New release: FGF signalling orchestrates multiple roles during salivary gland branching morphogenesis
May 26th, 2026
A new bulk RNA-seq dataset from King’s College London is now available in FaceBase!
Contributors: Abigail S. Tucker, Marta Perera, Joshua Brickman (King’s College London)
Description:
This study examined the role of the fibroblast growth factor (FGF) signalling pathway during branching morphogenesis in the murine embryonic submandibular salivary gland. The data compare pharmacological FGFR inhibition with conditional deletion of Fgfr2 (K14Cre;Fgfr2fl) from E13.5 +48 hours, revealing a multitude of roles for FGF signalling — including effects on fate decisions and tissue interactions. The dataset includes bulk RNA-Seq fastq files and the related counts matrix.
FaceBase Dataset:
Joshua Brickman, Abigail S. Tucker, Marta Perera. FGF signalling orchestrates multiple roles during salivary gland branching morphogenesis. FaceBase Consortium https://doi.org/10.25550/AH-J1XR (2026).
Image: Salivary gland stained with BrdU (proliferative cells, magenta) and DAPI (cyan). Image courtesy of Marta Perera.
New release: Amelogenin phosphorylation affects key regulatory genes in the enamel organ
April 30th, 2026A new amelogenin dataset is now available on FaceBase!
Contributors: Elia Beniash, Henry Margolis at the University of Pittsburgh (University of Pittsburgh)
Description:
Amelogenin (AMELX) is the predominant enamel matrix protein and has a single phosphorylation site at Serine 16 (S16), which enhances its ability to stabilize amorphous calcium phosphate in vitro. To investigate the in vivo role of AMELX phosphorylation, a knock-in mouse model (AmelxS16A) was generated in which S16 is substituted with Alanine to prevent phosphorylation. KI enamel is hypoplastic, lacks enamel rods, and features multiple ectopic calcifications; KI ameloblasts also lack Tomes’ processes and show progressive cell pathologies.
To characterize these effects comprehensively, single-cell RNA sequencing was performed on incisal enamel organs from WT and KI mice. 624 genes were differentially expressed across total enamel organ cell populations. Notably, Shh was downregulated 5.1-fold and Wnt5a was upregulated 8.1-fold in KI secretory ameloblasts compared to WT. Ten distinct cell populations were identified, with secretory ameloblasts showing the greatest transcriptomic impact, indicating that AMELX phosphorylation influences not only extracellular enamel matrix processes but also key intracellular pathways governing ameloblast biology.
FaceBase Dataset:
Elia Beniash, Henry Margolis. Amelogenin phosphorylation affects key regulatory genes in the enamel organ. FaceBase Consortium https://doi.org/10.25550/AF-V3VC (2026).
New release: Mandible vs tongue involvement in cleft palate in mouse models
April 22nd, 2026A new dataset is now available on FaceBase from Goodwin, Green, and colleagues at the University of Pittsburgh. Their study examines the respective contributions of mandibular hypoplasia and tongue malposition to cleft palate in Pierre Robin sequence (PRS), using two complementary mouse models. A related manuscript has been accepted for publication in the Journal of Dental Research.
Comparison of palate outcomes in the Sox9fl/fl;mtHand2Cre Pierre Robin sequence model (left) and the DTA/+;mtHand2Cre micrognathia/microglossia model (right). Image courtesy of Alice Fitzgerald Goodwin.
Contributors: Alice Fitzgerald Goodwin, Jeremy Green (University of Pittsburgh)
Description:
To investigate cleft palate in Pierre Robin sequence (PRS), we generated a mouse model with Sox9 deleted specifically in the mandibular mesenchyme (Sox9fl/fl;mtHand2Cre), which resulted in mandibular hypoplasia and retrognathia, palatal shelf elevation delay, and fully penetrant cleft of the secondary palate. To determine the relative contributions of mandible vs tongue malposition to cleft palate in PRS, we generated a micrognathia and microglossia model (DTA/+;mtHand2Cre). The majority of these animals had a normally formed palate, suggesting that tongue obstruction of palatal shelf elevation is the primary contributor to cleft palate in PRS.
Data deposited on FaceBase include microCT scans of Sox9fl/fl;mtHand2Cre and control embryos at E18.5; H&E-stained coronal sections at E12.5, E13.5, E14.5, and E16.5; proliferation and apoptosis assays at E12.5 and E14.5 in the Meckel’s cartilage; immunofluorescence with antibodies against Pax7 and MHC at E14.5; RNAscope with probes against osteogenic markers at E14.5; palatal shelf explant studies at E13.5; and H&E staining and TUNEL apoptosis staining of DTA/+;mtHand2Cre and control embryos.
FaceBase Dataset:
Alice Fitzgerald Goodwin, Jeremy Green. Mandible vs tongue involvement in cleft palate in mouse models. FaceBase Consortium https://doi.org/10.25550/AB-SJQA (2026).
Publication:
Alice Fitzgerald Goodwin, Jeremy Green; Intrinsic tension drives palatal shelf reorientation post tongue retraction. Journal of Dental Research 2026. (accepted April 21, 2026 — DOI to be added upon publication)
New release: Six2 and CTCF ChIP-seq datasets of wildtype mouse embryonic facial tissues (E10.5 - E13.5)
April 16th, 2026New ChIP-seq datasets are now available in FaceBase, profiling Six2 transcription factor binding and CTCF-defined topologically associating domains in wildtype mouse embryonic facial tissues at stages E10.5 through E13.5. Input libraries are included as controls. Together these data support investigation of gene regulatory networks and chromatin architecture during craniofacial morphogenesis.
Contributors: Jingyue Xu, Han Liu and Rulang Jiang (Cincinnati Children’s Hospital, Medical Center)
Description:
We performed a ChIP-seq assay using a Six2 antibody to identify endogenous Six2-binding genomic loci in mouse embryonic facial tissues. We performed a ChIPseq assay using the CTCF antibody to identify topologically associating domains and boundaries. We generated ChIP libraries and sent them for next-generation sequencing. We also generated input libraries as control samples.
FaceBase Dataset:
Jingyue Xu, Han Liu, Rulang Jiang. Six2 and CTCF ChIP-seq datasets of wildtype mouse embryonic facial tissues (E10.5 - E13.5). FaceBase Consortium https://doi.org/10.25550/7Z-41CW (2026).
New release: Phenotypic impacts of embryonic exposure to the CSF1R inhibitor PLX5622 on craniofacial development
April 9th, 2026A new dataset is now available on FaceBase from Ma, Rosin, and colleagues at The University of British Columbia. Their study examines how disrupting CSF1R signaling, which is critical for macrophage and osteoclast development, affects craniofacial morphogenesis during embryonic development. A related manuscript is released on Development.
Control (left) and PLX5622-exposed (right) mouse crania stained for bone (red) and cartilage (blue), revealing craniofacial structural disruptions following prenatal CSF1R inhibition. Image courtesy of Felix Ma and Jessica M. Rosin.
PI: Jessica M. Rosin (the University of British Columbia)
Description:
Despite a wealth of knowledge on the mechanisms underlying craniofacial morphogenesis during gestation, the roles of fetal macrophages and osteoclasts during this process remain less well characterized. Here, we used the pharmacological inhibitor PLX5622 to disrupt colony stimulating factor-1 receptor (CSF1R) signaling, which is essential for macrophage and osteoclast proliferation, differentiation, and survival. Prenatal PLX5622 exposure resulted in ∼50% depletion of CSF1R+ macrophages, with complete loss of osteoclasts. While there were no notable changes in craniofacial nerve or muscle development, prenatal exposure to PLX5622 resulted in skull doming and cranial suture impairments, in addition to disruptions to development of the premaxilla, mandible, ear ossicles, palate, and cranial base. In response to PLX5622 exposure, cytokine and chemokine signaling was altered and neural crest proliferation was impaired. Our data also highlight sex- and strain-specific differences in PLX5622 phenotypes and together demonstrate that CSF1R+ macrophages and osteoclasts are essential for craniofacial morphogenesis.
Data deposited on FaceBase include images of control and PLX5622-exposed whole-mount E11.5, E12.5, and E13.5 nerve (2H3) and muscle (MF 20) antibody staining and P1 skeletal staining.
FaceBase Dataset:
Felix Ma, Jessica M. Rosin. Phenotypic impacts of embryonic exposure to the CSF1R inhibitor PLX5622 on craniofacial development. FaceBase Consortium https://doi.org/10.25550/A9-12PJ (2026).
Publication:
Felix Ma, Rose Ru Jing Zhou, Matthew Rosin, Iris Zhou, Sabrina Ownsworth, Rouzbeh Ostadsharif Memar, Vincent B. Wong, Jessica M. Rosin; CSF1R+ macrophage and osteoclast depletion impairs neural crest proliferation and craniofacial morphogenesis. Development 2026; dev.205423. doi: https://doi.org/10.1242/dev.205423