ArticleDevelopment (Cambridge, England)2025
Cdh2, a downstream target of Hes7, regulates somitogenesis by supporting FGF signalling.
Article in Development (Cambridge, England), 2025. 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
3 authors.
Funding
Abstract
In the segmentation clock, Hes7 expression oscillates synchronously in the presomitic mesoderm (PSM), regulating periodic somite formation. Despite intensive studies, the whole regulatory gene networks of the segmentation clock remain to be analysed. To identify the direct target genes of Hes7, we performed chromatin immunoprecipitation with sequencing analysis using an anti-Hes7 antibody and knocked out the identified genes from mouse embryonic stem cells carrying a Hes7 reporter. These cells were induced to differentiate into PSM-like tissue, and live imaging of Hes7 oscillations was conducted. Among the tested genes, Cdh2 knockout resulted in downregulation of fibroblast growth factor (FGF) signalling and premature cessation of Hes7 oscillations. Conversely, Cdh2 overexpression led to upregulation of FGF signalling and prolonged Hes7 oscillations. Whereas Cdh2 mRNA showed dynamic expression through repression by Hes7 oscillations, Cdh2 protein exhibited a rather steady gradient with higher levels in the posterior PSM and lower levels in the anterior PSM. Thus, Hes7-controlled Cdh2 regulates FGF signalling, leading to the proper maintenance of Hes7 oscillations, suggesting that the interplay between Hes7 and Cdh2 governs the timing mechanism of PSM differentiation.
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.