Him is regulated by Tin to suppress cardiogenic cell fate.
| Autor: | Ming-Wei Kuo, 郭明偉 |
|---|---|
| Rok vydání: | 2008 |
| Druh dokumentu: | 學位論文 ; thesis |
| Popis: | 96 The homeobox containing gene, tinman (tin) plays a pivotal role in heart development as well as cardiac function of Drosophila. Loss of tin function during embryogenesis, leads to the abolishment of heart precursor cells and the mature heart. However, depleting the function of tin at late embryogenesis, the heart formed initially, but lack of various cardial cell types. Thus, the heart can not perform normal physiological function. This suggests that tin is required early for the specification of cardial precursors, lately for the diversification of cardial cell and function. It is generally believed that tin can not act alone in all aspects of developing heart. It has been proposed that tin exerts its function by activating down-stream genes or acting synergistically with other genes to fulfill its role for the formation of functional heart in Drosophila. In this study, we have identified a cardiogenic gene, Him, that may act downstream of tin. Like tin, Him does exhibit pan-mesodermal expression pattern but its expression is later than that of tin. Later, the expressions of tin and Him are restrict in cardiac cells and pericardial cells. Comparing the dynamic expression patterns of both tin and Him, we hypothesized that Him is a downstream target of tin. Furthermore, we have found that down-regulation of Him by RNA interference promotes cardial cell fates. By contrast, mesodermally specific expression of Him suppresses cardial cell fate. This suggests that Him functions as a cardial cell suppressor. Since the both expression patterns of tin and Him are overlapped, we believed that Him may be a directed target of tin. The cardial specific enhancer of Him has been identified. Sequence analysis revealed that three tin consensus binding sites are present in the enhancer regions. The enhancer activity were down regulated in tin mutant background or when dominant negative allele of tin are co-expressed. By contrast, ectopic tin activates Him cardial enhancer. In addition, Tin can binds to the consensus binding sites in vitro. Thus, we concluded that tin is an upstream regulator of Him. |
| Databáze: | Networked Digital Library of Theses & Dissertations |
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