Reference Report

Reference
Citation	Helms, W., Lee, H., Ammerman, M., Parks, A.L., Muskavitch, M.A., Yedvobnick, B. (1999). Engineered truncations in the Drosophila mastermind protein disrupt Notch pathway function. Dev. Biol. 215(2): 358--374. (Export to RIS)
FlyBase ID	FBrf0111904
Publication Type	Research paper
PubMed ID	10545243
PubMed Abstract	The phenotypes and genetic interactions associated with mutations in the Drosophila mastermind (mam) gene have implicated it as a component of the Notch signaling pathway. However, its function and site of action within many tissues requiring Notch signaling have not been thoroughly investigated. To address these questions, we have constructed truncated versions of the Mam protein that elicit dominant phenotypes when expressed in imaginal tissues under GAL4-UAS regulation. By several criteria, these effects appear to phenocopy loss of function for the Notch pathway. When expressed in the notum, truncated Mam results in failure of lateral inhibition within proneural clusters and perturbations in cell fate specification within the sensory organ precursor cell lineage. Expression in the wing is associated with vein thickening and margin defects, including nicking and bristle loss. The truncation-associated wing margin phenotypes are modified by mutations in Notch and Wg pathway genes and are correlated with depressed expression of wg, cut, and vg. These data support the idea that Mam truncations have lost key effector domains and therefore behave as dominant-negative proteins. Coexpression of Delta or an activated form of Notch suppresses the effects of the Mam truncation, suggesting that Mam can function upstream of ligand-receptor interaction in the Notch pathway. This system should prove useful for the investigation of the role of Mam within the Notch pathway.
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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 (3)
	C(1)DX Df(1)N-54l9 Df(3R)Espl1
Alleles (59)
	arm¹ arm^{S2.Scer\UAS.T:Hsap\MYC} arm^{S10.Scer\UAS.T:Hsap\MYC} ct^53d Dl^BX9 Dl^Scer\UAS.cJa dsh³ dsh^Scer\UAS.cAa dx¹ dx^Scer\UAS.cMa Ecol\lacZ^{Dvir\Mef2.-9894:-9094} Ecol\lacZ^Mef2.5.4 Ecol\lacZ^{Mef2.-5662:-5180} Ecol\lacZ^{Mef2.-5808:-5180} Ecol\lacZ^{Mef2.-5898:-5180} Ecol\lacZ^{Mef2.-5940:-5180} Ecol\lacZ^{Mef2.-5940:-5656} Ecol\lacZ^{Mef2.-5942:-3650} Ecol\lacZ^{Mef2.-5990:-5180} Ecol\lacZ^{Mef2.-5990:-5322} Ecol\lacZ^{Mef2.-5990:-5517} Ecol\lacZ^{Mef2.-5990:-5627} Ecol\lacZ^{Mef2.-6389:-4640} Ecol\lacZ^{Mef2.-8765:-5942} Ecol\lacZ^Mef2.mE Ecol\lacZ^{Mef2.mtin1.mtin2} Ecol\lacZ^Mef2.mtin1 Ecol\lacZ^Mef2.mtin2 Ecol\lacZ^vg.806 fz2^{ECD.GPI.Scer\UAS.T:Hsap\MYC} fz2^Scer\UAS.cCa gro^E48 H¹ H^Scer\UAS.cGa mam¹ mam¹⁰ mam^H.Scer\UAS mam^N.Scer\UAS mam^R.Scer\UAS N^{int.G.Scer\UAS} N^nd-1 pan^13a pan^Scer\UAS.cWa Scer\GAL4³⁰⁹ Scer\GAL4^bbg-C96 Scer\GAL4^dpp.blk1 Scer\GAL4^GMR.PF Scer\GAL4^hs.2sev Scer\GAL4^pnr-MD237 Ser^Bd-3 Ser^rev6-1 Ser^Scer\UAS.cGa sgg^M11 sgg^Scer\UAS.cSa Su(H)⁸ Su(H)¹⁶ Su(H)^Scer\UAS.cGa w^+mC wg^l-17
Constructs (39)
	P{arm-cmyc} P{Dvir\Mef2-lacZ} P{GAL4-dpp.blk1} P{GAL4-Hsp70.sev} P{GAL4-ninaE.GMR} P{Mef2-lacZ.2} P{Mef2-lacZ.3} P{Mef2-lacZ.4} P{Mef2-lacZ.5} P{Mef2-lacZ.6} P{Mef2-lacZ.7} P{Mef2-lacZ.8} P{Mef2-lacZ.9} P{Mef2-lacZ.10} P{Mef2-lacZ.11} P{Mef2-lacZ.12} P{Mef2-lacZ.13} P{Mef2-lacZ.mE} P{Mef2-lacZ.mtin1.mtin2} P{Mef2-lacZ.mtin1} P{Mef2-lacZ.mtin2} P{Mef2-lacZ-II} P{UAS-arm.S2} P{UAS-arm.S10} P{UAS-Dl.J} P{UAS-dsh.A} P{UAS-DxA89} P{UAS-fz2.C} P{UAS-fz2(ECD)-GPI} P{UAS-H.G} P{UAS-mamH} P{UAS-mamN} P{UAS-mamR} P{UAS-N.intra.G} P{UAS-pan.dTCF} P{UAS-Ser.G} P{UAS-sgg.S} P{UAS-Su(H).G} P{vg(806)-lacZ}
Genes (22)
	ac arm ct Dl ds dsh dx Ecol\lacZ futsch fz2 gro H mam N pan Scer\GAL4 Ser sgg Su(H) T:Hsap\MYC w wg
Insertions (4)
	P{GAL4}309 P{GawB}bbg^C96 P{GawB}pnr^MD237 P{UAS-sgg.S}310A