ArticleInvestigative ophthalmology & visual science2026
Genetic Regulation of Wnt/PCP Components Through Fgf10/Fgfr2/Sox9 Module in Tear Duct Development.
Article in Investigative ophthalmology & visual science, 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
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Tear duct obstruction can lead to a range of ocular surface disorders. Although Fgf signaling has been implicated in congenital tear duct obstruction, the associated signaling networks remain incompletely understood. To better elucidate the developmental biology and molecular genetics of the tear drainage system, we investigated genetic interactions between the Fgf and Wnt/planar cell polarity (PCP) pathways. Methods: Mutant mice with disruptions of Fgf10, Fgfr2, or Sox9 were generated. Tear duct development was evaluated using immunohistochemistry and in situ hybridization with a set of molecular markers. Single-cell RNA sequencing combined with CUT&Tag analysis was used to define tear duct molecular identity and identify potential targets of the Fgf signaling pathway. A luciferase reporter assay and electrophoretic mobility shift assay (EMSA) were performed to validate Sox9 target genes. Results: Fgf10 and Fgfr2 are required for tear duct formation by controlling the proliferation and survival of tear duct progenitors. The Fgf10/Fgfr2/Sox9 module genetically regulates a subset of Wnt/PCP genes involved in embryonic tear duct elongation. In particular, we show that Sox9 binds to and activates the promoter of Prickle1, a core Wnt/PCP component previously implicated in tear duct development. Finally, Fgf signaling appears to act unidirectionally on Wnt/PCP components, as neither Fgfr2 nor Sox9 expression is altered in Prickle1 mutants. Conclusions: This study uncovers a previously unrecognized direct genetic link between Fgf signaling and Wnt/PCP pathway in tear duct formation, suggesting that Wnt/PCP components may represent potential risk factors for congenital nasolacrimal duct obstruction (CNLDO), warranting further investigation.
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.