Reference Report

Reference
Citation	Begemann, G., Michon, A.M., van der Voorn, L., Wepf, R., Mlodzik, M. (1995). The Drosophila orphan nuclear receptor Seven-up requires the Ras pathway for its function in photoreceptor determination. Development 121(1): 225--235. (Export to RIS)
FlyBase ID	FBrf0076133
Publication Type	Research paper
PubMed ID	7867504
PubMed Abstract	The Drosophila seven-up (svp) gene specifies outer photoreceptor cell fate in eye development and encodes an orphan nuclear receptor with two isoforms. Transient expression under the sevenless enhancer of either svp isoform leads to a dosage-dependent transformation of cone cells into R7 photoreceptors, and at a lower frequency, R7 cells into outer photoreceptors. To investigate the cellular pathways involved, we have taken advantage of the dosage sensitivity and screened for genes that modify this svp-induced phenotype. We show that an active Ras pathway is essential for the function of both Svp isoforms. Loss-of-function mutations in components of the Ras signal transduction cascade act as dominant suppressors of the cone cell transformation, whilst loss-of-function mutations in negative regulators of Ras-activity act as dominant enhancers. Furthermore, Svp-mediated transformation of cone cells to outer photoreceptors, reminiscent of its wild-type function in specifying R3/4 and R1/6 identity, requires an activated Ras pathway in the same cells, or alternatively dramatic increase in ectopic Svp protein levels. Our results indicate that svp is only fully functional in conjunction with activated Ras. Since we find that mutations in the Egf-receptor are also among the strongest suppressors of svp-mediated cone cell transformation, we propose that the Ras activity in cone cells is due to low level Egfr signaling. Several models that could account for the observed svp regulation by the Ras pathway are discussed.
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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 (9)
	Df(2L)ast2 Df(2R)rl10a Df(2R)trix Df(3L)gilΔ4 Df(3R)by10 Df(3R)by62 Df(3R)Espl4 Df(3R)p13 Tp(3;2)by62
Alleles (55)
	aop^A141 aop^yan-1 aos^A254Δ15 Cdc37^e1E csw^Esev1A-eOP drk^E(sev)2B E(sev)3D^e0Q Ecol\lacZ^klg-H214 Ecol\lacZ^svp-07842 Egfr^E3 Egfr^f11 Egfr^t1 faf^BX4 gl² gl³ Hsp83^e1D Jra^{bZIP.hs.sev.T:Ivir\HA1} mam³³ N^55e11 phl::tor^12D.hs.sev phl¹ phl⁷ phyl^odin3G6 phyl^odin17L1 pnt^Δ88 Ras85D^e2F Ras85D^V12.sev RasGAP1^rI533 rho⁶ rl¹⁰ rl^10a rl^Sem ro¹ ro^x63 ry^+t7.2 S^KP347 sca^BP2 sev^{S11.T:Hsap\MYC} sina¹ sina² sina³ sina⁴ sina⁵ sina⁶ sina^P21 so¹ Sos^e4G Sos^JC2 spi¹ svp^1.sev svp¹ svp^2.sev svp³ svp⁰⁷⁸⁴² usp³
Constructs (5)
	P{sE-jun^bZip} P{sE-raf^torY9} P{sevRas1.V12} P{sev-svp1} P{sev-svp2}
Genes (39)
	aop aos ato Cdc37 csw Dl drk E(sev)3D Ecol\lacZ Egfr faf gl Hsp83 Jra klg mam N phl phl::tor phyl pnt Ras85D RasGAP1 rho rl ro ry S sca sev sina so Sos spi svp T:Hsap\MYC T:Ivir\HA1 tor usp
Insertions (2)
	P{HZ}klg^H214 P{PZ}svp⁰⁷⁸⁴²