ArticleScientific reports2021
SPECC1L-deficient primary mouse embryonic palatal mesenchyme cells show speed and directionality defects.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Loss of SPECC1L in cranial neural crest cells results in increased hedgehog signaling and frontonasal dysplasia.bioRxiv : the preprint server for biology · 2025Article
- Genetic interaction ofbioRxiv : the preprint server for biology · 2025Article
- Novel insights into palatal shelf elevation dynamics in normal mouse embryos.Frontiers in cell and developmental biology · 2025Article
- Structure and interactions of the endogenous human Commander complex.Nature structural & molecular biology · 2024Article
- SPECC1L: a cytoskeletal protein that regulates embryonic tissue dynamics.Biochemical Society transactions · 2023Article
- Transcriptome sequencing analysis of the role of β-catenin in F-actin reorganization in embryonic palatal mesenchymal cells.Annals of translational medicine · 2022Article
- TWIST1 interacts with β/δ-catenins during neural tube development and regulates fate transition in cranial neural crest cells.Development (Cambridge, England) · 2022Article
- In-frame deletion of SPECC1L microtubule association domain results in gain-of-function phenotypes affecting embryonic tissue movement and fusion events.Human molecular genetics · 2021Article
- Isolation and Time-Lapse Imaging of Primary Mouse Embryonic Palatal Mesenchyme Cells to Analyze Collective Movement Attributes.Journal of visualized experiments : JoVE · 2021Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Cleft lip and/or palate (CL/P) are common anomalies occurring in 1/800 live-births. Pathogenic SPECC1L variants have been identified in patients with CL/P, which signifies a primary role for SPECC1L in craniofacial development. Specc1l mutant mouse embryos exhibit delayed palatal shelf elevation accompanied by epithelial defects. We now posit that the process of palate elevation is itself abnormal in Specc1l mutants, due to defective remodeling of palatal mesenchyme. To characterize the underlying cellular defect, we studied the movement of primary mouse embryonic palatal mesenchyme (MEPM) cells using live-imaging of wound-repair assays. SPECC1L-deficient MEPM cells exhibited delayed wound-repair, however, reduced cell speed only partially accounted for this delay. Interestingly, mutant MEPM cells were also defective in coordinated cell movement. Therefore, we used open-field 2D cultures of wildtype MEPM cells to show that they indeed formed cell streams at high density, which is an important attribute of collective movement. Furthermore, activation of the PI3K-AKT pathway rescued both cell speed and guidance defects in Specc1l mutant MEPM cells. Thus, we show that live-imaging of primary MEPM cells can be used to assess mesenchymal remodeling defects during palatal shelf elevation, and identify a novel role for SPECC1L in collective movement through modulation of PI3K-AKT signaling.
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