Anatomical and physiological characterisation of the Fgf10-deficient mice during embryonic development
- Research Opportunity
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- Royal Children’s Hospital/Murdoch Childrens Research Institute
|Associate Professor Warwick Teaguefirstname.lastname@example.org||Personal web page|
|Doctor Gulcan Sarilaemail@example.com|
Summary This study will characterise the anatomical development of the Fgf10-deficient mice during embryogenesis (embryonic day E11.5 to 18.5) using immunohistochemical staining. The project will yield key insights into the anatomy and physiology of the Fgf10-deficient mice impacting the design of new diagnostic and therapeutic options for DA.
Fibroblast Growth Factor 10 (Fgf10) is a protein coding gene, from the FGF family, known to play an important role in the regulation of embryonic development, cell differentiation and proliferation. FGF proteins bind to four Fgf receptors to initiate signalling events that mediate various biological functions in target cells, with Fgf receptor 1 and 2 (Fgfr1, -2) appearing to be the most common. In 30-50% of mice embryos with Fgf10/Fgfr2 genetic deletion results in a congenital obstruction of the duodenum known as duodenal atresia (DA). Fgf10-deficient mice also show impaired lung/trachea development, colonic atresia, absence of limb bud formation, cranio-facial anomalies and impaired wound healing. The cause of DA in humans is not known, however these findings, in addition to the genetic association of DA to trisomy 21, support a genetic aetiology for this disease. Despite numerous studies, the molecular mechanism of this genetic link still remains unclear, highlighting its unique and complex properties within different aspects of health and disease. This study will characterise the anatomical development of the Fgf10-deficient mice during embryogenesis (embryonic day E11.5 to 18.5) using immunohistochemical staining. Embryos derived from heterozygous Fgf10 mice will be embedded into paraffin and sectioned to generate a physiological atlas of the mice and to determine the presence/type of DA. We hypothesised that Fgf10-deficient mice with DA will display distinctive changes in the developmental and apoptotic signalling pathways, as well as a physical disruption of normal duodenal morphology. The project will yield key insights into the anatomy and physiology of the Fgf10-deficient mice impacting the design of new diagnostic and therapeutic options for DA.
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Research NodeRoyal Children’s Hospital/Murdoch Childrens Research Institute
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