Effect of the absence of the transcription factor hand2 on the fibronectin expression during Jaw Development of Zebrafish (Danio rerio)
In jaw development, various transcription factors contribute to the definition of cell fate and the organization of the extracellular matrix. One of these transcription factors is Hand2. Its absence in other tissue contexts has shown to affect fibronectin expression and distribution, an essential co...
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| Tipo de recurso: | tesis de maestría |
| Estado: | Versión aceptada para publicación |
| Fecha de publicación: | 2023 |
| País: | Colombia |
| Institución: | Universidad de los Andes |
| Repositorio: | Séneca: repositorio Uniandes |
| Idioma: | inglés |
| OAI Identifier: | oai:repositorio.uniandes.edu.co:1992/73873 |
| Acceso en línea: | https://hdl.handle.net/1992/73873 |
| Access Level: | acceso embargado |
| Palabra clave: | Jaw development Zebrafish Fibronectin Hand2 transcriptor factor Gene expression Biología |
| Sumario: | In jaw development, various transcription factors contribute to the definition of cell fate and the organization of the extracellular matrix. One of these transcription factors is Hand2. Its absence in other tissue contexts has shown to affect fibronectin expression and distribution, an essential component of the extracellular matrix. In fact, previous studies have shown that the absence of the transcription factor Hand2 leads to fibronectin overexpression in the heart. These changes could also affect jaw development in zebrafish (Danio rerio). However, it is not known yet if there is any effect of fibronectin misexpression during jaw development. Therefore, we are evaluating how the absence of the transcription factor Hand2 changes the fibronectin expression and distribution in the context of jaw development. Thus, we evaluate fibronectin expression in zebrafish at stages 24hpf, 36hpf, 48hpf, 72hpf by RT-PCR. We are also evaluating through in situ hybridization other markers like pitx2 and notch2 to identify the expression patterns in hand2 loss-of-function mutant embryos and their wild-type siblings. Our results will help us to understand some of the causes of mandibular defects such as those produced in the Apert and Sturge- Weber syndromes caused by alterations in the expression of hand2 in its role regulating fibronectin protein expression. |
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