Reference Report

Reference
Citation	Staehling-Hampton, K., Ciampa, P.J., Brook, A., Dyson, N. (1999). A genetic screen for modifiers of E2F in Drosophila melanogaster. Genetics 153(1): 275--287. (Export to RIS)
FlyBase ID	FBrf0111491
Publication Type	Research paper
PubMed ID	10471712
PubMed Abstract	The activity of the E2F transcription factor is regulated in part by pRB, the protein product of the retinoblastoma tumor suppressor gene. Studies of tumor cells show that the p16(ink4a)/cdk4/cyclin D/pRB pathway is mutated in most forms of cancer, suggesting that the deregulation of E2F, and hence the cell cycle, is a common event in tumorigenesis. Extragenic mutations that enhance or suppress E2F activity are likely to alter cell-cycle control and may play a role in tumorigenesis. We used an E2F overexpression phenotype in the Drosophila eye to screen for modifiers of E2F activity. Coexpression of dE2F and its heterodimeric partner dDP in the fly eye induces S phases and cell death. We isolated 33 enhancer mutations of this phenotype by EMS and X-ray mutagenesis and by screening a deficiency library collection. The majority of these mutations sorted into six complementation groups, five of which have been identified as alleles of brahma (brm), moira (mor) osa, pointed (pnt), and polycephalon (poc). osa, brm, and mor encode proteins with homology to SWI1, SWI2, and SWI3, respectively, suggesting that the activity of a SWI/SNF chromatin-remodeling complex has an important impact on E2F-dependent phenotypes. Mutations in poc also suppress phenotypes caused by p21(CIP1) expression, indicating an important role for polycephalon in cell-cycle control.
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Language of Publication	English
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Publication Type	Journal
Abbreviation	Genetics
Title	Genetics
Publication Year	1916-
ISBN/ISSN	0016-6731
Data from Reference
Aberrations (14)
	Df(1)C128 Df(2L)net-PM47C Df(2L)net-PMF Df(2L)TE21A Df(2R)59AB Df(2R)H81 Df(2R)Pu-D17 Df(2R)vg56 Df(3L)brm11 Df(3L)HR370 Df(3L)M21 Df(3L)th102 Df(3R)DG2 In(2R)Pcl¹¹
Alleles (84)
	aop¹ aop^A141 BacA\p35^GMR.PH brm² brm^ksh-6 brm^ksh-7 brm^ksh-8 brm^pjc-2 btl⁰⁰²⁰⁸ cdc2^216A cdc2^E10 CycA⁵ CycE² CycE^AR95 dap^GMR.PdN Dll⁵ Dll⁹ Dll¹² Dp^49Fk-1 Dp^GMR.PD E2f⁰⁷¹⁷² E2f^GMR.PD E2f^rM729 E(E2f)2B^ksh-5 E(E2f)2B^pjc-1 E(E2f)2B^pjc-10 Egfr^E1 Egfr^f2 esc¹ Hsap\CDKN1A^GMR.PH kis¹ ksh-15^ksh-15 ksh-16^ksh-16 ksh-17^ksh-17 ksh-18^ksh-18 ksh-19^ksh-19 kto¹ mor¹ mor² mor⁵ mor^ksh-9 mor^ksh-10 osa² osa^E65 osa^ksh-11 osa^ksh-12 osa^ksh-13 osa^pjc-3 Pc¹ Pc⁷ phl¹ pho¹ pjc-16^pjc-16 pnt^05484Δ33 pnt^07825Δ78 pnt^ksh-14 pnt^pjc-5 pnt^pjc-6 Ras85D^e1B Ras85D^e2F RasGAP1^3ij RasGAP1^A13D Rho1^GMR.PH rl^Sem rl^x162 rpr^GMR.PW Scm^D1 sev¹⁴ spen^16H1 spen^16T1 spen^ksh-1 spen^ksh-2 spen^ksh-3 spen^ksh-4 spen^pjc-4 spen^pjc-7 spen^pjc-15 spen^poc231 spen^poc361 stg² stg⁷ sxc¹ trx¹ trx^E2
Constructs (7)
	P{GMR-dap} P{GMRdDP} P{GMRdE2F} P{GMRp21^B} P{GMRP35} P{GMR-Rho1} P{GMR-rpr.W}
Genes (49)
	aop b BacA\p35 brm btl cdc2 cdc2c CycA CycE dap Dll Dp dp e E2f E(E2f)2B Egfr esc h Hsap\CDKN1A kis ksh-15 ksh-16 ksh-17 ksh-18 ksh-19 kto mor osa Pc phl pho pjc-16 pnt px Ras85D RasGAP1 Rho1 rl RnrS rpr Scm sev sp spen stg sxc th trx