Publications by authors named "Jeffry M Cesario"
Development of the teeth requires complex signaling interactions between the mesenchyme and the epithelium mediated by multiple pathways. For example, canonical WNT signaling is essential to many aspects of odontogenesis, and inhibiting this pathway blocks tooth development at an early stage. R-spondins (RSPOs) are secreted proteins, and they mostly augment WNT signaling.
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- The calvaria, or upper part of the skull, develops from mesenchyme around the brain, with specific regions (like supra-orbital mesenchyme) promoting bone growth while others (early migrating mesenchyme) do not.
- Researchers discovered Lmx1b, a gene that acts as an anti-osteogenic factor in early migrating mesenchyme, helping to differentiate areas with varying capacities for bone development.
- Altering the expression of Lmx1b can lead to abnormal bone growth and conditions like craniosynostosis, highlighting its crucial role in the proper formation and organization of the skull.
Development of the face is regulated by a large number of genes that are expressed in temporally and spatially specific patterns. While significant progress has been made on characterizing the genes that operate in the oral region of the face, those regulating development of the aboral (lateral) region remain largely unknown. Recently, we discovered that transcription factors LIM homeobox (LHX) 6 and LHX8, which are key regulators of oral development, repressed the expression of the genes encoding forkhead box transcription factors, Foxp1 and Foxp2, in the oral region.
View Article and Find Full Text PDFOocytes segregate chromosomes in the absence of centrosomes. In this situation, the chromosomes direct spindle assembly. It is still unclear in this system which factors are required for homologous chromosome bi-orientation and spindle assembly.
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- Cleft palate is a common birth defect, and understanding its molecular genetics, specifically the roles of Lhx6 and Lhx8 genes, is crucial for science and medicine.
- In mice lacking Lhx6 and Lhx8, severe craniofacial issues arose, linked to impaired palate growth due to decreased cell proliferation, revealing the involvement of the cell cycle inhibitor p57(Kip2).
- The study demonstrates that Lhx6 and Lhx8 regulate p57(Kip2) through both direct and indirect mechanisms, highlighting a new pathway that connects cell proliferation and palate development.
Development of the mammalian face requires a large number of genes that are expressed with spatio-temporal specificity, and transcriptional regulation mediated by enhancers plays a key role in the precise control of gene expression. Using chromatin immunoprecipitation for a histone marker of active enhancers, we generated a genome-wide map of candidate enhancers from the maxillary arch (primordium for the upper jaw) of mouse embryos. Furthermore, we confirmed multiple novel craniofacial enhancers near the genes implicated in human palate defects through functional assays.
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