Abstract
A series of inductive signals are necessary to subdivide the mesoderm in order to allow the formation of the progenitor cells of the heart. Mesoderm-endogenous transcription factors, such as those encoded by twist and tinman, seem to cooperate with these signals to confer correct context and competence for a cardiac cell fate. Additional factors are likely to be required for the appropriate specification of individual cell types within the forming heart. Similar to tinman, the zinc finger- and homeobox-containing gene, zfh-1, is expressed in the early mesoderm and later in the forming heart, suggesting a possible role in heart development. Here, we show that zfh-1 is specifically required for formation of the even-skipped (eve)-expressing subset of pericardial cells (EPCs), without affecting the formation of their siblings, the founders of a dorsal body wall muscle (DA1). In addition to zfh-1, mesodermal eve itself appears to be needed for correct EPC differentiation, possibly as a direct target of zfh-1. Epistasis experiments show that zfh-1 specifies EPC development independently the lineage gene that controls DA1 founder versus fate. We discuss the combinatorial control that specify the EPC cell fate in a spatially precise pattern within the embryo.
Original language | English |
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Pages (from-to) | 3241-3251 |
Number of pages | 11 |
Journal | Development |
Volume | 126 |
Issue number | 14 |
DOIs | |
Publication status | Published - 1999 Jul |
Externally published | Yes |
Keywords
- Cardiogenesis
- Cell fate
- Drosophila
- EGF receptor
- Even-skipped
- Heart
- Homeodomain
- Lineage
- Mesoderm
- Myocardium
- Myogenesis
- Notch
- Numb
- Pericardial cell
- Spitz
- Zinc finger
- zfh-1
ASJC Scopus subject areas
- Molecular Biology
- Developmental Biology