Reference Report

Reference
Citation	Metzstein, M.M., Krasnow, M.A. (2006). Functions of the nonsense-mediated mRNA decay pathway in Drosophila development. PLoS Genet. 2(12): e180. (Export to RIS)
FlyBase ID	FBrf0194265
Publication Type	Research paper
PubMed ID	17196039
PubMed Abstract	Nonsense-mediated mRNA decay (NMD) is a cellular surveillance mechanism that degrades transcripts containing premature translation termination codons, and it also influences expression of certain wild-type transcripts. Although the biochemical mechanisms of NMD have been studied intensively, its developmental functions and importance are less clear. Here, we describe the isolation and characterization of Drosophila "photoshop" mutations, which increase expression of green fluorescent protein and other transgenes. Mapping and molecular analyses show that photoshop mutations are loss-of-function mutations in the Drosophila homologs of NMD genes Upf1, Upf2, and Smg1. We find that Upf1 and Upf2 are broadly active during development, and they are required for NMD as well as for proper expression of dozens of wild-type genes during development and for larval viability. Genetic mosaic analysis shows that Upf1 and Upf2 are required for growth and/or survival of imaginal cell clones, but this defect can be overcome if surrounding wild-type cells are eliminated. By contrast, we find that the PI3K-related kinase Smg1 potentiates but is not required for NMD or for viability, implying that the Upf1 phosphorylation cycle that is required for mammalian and Caenorhabditis elegans NMD has a more limited role during Drosophila development. Finally, we show that the SV40 3' UTR, present in many Drosophila transgenes, targets the transgenes for regulation by the NMD pathway. The results establish that the Drosophila NMD pathway is broadly active and essential for development, and one critical function of the pathway is to endow proliferating imaginal cells with a competitive growth advantage that prevents them from being overtaken by other proliferating cells.
DOI	10.1371/journal.pgen.0020180
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Language of Publication	English
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Publication Type	Journal
Abbreviation	PLoS Genet.
Title	PLoS Genetics
Publication Year	2005-
ISBN/ISSN	1553-7404 1553-7390
Data from Reference
Aberrations (2)
	Df(1)exe2B Dp(1;Y)BSC1
Alleles (29)
	Adhⁿ⁴ Avic\GFP^{+I.E.Scer\UAS.Hsp70.3'UTR} Avic\GFP^{+I.E.Scer\UAS.SV40.3'UTR.ΔI} Avic\GFP^{+I.E.Scer\UAS.SV40.3'UTR} Avic\GFP^Act5C.PR Avic\GFP^{E.Scer\UAS.Hsp70.3'UTR} Avic\GFP^{E.Scer\UAS.SV40.3'UTR.ΔI} Avic\GFP^{E.Scer\UAS.SV40.3'UTR} Avic\GFP^{S65T.I167T.Scer\UAS.T:Myr-Src64B} Avic\GFP^{Scer\UAS.P\T.fs(1)K10.3'UTR} Avic\GFP^{Scer\UAS.SV40.3'UTR} Disc\RFP^{Scer\UAS.DsRed1.SV40.3'UTR} Disc\RFP^{Scer\UAS.DsRed2.SV40.3'UTR.T:Uuuu\nls6} His2Av^{T:Avic\GFP-S65T} Mmus\Cd8a^{Scer\UAS.T:Avic\GFP} nonC^32AP Scer\GAL4^btl.PS Scer\GAL4^da.G32 Scer\GAL4^e22c Scer\GAL4^ppk.1.9 Scer\GAL80^btl Upf1^13D Upf1^26A Upf2^14J Upf2^25G Upf2^29AA Upf2^+tMa Upf2^Scer\UAS.cMa W^GMR.PG
Constructs (23)
	P{ActGFP} P{btl-GAL80.M} P{GAL4-btl.S} P{GAL4-da.G32} P{GMR-hid} P{His2Av^{T:Avic\GFP-S65T}} P{ppk-GAL4.1.9} P{UAS-DsRed1-SV40} P{UAS-EGFP.+I.Hsp70} P{UAS-EGFP.+I.SV40} P{UAS-EGFP.+I.SV40ΔI} P{UAS-EGFP.Hsp70} P{UAS-EGFP.SV40} P{UAS-EGFP.SV40ΔI} P{UAS-GFP.SV40} P{UAS-mCD8::GFP.L} P{UAS-nls:DsRed2-SV40} P{UASp-GFP.K10} P{UAS-Src-GFP(S65T/I167T)} P{UAS-Upd2.M} P{Upf2^+tMa} P+PBac{XP5.WH5} PBac{WH}
Genes (18)
	Adh Avic\GFP Disc\RFP His2Av Mmus\Cd8a nonC Oda P Scer\GAL4 Scer\GAL80 Sxl T:nls-tra T:SV40\nls2 T:Uuuu\nls6 tra Upf1 Upf2 W
Insertions (5)
	P{btl-GAL80.M}X P{en2.4-GAL4}e22c P{XP}C3G^d00589 P+PBac{XP5.WH5}exe2B PBac{WH}Cht11^f02328
Natural transposons (1)
	P-element