Abstract
The way in which spatially patterned cellular identities are generated is a central question of organogenesis. In the case of Drosophila heart formation, the cardiac progenitors are specified in precise mesodermal positions, giving rise to multiple cell types in a highly ordered arrangement. Here, we study the mechanisms by which positional information conveyed by signaling pathways and a combinatorial code of activating and repressing transcription factors work together to confine the expression of the homeobox gene even-skipped (eve) to a small region of the dorsal mesoderm. By manipulating both expression patterns and binding sites for transcription factors, we show that a complex combination of regulatory activities converge on a single enhancer of eve to generate precisely targeted gene expression within the cardiac mesoderm. In particular, ladybird early (lbe), a homeobox gene expressed adjacent to eve, restricts the positive actions of factors downstream of wingless, decapentaplegic, and ras to generate the eve pattern. Mutation of a Lbe binding site causes dramatic expansion of expression and abolishes the responsiveness to repression by lbe. Conversely, eliminating eve in the mesoderm expands lbe expression into the normal eve-expressing territory, suggesting that mutual repression between eve and lbe is essential for delineating the spatial patterns of gene expression that specify cell types within the cardiac mesoderm.
| Original language | English |
|---|---|
| Pages (from-to) | 225-240 |
| Number of pages | 16 |
| Journal | Developmental Biology |
| Volume | 252 |
| Issue number | 2 |
| DOIs | |
| Publication status | Published - 2002 Jan 1 |
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Keywords
- Cell fate
- Even-skipped
- Heart
- Repression
- TGF-β
- ladybird
- tinman
- wingless
ASJC Scopus subject areas
- Molecular Biology
- Developmental Biology
- Cell Biology
Cite this
Transcriptional integration of competence modulated by mutual repression generates cell-type specificity within the cardiogenic mesoderm. / Han, Zhe; Fujioka, Miki; Su, Ming-Tsan; Liu, Margaret; Jaynes, James B.; Bodmer, Rolf.
In: Developmental Biology, Vol. 252, No. 2, 01.01.2002, p. 225-240.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Transcriptional integration of competence modulated by mutual repression generates cell-type specificity within the cardiogenic mesoderm
AU - Han, Zhe
AU - Fujioka, Miki
AU - Su, Ming-Tsan
AU - Liu, Margaret
AU - Jaynes, James B.
AU - Bodmer, Rolf
PY - 2002/1/1
Y1 - 2002/1/1
N2 - The way in which spatially patterned cellular identities are generated is a central question of organogenesis. In the case of Drosophila heart formation, the cardiac progenitors are specified in precise mesodermal positions, giving rise to multiple cell types in a highly ordered arrangement. Here, we study the mechanisms by which positional information conveyed by signaling pathways and a combinatorial code of activating and repressing transcription factors work together to confine the expression of the homeobox gene even-skipped (eve) to a small region of the dorsal mesoderm. By manipulating both expression patterns and binding sites for transcription factors, we show that a complex combination of regulatory activities converge on a single enhancer of eve to generate precisely targeted gene expression within the cardiac mesoderm. In particular, ladybird early (lbe), a homeobox gene expressed adjacent to eve, restricts the positive actions of factors downstream of wingless, decapentaplegic, and ras to generate the eve pattern. Mutation of a Lbe binding site causes dramatic expansion of expression and abolishes the responsiveness to repression by lbe. Conversely, eliminating eve in the mesoderm expands lbe expression into the normal eve-expressing territory, suggesting that mutual repression between eve and lbe is essential for delineating the spatial patterns of gene expression that specify cell types within the cardiac mesoderm.
AB - The way in which spatially patterned cellular identities are generated is a central question of organogenesis. In the case of Drosophila heart formation, the cardiac progenitors are specified in precise mesodermal positions, giving rise to multiple cell types in a highly ordered arrangement. Here, we study the mechanisms by which positional information conveyed by signaling pathways and a combinatorial code of activating and repressing transcription factors work together to confine the expression of the homeobox gene even-skipped (eve) to a small region of the dorsal mesoderm. By manipulating both expression patterns and binding sites for transcription factors, we show that a complex combination of regulatory activities converge on a single enhancer of eve to generate precisely targeted gene expression within the cardiac mesoderm. In particular, ladybird early (lbe), a homeobox gene expressed adjacent to eve, restricts the positive actions of factors downstream of wingless, decapentaplegic, and ras to generate the eve pattern. Mutation of a Lbe binding site causes dramatic expansion of expression and abolishes the responsiveness to repression by lbe. Conversely, eliminating eve in the mesoderm expands lbe expression into the normal eve-expressing territory, suggesting that mutual repression between eve and lbe is essential for delineating the spatial patterns of gene expression that specify cell types within the cardiac mesoderm.
KW - Cell fate
KW - Even-skipped
KW - Heart
KW - Repression
KW - TGF-β
KW - ladybird
KW - tinman
KW - wingless
UR - http://www.scopus.com/inward/record.url?scp=0036937281&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0036937281&partnerID=8YFLogxK
U2 - 10.1006/dbio.2002.0846
DO - 10.1006/dbio.2002.0846
M3 - Article
C2 - 12482712
AN - SCOPUS:0036937281
VL - 252
SP - 225
EP - 240
JO - Developmental Biology
JF - Developmental Biology
SN - 0012-1606
IS - 2
ER -