![]() PBM computes correspondences through an optimization process that seeks to minimize the information content (entropy) of the resulting shape model, thus maximizing its statistical power, relative to arbitrary descriptions of shape. In the PBM approach correspondence points, which are computed automatically, allow for a very detailed description of the geometric variability of anatomical structures, especially when that geometry is derived from high-resolution three-dimensional (3D) imaging, such as microCT. In a point-correspondence model, anatomical geometry is represented by many hundreds or thousands of landmark points called “correspondences”. PBM is a technique for examining the phenotype of a population that uses a point-correspondence model to represent homology across anatomical surfaces. The statistical shape analysis approach used in this study is called particle based-modeling (PBM). The Pax7-deficient mouse provides a model with which to test whether Pax7 deficiency is sufficient to induce antero-posterior shortening of the cranial base. The FGF signaling cascade has been shown to be necessary and sufficient to induce Pax3, but did not induce Pax7 expression after neural crest cells complete their migration towards the face 6. Dexamethasone (Dex) is commonly used in cancer treatment, but has also been shown to alter FGF signaling, repress Pax7 expression, and lead to disrupted cranial neural crest development 5. ![]() Several mouse models alter the expression of genes implicated in cartilage maturation (e.g., FGFR3), are known to cause premature fusion of cranial base sutures, antero-posterior shortening of the cranial base, reduction in the size of the foramen magnum, and impaired ossification in the frontal bone 4. However, the role of Pax7 in chondrocranium development has been largely unexplored. The Pax7-deficient mouse was later found to have a compelling defect in postnatal muscle growth 2, which was thereafter carefully clarified as a defect in postnatal muscle stem cell renewal 3, but not prenatal muscle patterning, therefore making it unlikely that Pax7 mutant craniofacial defects could be attributed to factors other than cranial patterning. 1 report no gross morphological abnormality in the neuronal derivatives of the cephalic neural crest. 1 also reported a reduced number of tubules in the serous glands of the nose, and the inferior lateral part of the nasal cavity is missing both nose phenotypes were attributed to neural crest defects. The craniofacial defects observed in Pax7-deficient mice were restricted to neural crest derived portions of the skull, and skeletal preparations showed apparently normal morphology at the cranial base sutures at P0. Disrupting both copies of Pax7 during embryogenesis resulted in underdevelopment (antero-posterior shortening) of the maxilla and lacrimal bones. ![]() Homozygous Pax7-deficient mice typically died within 2 weeks of birth. The role of Pax7 in patterning fetal craniofacial features was first described by Mansouri and colleagues 1.
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