ArticleFrontiers in cell and developmental biology2026
Actin disruption is associated with altered YAP/TAZ-responsive transcription and reduced migration during palatal shelf elevation.
Article in Frontiers in cell and developmental biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Palatal shelf elevation requires coordinated mesenchymal remodeling, but the relationship between actin organization, mechanosensitive transcription, and mesenchymal motility remains incompletely defined. This study examined how actin disruption relates to YAP/TAZ-responsive transcription and palatal mesenchymal behavior. Methods: Primary mouse embryonic palatal mesenchymal cells and E13.5 palate organ cultures were treated with latrunculin A (Lat-A). Actin organization, YAP localization, wound closure, and palatal shelf orientation were assessed. GA-017, a LATS1/2 inhibitor that can activate both YAP and TAZ, was used to examine responses in the Lat-A background. RNA sequencing and reanalysis of public single-cell multiomic and spatial transcriptomic datasets characterized the associated transcriptional programs. Results: Lat-A disrupted filamentous actin, reduced wound closure, and altered YAP localization. Reduced wound closure persisted in the presence of mitomycin. GA-017 partially opposed the Lat-A-associated changes in wound closure and transcription. RNA sequencing identified 674 genes with opposite-direction changes in the Lat-A-versus-control and Lat-A-plus-GA-017-versus-Lat-A comparisons, including Ccn1, Ccn2, Ankrd1, and Amotl2. In organ culture, Lat-A was associated with reduced F-actin, YAP, CCN1, and CCN2 signals and abnormal palatal shelf orientation. Public datasets provided complementary evidence for the developmental expression and spatial overlap of YAP/TEAD-, CCN-, actin-, and migration-related programs. Discussion: These findings link actin disruption to altered LATS-sensitive YAP/TAZ-responsive transcription and reduced palatal mesenchymal wound closure during palatal elevation. CCN1 and CCN2 are candidate components of this response.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.