Abstract
The zebrafish ventricular myosin heavy chain (vmhc) gene exhibits restricted expression in the ventricle. However, the molecular mechanism underlying this chamber-specific expression is unclear. Here, we exploited both transient and transgenic technologies to dissect the zebrafish vmhc promoter. We demonstrated that a combination of two transient assays in this animal model quickly identified chamber-specific cis-elements, isolating a 2.2 kb fragment upstream from the vmhc gene that can drive ventricle-specific expression. Furthermore, deletion analysis identified multiple cis-elements that exhibited cardiac-specific expression. To achieve chamber specificity, a distal element was required to coordinate with and suppress a proximal enhancer element. Finally, we discovered that Nkx2.5-binding sites (NKE) were essential for this repressive function. In summary, our study of the zebrafish vmhc promoter suggests that ventricle-specific expression is achieved through an inhibitory mechanism that suppresses expression in the atrium.
Original language | English (US) |
---|---|
Pages (from-to) | 1564-1573 |
Number of pages | 10 |
Journal | Developmental Dynamics |
Volume | 238 |
Issue number | 6 |
DOIs | |
State | Published - Jun 2009 |
Keywords
- Chamber specificity
- Promoter analysis
- Transgenic fish
- Vmhc
ASJC Scopus subject areas
- Developmental Biology