Reference Report

Reference
Citation	Yu, K., Sturtevant, M.A., Biehs, B., Francois, V., Padgett, R.W., Blackman, R.K., Bier, E. (1996). The Drosophila decapentaplegic and short gastrulation genes function antagonistically during adult wing vein development. Development 122(12): 4033--4044. (Export to RIS)
FlyBase ID	FBrf0091302
Publication Type	Research paper
PubMed ID	9012523
PubMed Abstract	TGF-beta-related signaling pathways play diverse roles during vertebrate and invertebrate development. A common mechanism for regulating the activity of TGF-beta family members is inhibition by extracellular antagonists. Recently, the Drosophila short gastrulation (sog) gene was shown to encode a predicted diffusible factor which antagonizes signaling mediated by the TGF-beta-like Decapentaplegic (Dpp) pathway in the early blastoderm embryo. sog and dpp, which are among the earliest zygotic genes to be activated, are expressed in complementary dorsal-ventral domains. The opposing actions of sog and dpp in the early embryo have been highly conserved during evolution as their vertebrate counterparts, chordin and BMP-4, function homologously to define neural versus non-neural ectoderm in Xenopus. Here we exploit the genetically sensitive adult wing vein pattern to investigate the generality of the antagonistic relationship between sog and dpp. We show that dpp is expressed in vein primordia during pupal wing development and functions to promote vein formation. In contrast, sog is expressed in complementary intervein cells and suppresses vein formation. sog and dpp function during the same phenocritical periods (i.e. 16-28 hours after pupariation) to influence the vein versus intervein cell fate choice. The conflicting activities of dpp and sog are also revealed by antagonistic dosage-sensitive interactions between these two genes during vein development. Analysis of vein and intervein marker expression in dpp and sog mutant wings suggests that dpp promotes vein fates indirectly by activating the vein gene rhomboid (rho), and that sog functions by blocking an autoactivating Dpp feedback loop. These data support the view that Sog is a dedicated Dpp antagonist.
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Language of Publication	English
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Publication Type	Journal
Abbreviation	Development
Title	Development
Publication Year	1987-
ISBN/ISSN	0950-1991
Data from Reference
Aberrations (1)
	Dp(1;Y)sog⁺
Alleles (25)
	dpp^BP.hs dpp^s1 Dys^det-1 rho^Mod rho^Stg Scer\GAL4^32B Scer\GAL4^69B sog⁶ sog^EP2 sog^EP3 sog^EP4 sog^EP5 sog^EP6 sog^EP7 sog^EP8 sog^EP9 sog^EP10 sog^EP11 sog^EP12 sog^EP13 sog^hs.PY sog^P1 sog^Scer\UAS.cYa tkv^unspecified w^+mC
Constructs (4)
	P{hs-dpp.BP} P{HS-rho} P{HS-sog} P{UAS-sog.Y}
Genes (7)
	dpp Dys rho Scer\GAL4 sog tkv w
Insertions (17)
	P{GawB}32B P{GawB}69B P{HS-rho}Mod P{HS-rho}Stg P{HS-sog}EP1 P{HS-sog}EP2 P{HS-sog}EP3 P{HS-sog}EP4 P{HS-sog}EP5 P{HS-sog}EP6 P{HS-sog}EP7 P{HS-sog}EP8 P{HS-sog}EP9 P{HS-sog}EP10 P{HS-sog}EP11 P{HS-sog}EP12 P{HS-sog}EP13