RESUMEN
The calvarial bones of the infant skull are connected by transient fibrous joints known as sutures and fontanelles, which are essential for reshaping during birth and postnatal growth. Genetic disorders such as Apert, Pfeiffer, Crouzon, and Bent bone dysplasia linked to FGFR2 variants often exhibit multi-suture craniosynostosis and a persistently open anterior fontanelle (AF). This study leverages mouse genetics and single-cell transcriptomics to determine how Fgfr2 regulates closure of the AF closure and its transformation into the frontal suture during postnatal development. We find that cells of the AF, marked by the tendon/ligament factor SCX, are spatially restricted to ecto- or endocranial domains and undergo regionally selective differentiation into ligament, bone, and cartilage. Differentiation of SCX+ AF cells is dependent on FGFR2 signaling in cells of the osteogenic fronts which, when fueled by FGF18 from the ectocranial mesenchyme, express the secreted WNT inhibitor WIF1 to regulate WNT signaling in neighboring AF cells. Upon loss of Fgfr2 , Wif1 expression is lost, and cells of the AF retain a connective tissue-like fate failing to form the posterior frontal suture. This study provides new insights into regional differences in suture development by identifying an FGF-WNT signaling circuit within the AF that links frontal bone advancement with suture joint formation.
RESUMEN
The integration of conflicting signals in response to environmental constraints is essential to efficient plant growth and development. The light-dependent and the stress hormone abscisic acid (ABA)-dependent signaling pathways play opposite roles in many aspects of plant development. While these pathways have been extensively studied, the complex nature of their molecular dialogue is still obscure. When mobilized by the Arabidopsis thaliana ß-glucosidase 1 (AtBG1), the glucose ester-conjugated inactive form of ABA has proven to be a source of the active hormone that is essential for the adaptation of the plant to water deficit, as evidenced by the impaired stomatal closure of atbg1 mutants in response to water stress. In a suppressor screen designed to identify the molecular components of AtBG1-associated physiological and developmental mechanisms, we identified the mutation variant of AtBG1 traits (vat1), a new mutant allele of the red light/far-red light photoreceptor PHYTOCHROME B (PHYB). Our study reveals that atbg1 plants harbor increased stomatal density in addition to impaired stomatal closure. We also provide evidence that the vat1/phyb mutation can restore the apparent transpiration of the atbg1 mutant by decreasing stomatal aperture and restoring a stomatal density similar to wild-type plants. Expression of key regulators of stomatal development showed a crosstalk between AtBG1-mediated ABA signaling and PHYB-mediated stomatal development. We conclude that the AtBG1-dependent regulation of ABA homeostasis and the PHYB-mediated light signaling pathways act antagonistically in the control of stomatal development.