Reference Report

Reference
Citation	Qian, L., Liu, J., Bodmer, R. (2005). Neuromancer Tbx20-related genes (H15/midline) promote cell fate specification and morphogenesis of the Drosophila heart. Dev. Biol. 279(2): 509--524. (Export to RIS)
FlyBase ID	FBrf0183861
Publication Type	Research paper
PubMed ID	15733676
PubMed Abstract	The Tbx family of transcription factors are prominently expressed in the early cardiac primordium throughout the animal kingdom. Mutations in Tbx genes result invariably in defective formation and function of the heart, including congenital heart disease in humans. Similar to their vertebrate counterpart, the Drosophila Tbx20 gene pair, neuromancer1 (nmr1, FlyBase:H15) and neuromancer2 (nmr2, Flybase:mid), exhibits a dynamic expression pattern, including in all contractile myocardial cells. Deletion mutants of nmr1 combined with mesoderm-specific knock-down of nmr2 exhibit phenotypes that suggest nmr is critical for correct specification of the cardiac progenitor populations as well as for morphogenesis and assembly of the contractile heart tube. Loss-of-nmr-function causes a switch in cell fates in the cardiogenic region, in that the progenitors expressing the homeobox gene even skipped (eve) are expanded accompanied by a corresponding reduction of the progenitors expressing the homeobox gene ladybird (lbe). As a result, the number of differentiating myocardial cells is severely reduced whereas pericardial cell populations are expanded. Conversely, pan-mesodermal expression of nmr represses eve, while causing an expansion of cardiac lbe expression, as well as ectopic mesodermal expression of the homeobox gene tinman. In addition, nmr mutants with less severe penetrance exhibit cell alignment defects of the myocardium at the dorsal midline, suggesting nmr is also required for cell polarity acquisition of the heart tube. In exploring the regulation of nmr, we find that the GATA factor Pannier is essential for cardiac expression, and acts synergistically with Tinman in promoting nmr expression. Moreover, reducing nmr function in the absence of pannier further aggravates the deficit in cardiac mesoderm specification. Taken together, the data suggest that nmr acts both in concert with and subsequent to pannier and tinman in cardiac specification and differentiation. We propose that nmr is another determinant of cardiogenesis, along with tinman and pannier.
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Language of Publication	English
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Publication Type	Journal
Abbreviation	Dev. Biol.
Title	Developmental Biology
Publication Year	1959-
ISBN/ISSN	0012-1606
Data from Reference
Aberrations (1)
	Df(2R)520
Alleles (16)
	Ecol\lacZ^H15-H-15 eve^Scer\UAS.cBa H15^nmr-210 H15^nmr-614 H15^Scer\UAS.cQa mid^{dsRNA.Scer\UAS} mid^Scer\UAS.cQb pnr^Scer\UAS.cHa pnr^VX6 Scer\GAL4^da.G32 Scer\GAL4^how-24B Scer\GAL4^tin.CΔ4 Scer\GAL4^twi.PG tin³⁴⁶ tin^Scer\UAS.cRa w^+mC
Constructs (9)
	P{GAL4-da.G32} P{GAL4-twi.G} P{tinC-Gal4.Δ4} P{UAS-eve.B} P{UAS-H15.Q} P{UAS-mid.dsRNA} P{UAS-mid.Q} P{UAS-pnr.H} P{UAS-tin.R}
Genes (17)
	Dg dlg1 Ecol\lacZ en eve H15 His3 lbe Mef2 mid odd pnr Scer\GAL4 tin w wg α-Spec
Insertions (2)
	P{GawB}how^24B P{PZ}H-15