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. 2005 Nov;171(3):1137–1152. doi: 10.1534/genetics.105.044453

TABLE 3.

Deficiency screen for modifiers of GMR>H

Name Cytology Modificationa Candidate genesb Modificationc Cell deathd
Df(1)N-8 3C2-3; 3E3-4 E2 Notch(N5419) Lethal +
diminuitive (dm1) Lethal
Df(1)C52 8E; 9C-D S1 nejire(nej3) S1 +
Df(1)v-N48 9F; 10C3-5 E2 dishevelled(dsh1) E3 +
Df(1)N105 10F7; 11D1 S1 smrter (smrG0361) S1
Df(1)N12 11D1-2; 11F1-2 S1 hemipterous (hepv39, v75) S1 +
multiple edematous wings (mewM6) S1
Df(1)sd72b 13F1; 14B1 S1 scalloped(sdETX4) S1
Df(1)4b18 14B8; 14C1 Lethal Dorsal switch protein(Dsp1) Lethal +
Df(1)r-D1 14C2-4; 15B2-C1 S2 inflated (ifB2) S1
Rho-kinase (rok1) S1
Df(1)B25 15D3; 16A4-6 E1 Bar (B1) E1
bazooka (baz4) S1 +
Df(1)BK10 16A2; 16C7-10 E1 Bar (B1) E1
Df(1)HF396 18E1-2; 20E-F S1 amnesiac(amn1) S1
Df(2L)dp-79b 22A2-3; 22D5-E1 S1 anterior open(aop1) S1 +
Df(2L)C144 22F3-4; 23C3-5 S2 lilliputian (lilliA17-2, 00632) S2 +
Df(2L)JS17 23C1-2; 23E1-2 S1 lilliputian (lilliA17-2, 00632) S2 +
Df(2L)sc19-8 24C2-8; 25C8-9 S1 echinoid (edk01102) S1
fat (ftG-rv) S2
turtle (tutlk14703) S1 +
Df(2L)sc19-4 25A5; 25E5 E1 thick veins (tkv1) S1/2 nt
Df(2R)cn9 42E; 44C E1 sine oculis (so1) E1 +
Df(2R)B5 46A; 46C E1 crossbronx (cbx05704) S1
dacapo (dap4) S2
Df(2R)X1 46C; 47A1 S1 crossbronx (cbx05704) S1
leonardo (leo07103) S1 +
Df(2R)Jp8 52F5-9; 52F10-53A1 E2 Rho1 (Rho1E.10) E2 +
Df(2R)X58-12 58D1-2; 59A E2 Cyclin B (CycB2) E1 +
defective proventriculus (dve01738) S1 +
Df(3L)HR232 63C1; 63D2 S1 sprouty (sty226) S1/2
Df(3L)GN24 63F6-7; 64C13-15 S1 Rpd3(Rpd304556) S1
Df(3L)vin2 67F2; 68D6 S2 klumpfuss (klu09036) S1/2 +
Df(3L)brm11 71F1-4; 72D1-10 E2 brahma (brm2) E2/3 +
thread(th4) E2 +
Arflike at 72A (Arf72AN6) E2 +
Df(3R)p712 84D4-6; 85B6 E1/2 puckered (pucE69) E2 +
Df(3R)e-N19 93B; 94A E1 Calcium/calmodulin dependent
protein kinase (CakiX-307) E1
Df(3R)TI-P 97A; 98A1-2 E1 Serrate (SerRX102) E1

Listed are those modifying deficiencies in which the responsible loci were identified. Underlined are deficiencies that affect genes also found in the gain-of-function screen and showing an opposite interaction with GMR>H. See Table S2 at http://www.genetics.org/supplemental/ for further modifying deficiencies where no candidates could be assigned.

a

Modifications were phenotypically categorized according to Figure 2: S, suppressors; E, enhancers.

b

Identified modifiers with full name (alleles used for the crosses are given in parentheses). Those genes also found in the gain-of-function screen are underlined. Candidate genes that did not interact with GMR>H are listed in Table S2.

c

Phenotypic classification is according to Figure 2: S, suppressors; E, enhancers.

d

Interaction with apoptosis-inducing factors were observed (+) or were not observed (−) (for details, see text and Table 2).