ALT Fig. 2. Prof. Sally Dunwoodie presented awards to the winners of the best poster presentation.

ALT xZnf131-depleted embryos exhibit gastrulation defects

ALT Fig. 2. Model of endocardial cushion EndMT. This figure illustrates the developmental progression of endocardial cushion EndMT. Firstly, the cardiac jelly is generated between the endocardium and myocardium. Secondly, endocardial cells (ECs) sense blood flow shear forces, lose their primary cilia, and initiate EndMT. ECs detach from the endocardium, migrate into the cardiac jelly, and transform into mesenchymal cells. During post-EndMT development, mesenchymal cells undergo proliferation, migration, and secretion of extracellular matrix, participating in the shaping of valves and the atrioventricular septum.

ALT Fig. 1. Clinical and radiological features of the proband with acromesomelic dysplasia, Maroteaux type (AMDM).

ALT Fig. 3. Image Analysis reveals proliferation differences based on differentiation stimuli. (A) Confluency seen within each well is graphed over the measurement period. (B) Representative images comparing macrophages at day 0 and day 18, with the differentiation agent concentration increasing down the image pairs.

ALT Fig. 4. Table of all sgRNAs designed and tested in this study

ALT Fig. 7. Proposed model for promoter-level reciprocal repression during Xenopus gastrulation. In ventral mesodermal regions, BMP signaling activates Ventx1.1 expression through Smad1/5/8–Smad4 signaling. Ventx1.1 represses gsc transcription through VRE elements within the proximal gsc promoter. In the neuroectodermal domain, reduced BMP signaling permits Foxd4l1.1 expression, which further represses gsc transcription through BRE/FRE-containing promoter region. In dorsal organizer regions, Activin/Nodal signaling activates gsc through Smad2/3–Smad4 signaling, and Gsc represses ventx1.1 transcription through the GRE1-containing region of the ventx1.1 promoter. The FRE partially overlaps with VRE2 on the reverse strand, suggesting spatially distinct promoter occupancy by Ventx1.1 and Foxd4l1.1 during gastrulation.

ALT Fig. 1. Sagittal histological section of the developing foot showing the anatomical localization of the human heel fat pad (HHFP) (CRL 177 mm; 19 GW). The calcaneus and overlying skin are identified. The inset highlights the region of interest for HHFP development. Scale bar: 100 μm.

ALT Fig. 1. DEL1 is highly expressed and secreted during osteoclast differentiation.

ALT Fig. 6. Proposed model of the IHH signaling pathway modulation by RAB23-GDP, -GTP and -Resveratrol molecular interactions. The rendered images represent the functional state of RAB23 protein (active or inactive) according of molecular docking with GDP, GTP and Resveratrol, and its impact in the IHH gene transcription (promotion or inhibition) induced by GLI1 transcription factor, in l-PDLCs cultivated in osteogenic medium with and without resveratrol pretreatment (OM and OM/RESV groups, respectively).

ALT Call for papers! Submit to the Splicing in Development and Disease special issue by June 30, 2026.

ALT Fig. 2. Roles of SRSF3 in RNA metabolism. SRSF3 (magenta) contributes to alternative RNA splicing, binding to m6A modifications, transcription termination, polyadenylation, transcript stability, nuclear export and miRNA biogenesis. Pol II, RNA polymerase II; YTHDC1, YTH domain-containing protein 1; NEXT, nuclear exosome targeting complex; NXF1, nuclear RNA export factor 1.

ALT Fig. 1. The core mechanisms of NNMT-mediated fibrosis: NAD depletion, methylation imbalance, inflammation, and oxidative stress NAD+, Nicotinamide adenine dinucleotide; MAPK, Mitogen-activated protein kinase; SAH, S-adenosyl-L-homocysteine; SAA, Serum amyloid A; NAM, Nicotinamide; ROS, Reactive oxygen species; SAM, S-Adenosylmethionine; NNMT, Nicotinamide N-methyltransferase; MNA, 1-Methylnicotinamide; Hcy, Homocysteine; PARPs, Poly (ADP-ribose) polymerases.

ALT Fig. 3. Differentiation strategies employed for brown adipocyte induction from human stem cells. (A) Schematic representation of genetic factors and their mode of modulation (overexpression or knockdown) across different cell sources, indicating whether each manipulation enhanced or reduced brown adipocyte differentiation. (B) Diagrammatic summary of non-genetic factors applied to various human cell sources, depicting the range of stimuli such as growth factors, small molecules, hormones, phytochemicals, and physiological or developmental cues reported to promote brown adipocyte differentiation.

ALT Fig. 1. | Generation of scBAP1, sh1BAP1, sh2BAP1 stable cell lines and differentiation into neuronal progenitor cells (a) Post lentiviral transduction of human embryonic stem cells (hESCs) with scBAP1, sh1BAP1 and sh2BAP1 lentiviruses, was verified by enhanced green fluorescence protein (EGFP) at day 4, in absence of doxycycline (Dox-). DAPI (blue) was used to stain the nucleus. (Magnification: 20X)

ALT Fig. 1. Basal characterization of the epigenetic mark H3K27me3, the epigenetic enzymes associated with H3K27me3 levels and key osteogenic genes.

ALT Fig. 2. Characterization of bone fragments A. Representative H&E stained section of bone fragment showing abundant adipocytes in the bone marrow next to mineralized bone with osteocytes. Bar = 100 μm. B. Representative histological slides of BGLAP (Bone Gamma-Carboxyglutamate Protein) immunoreactivity in human bone samples. The black arrows point out the presence of lining osteoblasts expressing BGLAP. Bar = 50 μm.

ALT Fig. 1. Creation of three new embryonic mouse PTA-based population averages and matching atlases. (A) Sagittal view of E12.5 population average created from 11 wild type embryos at a voxel size of 7 μm3, (B) E15.5 population average created from 32 wild type embryos at voxel size of 14 μm3, (C) E17.5 population average created from 22 wild type embryos at voxel size of 14 μm3 which was resized to 28 μm3. (D–F) Corresponding atlases at (D) E12.5 with 43 labels, at (E) E15.5 with 47 labels and at (F) E17.5 with 46 labels. Only a subset of labels are shown for illustrative purposes. Scale bar = 2 mm.

ALT Fig. 3. Her9 mutants display pigmentation defects. A-B′) Lateral (A-B) and dorsal (A′-B′) views of melanophore patterning in WT/heterozygous and her9 mutant larvae at 6 dpf. Black arrowheads, dorsal stripe; green arrowheads, lateral stripe; blue arrowheads, ventral stripe; red arrowheads, yolk stripe; SB, swim bladder. C-D) H&E staining of WT/heterozygous and her9 mutant retina at 7 dpf; the retinal pigmented epithelium (RPE) is indicated with a white arrow. E-F′) Xanothophore (xan) and iridophore (ir) patterning in WT/heterozygous and her9 mutant larvae. Her9 mutants have reduced abundance of iridiphores (asterisks) and greater spread of xanthophores (yellow) than WT or heterozygous siblings. G-I′) Dorsal view of iridiphores and melanophores on the heads of WT/heterozygous and her9 mutant larvae.

ALT "Type H vessels in osteogenesis, homeostasis, and related disorders," by Xiaoru Qin et al. Fig. 1. Vascular distributions in long bones. Type H vessels are located in the metaphysis and along the periosteal and endosteal surface, whereas type L vessels are located in the diaphysis's bone marrow cavity. Secretion of PDGFA, PDGFB, TGF-β1, TGF-β3, and FGF1 from type H ECs is significantly higher than that from type L ECs. More RUNX2+ and OSX+ osteoprogenitors and osteoblasts surround type H vessels.

ALT Fig. 9. Immunofluorescence staining for MyoD at passage 15th, Scale bar: 100 μm. (A) Cells stained with MyoD (Red fluorescence); (B) Cells stained with DAPI; (C) Merged (MyoD & DAPI).

ALT Call for Papers! Submit to the Splicing in Development and Disease special issue

ALT Fig. 3. Histological analysis of TMJ in fetal mice from the experimental and control groups at postnatal weeks 1–3 using H&E and Masson's trichrome staining. B: Masson's trichrome staining; red dashed lines indicate the boundary between the chondrocyte layer and prechondrocyte layer, while yellow dashed lines indicate the boundary between the chondrocyte layer and hypertrophic chondrocyte layer. (N = 6. Scale bar = 100 μm)

ALT Fig. 1. Conservation of zinc finger domains of Osr1 and Osr2 in vertebrates. (A) Amino acid sequence alignment of Osr1 using MafftWS sequence alignment reveals high conservation of the zinc finger binding domains. B) Amino acid sequence alignment of Osr2 using MafftWS sequence alignment reveals high conservation of zinc fingers 1–3 in all species. Zinc fingers 4 and 5 are only conserved in chick, mouse, and humans. Zinc finger domains 1–3 and 4–5 are indicated by red and purple bars, respectively, shown above the amino acid sequence of interest. OSR2B, the alternatively spliced protein product has only been identified in mammals and was therefore omitted from the protein conservation analysis. Conservation is depicted below the corresponding amino acid sequence.

ALT Fig. 1. Illustration of the triad system in tissue engineering, representing the interaction between cell types, scaffolds, and external factors.

ALT Fig. 2. Interconnection between gut and oral microbiota in regulating bone and immune function. Dysbiosis in either site contributes to systemic and local inflammatory responses, influencing bone remodelling and promoting diseases such as periodontitis and osteoporosis through immune signalling pathways.

ALT Graphical abstract

ALT Graphical abstract

ALT Fig. 5. Dmxl1 embryos show no signs of craniofacial dysmorphism or micrognathia. (A–H) Skeletal preparations to highlight craniofacial structures (A–D) and dissociated mandibles at E18.5 (E–H).

ALT Fig. 2. Dermal bone mineralization was not generally accelerated in fam20b−/− embryos.

ALT Screenshot of presentation titled "Enteric neural crest development in Astyanax mexicanus surface fish and cavefish"

ALT Biological Differentiation Across the Scales • November 14, 2025, at 12:00 p.m. Central • Register Now

ALT Fig. 2. According to the traditional concept of mesenchyme, during embryonic development, mesenchymal-like tissues form through EMT from epithelial-shaped tissues in two major steps at the early stages of gastrulation. Specifically, the primary mesenchyme originates from the epiblast to form mesoderm and primitive endoderm; this process is regarded as the prototype of EMT. Subsequently, the mesoderm reverts to an epithelial morphology to generate transient embryonic structures, including somites, which then undergo a further round of EMT to generate secondary mesenchyme. Secondary mesenchyme is considered the embryonic connective tissue and provides the precursors of the connective tissues of the adult body.

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ALT September/October cover of Differentiation. Fluorescence micrograph of Drosophila melanogaster testis tip. Merged testis image displays DAPI (yellow), anti-Mettl3 (cyan) and anti-Vasa (magenta) stains. Nuclear DAPI stain in combination with antibody against m6A methyltransferase Mettl3 and germline marker Vasa, indicates localization pattern of methyltransferase in cells of the apical tip during spermatogenesis.

ALT Fig. 3. The most effective MSC exosomes-derived microRNAs applied for therapeutic approaches.

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ALT Fig. 3. Effects of OPG on localization of CD44, CD47, DC-STAMP, ATP6V0D2 and Connexin43 in fusing OCs and precursors. From "Exploring the impact of osteoprotegerin on osteoclast and precursor fusion: Mechanisms and modulation by ATP," by Yunwen Peng et al.

ALT Fig. 6. WNT5b mediates the Pi-induced suppression of OS cells migration. (A) Transwell assay was performed to evaluate the migration ability of NOS-10 (5 days) and SJSA-1 (10 days) cells with knock-down of WNT5b by siRNAs treated with osteogenic supplement medium. The analyses were performed at 24 h after seeding the cells into the culture inserts (n = 4). Scale bar = 500 μm.

ALT Fig. 3. Histological section of the human placental bed from the late first trimester stained with pan-cytokeratin antibodies. Anchoring placental villi (V) with immunoreactive trophoblast lining are seen on the top. Numerous dissociated cytokeratin-positive extra-villous trophoblastic cells of ovoid or elongated shape are seen invading the underlying decidua (bottom). These cells arise from the solid trophoblastic columns that anchor the placental villi to the endometrium (arrows) through an epithelial-mesenchymal transition (EMT) process.

ALT Fig. 5. PI3K inhibitor reduced the levels of p-AKT protein and the macrophage marker CD11b in macrophages differentiated from THP-1 cells. (A) PI3K inhibitor LY294002 reduced the levels of p-AKT protein in PMA-induced THP-1 cells. Negative control and NONO K.D. THP-1 cells were treated with 10 μM LY294002 dissolved in DMSO or an equal volume of DMSO (solvent control) for 30 min, followed by the addition of 100 ng/mL PMA for 48 h. The expression of AKT and p-AKT proteins were then detected using Western blotting. β-actin was used as a loading control. The experiment was repeated three times.

ALT Fig. 2. Role of alternative splice in palate development.

ALT Fig. 7. Representative histological staining grid using Alizarin red, Collagen X and Von Kossa following osteogenic differentiation.

ALT Fig. 7. Atg13 knockdown in vivo enhanced the role of sirolimus in alleviating bone loss in OVX mice. OVX-operated female mice were treated with sirolimus (10 mg/kg, orally, 5 times/week) along with Cont-shRNA-AAVs or Atg13-shRNA-AAVs (5 × 1010 PFU/mL, marrow-cavity injection) for 45 days. (A) Representative 3D micro-CT reconstructed images of the tibiae from each group. Scale bar, 1 mm. (B) Representative H&E-stained tibial sections from each group. Scale bar, 20 μm. (C) LC3-puncta formation in bone marrow RANK+ CSF1R+ cells sorted by FACS was evaluated via immunofluorescence staining. Representative images of LC3 puncta, including single and merged fluorescence, were obtained under a fluorescent microscope. Scale bar, 25 μm.

ALT Fig. 2. WNT7A gene expression in vertebrates. C, Section radioactive in situ hybridization of transverse section of CS (Carnegie Stage) 15 human embryo showing WNT7A expression in the telencephalon and spinal cord. D, Section radioactive in situ hybridization of coronal section of E12.5 mouse embryo showing Wnt7a expression (red) in the forebrain.

ALT Fig. 4. Timeline of key discoveries and progress of piRNA.

ALT Fig. 5. Osteogenesis imperfecta observed in X-rays of patients homozygous for WNT1 loss of function alleles. A) Limb fracture. B) Vertebral compression and deformation. C) Severe leg deformities.

ALT Fluorescence micrographs of testes stained with DAPI (blue), anti-Mettl3 (red) and anti-Vasa (green), as well as merged images”. A-A‴) control testis (UAS Mettl3 RNAi) (n = 19). B-B‴) nos-Gal4 knockdown testis (n = 18). C-C‴) bam-Gal4 knockdown testis (n = 14). Vasa stains spermatogonia and spermatocytes. Asterisk denotes hub. Scale bars indicate 25 μm.