μm (upper) and 5 μm (lower). Schematic diagram of the experiment in which PS exposure was detected in control and Cdc50a cKO neurons in vitro. After 6 DIV, cortical Cdc50afl/fl neurons were transfected with either hSyn-mCherry or hSyn-Cre-p2a-dTomato to generate control and Cdc50a cKO neurons, respectively. Representative live confocal z-stack images showing PS exposure (pSIVA, green) in mCherry/dTomato (red)-expressing neurons. Scale bar, 20 μm.
F. RT-QPCR analysis of Gemc1 in trachea, oviduct and ovary tissue from Gemc1+/+ and Gemc1-/- mice shows that the knockout reduces Gemc1 mRNA to undetectable levels. Mean and standard deviation of duplicate samples from 2 female mice are plotted. Additional examples from other Gemc1-/- tissues are shown in Appendix Fig S1.
GC92 SV40 immortalized human fibroblasts containing the I-SceI NHEJ reporter were transfected with the indicated siRNA oligos and I-SceI. 48 h later genomic DNA was extracted and repair of I-SceI cut-sites analyzed through junction analysis (n= independently derived sequences, see materials and methods for details).
C. ERK71 mutants fail to maximally downregulate sugarbabe expression upon fasting (N=4 replicates of 10 larvae/replicate for each genotype).
(A) Immunodetection of PERK in WT and Mfn2 KO cells stably expressing a scrambled shRNA (Scr) or a shRNA directed against PERK (PERK KD).
MISTRG mice were reconstituted or not at birth with ~200.000 human CD34+ cord blood HSPCs, and subcutaneously transplanted with 10x106 U-2932 cells at six weeks of age. tumor weights and volumes at the study endpoint in D, where each data point represents one tumor.
(B) Expression of the DSCR1 mRNA in Ts65Dn mouse was increased about 2.5 folds compared to that of wild type. However, Ts65Dn/DSCR1+/- mouse showed normal level of DSCR1 mRNA transcript. Values are shown as mean ± SEM and tested for statistical significance by one-way ANOVA followed by Bonferroni post hoc test. N=3 for each condition, *P< 0.05.
Bisulfite genomic sequencing of the promoter regions of Oct4 and Nanog in iPSCs, ESCs and MEFs. Open circles indicated unmethylated CpG dinucleotides, while closed circles indicated methylated CpGs.
A, Immunofluorescence confocal microscopy of ARPE-19 cells overexpressing TFEB-FLAG-WT or TFEB-FLAG-C212A showing the subcellular distribution of recombinant TFEB in response to treatments with EBSS for 4 h or 250 μM NaAsO2 for 1 h. Scale bars, 10 μm.
A-E mRNA expression levels of Coq9 (A), Coq7 (B), Adck3 (C), Coq5 (D) and Coq6 (E) on cerebrum of Coq9+/+, Coq9Q95X and Coq9Q95X mice at 3 months of age. **P < 0.01; ***P < 0.001; Coq9Q95X and Coq9R239Xmice versus Coq9+/+mice. ###P < 0.001; Coq9Q95X versus Coq9R239Xmice.F-J mRNA expression levels of Coq9 (F), Coq7 (G), Adck3 (H), Coq5 (I) and Coq6 (J) on kidney of Coq9+/+, Coq9Q95X and Coq9Q95Xmice at 3 months of age. ***P < 0.001; Coq9Q95X and Coq9R239Xmice versus Coq9+/+mice. #P < 0.05; ###P < 0.001; Coq9Q95X versus Coq9R239Xmice.K-O mRNA expression levels of Coq9 (K), Coq7 (L), Adck3 (M), Coq5 (N) and Coq6 (O) on triceps surae of Coq9+/+, Coq9Q95X and Coq9Q95Xmice at 3 months of age. *P < 0.05; ***P < 0.001; Coq9Q95X and Coq9R239Xmice versus Coq9+/+mice. #P < 0.05; Coq9Q95X versus Coq9R239Xmice.
(C) The GFP of Spindly was removed with PreScission protease, and the resulting objects were imaged by negative stain EM. Scale bar: 200 nm. Data information: Experiments were technically replicated at least three times.
B Moving the Hsc70 binding site away from the trimerization domain reduces the rate of Hsc70/DnaJB1-mediated dissociation of HSE-DNA-bound Hsf1. Hsf1_t10/20/30, region 202-213 moved by 10, 20, or 30 residues towards the C-terminus.
(A) The overall structure of OTULINWT (3ZNV) is depicted with its catalytic triad (C129, H339, N341; pale cyan) and positions of variants identified in this study (M86, W167).
E. Schematics of astrocytic calcium imaging and representative images of spontaneous calcium signaling (green) of Daam2 cHet and cKO mice injected with AAV-GfaABC1D-GCaMP6f virus in OB. Approximate territory of astrocytes including soma and multiple microdomains is outlined in yellow. Representative traces of GCaMP6f signal in Daam2 cHet and cKO astrocytes are shown in black and red respectively. F-H. Quantification of amplitude (F), frequency (G), and area under curve (AUC) (H) of ∆F/F GCaMP6f signal events in OB. Amplitude and AUC of Daam2-deficient astrocytes are significantly increased in OB. Data is presented as mean ± SEM. Total number of cells is n=16, 15 (F-H) from N=3-4 mice of each genotype. Student's t-test was used for statistics, *p<0.05.
H Graph of TOPflash (TOP) to FOPflash (FOP) luciferase reporter ratios ± s.e.m. (n = 3 independent experiments) in transfected 293FT cells treated with conditioned mediums collected from L-WRN cells and diluted as indicated. L-WRN CM had been produced in the presence or absence of the porcupine inhibitor C59 (10-fold dilutions, 10 µM to 1 pM). *p<0.05, ***p<0.001, ****p<0.0001 by 1-way ANOVA and Dunnett's post-test compared to 0% L-WRN CM group.
(D) Control and spt5-AID strains were grown at 30°C in rich medium, before addition of auxin (0.5 mM 3-indoleacetic acid or IAA) for 1 hour. Spt5 protein was monitored in cell extracts by immunoblotting.
C Western blot analysis of candidate substrates reproducibly cleaved by GlpG from the screen. Data information: In (C rhomboid substrates that are uncleaved, cleaved by GlpG are marked by black, red, arrows, respectively. Controls, inactive enzymes and wild-type S. sonnei (Ss).
A. 3.8 Å cryoEM map of V1 in complex with subunit C, highlighting the hitherto unseen density (red) wedged between subunits B and C and the N-terminal part of peripheral stator EG2.
(A) Left: qRT-PCR analysis of mRNA expression of MAPK12 (p38gamma) and MAPK13 (p38delta) in liver extracts prepared from obese patients with alcoholic fatty liver disease (NAFLD) and control individuals without NAFLD. mRNA expression was normalized to the amount of Gapdh mRNA. Right: Representative H&amp;amp;E-stained liver sections. Scale Bar: 50μm. (n= 11-74)
A A selection of genes down-regulated in atosPBG mutant macrophages compared to the control, chosen for their >5 fold change in expression as well as an identified biological function.
d, Macrophages were infected as in c with or without IPTG induction. Intracellular bacterial replication was determined using a gentamicin-protection assay. Shown is fold replication compared to 2 h post infection. Clear triangles, wild type; filled triangles, wild type + IPTG; clear circles, iLLO; filled circles, iLLO + IPTG. Mean ± s.e.m. or range for three (wild type, wild type + IPTG, iLLO + IPTG) or two (iLLO-IPTG) independent experiments, respectively.
(A) Endolysosomal membranes from MSD, MPS‐IIIA and WT MEFs were treated with 1% Triton X‐114 and loaded on a sucrose gradient. Immunoblots with Flotillin‐1 identified DRMs in fractions 2, 3 and 4 (arrows). The fractions at the bottom of the gradient (12 and 13) correspond to high‐density detergent soluble fractions, whereas the remaining ones were defined as intermediate fractions (intermediate‐I: 5, 6, 7 8; intermediate‐II: 9, 10 and 11). The percentage of Flotillin‐1 in DRMs was calculated from the densitometric quantification of immunoblots.
serum FITC-Dextran level, of colonic section from the Angfl/fl and LyzMcre;Angfl/fl mice on day 8 with (n = 7) or without (n = 3) 2.5% DSS treatment.
(B) Cxcr4 mRNA expression in MM cells transfected with shCxcr4 (pools 1 and 2) relative to MM cells transfected with shScramble (AB1 shCTR), one biological replicate, in technical triplicate.
A HeLa cells expressing Dox-inducible RIPK3 WT, K518R or 3xKR were treated with 1 µg/ml Dox and/or 10 µM NSA and 20 µM Dab overnight. Protein levels of inducible RIPK3 expression and phosphorylated MLKL were examined by Western blotting. β-Actin was used as a loading control.
The yellow spark represents the initial exposure of the seedling to light. Photo-initiation is mediated by PAP8 and PAP5 rapid accumulation in early photo-morphogenesis (φMG): the Pr state of phytochrome B (PHYBPr) is converted in the Pfr state (PHYBPfr), which enters the nucleus, accumulates in early photobodies (small green discs) that regroup in late photobodies (large green discs) while promoting the destabilization of PIFs (PIF1 and PIF3 in particular). The red arrow in the timeline represents the albino block observed in pap8-1 that may represent a key feature of the PAP syndrome. The dark induces ubiquitination and degradation of HY5Ub impeding recognition of a cis-regulatory element in the promoter of PAP8 (yellow box). Light induces transcriptional activation of PAP8 in palisade cells likely through the HY5 pathway (dashed yellow arrow on PAP8 promoter); this part of the model is supported by transient assays, in vitro experiments, and in vivo genome-wide ChIP sequencing data. The cTP pre-sequence of PAP8 allows plastid import and then PAP8 assembly within the PEP-PAP complex. Using an unknown trafficking route such as travelling across the plastid envelope (?), part of the processed PAP8 pool is found in the nucleus where its action could be necessary for the PHYB-mediated transcriptional activation of GLK1 directly through HY530 (dashed yellow arrow) or other light responsive factors (LR), which in turn can activate the Photosynthetic Associated Nuclear Genes (PhANGs) concomitantly to the (PEP-PAP)-driven expression of the Photosynthetic Associated Plastid Genes (PhAPGs) essential for the building of the photosynthetic apparatus (PS) in the functional chloroplast.
(D) Quantitative data. Bars depict the percentages of cells exhibiting the accumulation of RFP-LC3 in puncta (RFP-LC3vac). (B and D) Means ± SEM; n = 3; *, P < 0.05.
B-G Immunofluorescence of unpermeabilized cells co-expressing FLAG-tagged wt UMOD (green) and the indicated HA-tagged isoforms (red). UMOD R415A does not incorporate into polymers that only contain wt protein (C). UMOD ΔFA has a dominant negative effect on wt protein polymerization (D) that is rescued in a double mutant carrying both ZP-N and ZP-C mutations (F). Similarly, the dominant negative effect of a CCS mutation (4A) that prevents EHP dissociation (E) is suppressed by the introducing the R415A mutation in the 4A isoform (G). Scale bar: 50 µm.
B Heatmap of selected immune mediator levels in plasma samples of healthy controls, vaccinated close contacts, COVID-19 vaccine breakthrough cases, and unvaccinated COVID-19 patients with primary infection. Each color represents the relative concentration of a particular analyte. Blue and red indicate low and high concentration, respectively.
A-D. Bright-field pictures of K8-eYFP (Left) and Z-projections of time series (Right) of live LB K8-eYFP embryos imaged using two-photon laser with time intervals between 20 and 30 min, focusing on regions corresponding to dashed white areas. A. Lateral view showing extension of K8 containing cables (white arrows) attached to the amnion and ExE wall (n=10). B. Anterior view showing chorion retraction at the Anterior Separation Point (white arrows) (n=6). C. Lateral and D. Posterior views showing allantois growth over time (n=12 and 3). Allantois cortex and mesenchyme are indicated with yellow and magenta arrows, respectively.
K: Sample traces of AMPA and NMDA receptor-mediated currents recorded from CA1 pyramidal cells.
Means ± SD of duplicates from two independent experiments are presented in the graph (n=2). When applicable, student t-test was performed to determine statistical significance (**P<0.01;***P<0.001).