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

TABLE 1.

Novel modifying EP or UAS lines of GMR>H

Genea Map GOF linesb GMRc GMR>H/+d Deficiency/allelee Breakpointsf GMR>H/+g Cell deathh Referencei
JNK pathway
basket 31B3 UASDN Little small S1/2 bsk1 S1 Not tested
misshapen 62E6-7 549 Wild type E1 msn06946 S1 Not tested Kraut et al. (2001)
GTPases, protein kinases and phosphatases
raspberry 9E1-2 1098 Wild type E1 Df(1)HC133 9B9; 9F4 S1 Not tested Bidet et al. (2003); Peña-Rangel et al. (2002)
CG2446 10D6-7 1503 Little big S1 Df(1)m259-4 10C2; 10E2 0 + Abdelilah-Seyfried et al. (2000)
Casein kinase I 11B7 1555 Little big S1 Df(1)HF368 11A2; 11B9 0 +
CG5261 27F6 816 Wild type S1 Df(2L)RF 27E3-F; 28B3-4 0 +
connector enhancer of ksr 54B9-11 576 Little big E1 cnkE-2083 E1 Not tested
Drac2 66A1 3118 Slits E4 Df(3L)pbl-X1 65F3; 66B10 S1 + Bidet et al. (2003); Peña-Rangel et al. (2002); Tseng and Hariharan (2002)
Malic enzyme 87C6-7 1250 Little big E1 Df(3R)kar31 87C2; 87D1 0 Not tested Bidet et al. (2003); Peña-Rangel et al. (2002)
widerborst 98A8 3113; 3559 Little big S2 wdbdw E1/2 + Abdelilah-Seyfried et al. (2000); Kraut et al. (2001)
UASDN E1/2
General transcriptional regulators/chromatin-remodeling factors
nejire 8F-9 1149; 1179; 1410 Small E2 Df(1)C52; nejQ7 8E; 9C-D S1 + Abdelilah-Seyfried et al. (2000); Peña-Rangel et al. (2002)
Dorsal switch 14B15-16 355 Wild type S2 Df(1)19 13F2-18; 14E Lethal + Kraut et al. (2001); Peña-Rangel et al. (2002)
protein Df(1)4b18 14B8; 14C1 Lethal
longitudinals 47A11-13 2537 Wild type E2 Df(2R)E3363 47A; 47F S1 Not tested Abdelilah-Seyfried et al. (2000)
lacking
Rpd3 64B12 3672 Wild type E1 Df(3L)GN24 63F6-7; 64C13-15 S1 Not tested
Regena 83B5-6 3713 Wild type E1 Not tested
Genes acting in protein transport or regulation of translation
IGF-II mRNA 9F5 1433 Little big S3 Df(1)HC133 9B9; 9F4 E1 + Kraut et al. (2001)
bind. protein
blue cheese 26A1 2299 Little small E2 Mutants not available or not tested + Abdelilah-Seyfried et al. (2000); Kraut et al. (2001)
Sec 61α 26D7-8 2567 Wild type E1 Mutants not available or not tested Not tested
eclair 85E4 469 Little small E1 Df(3R)GB104 85D12; 85E10 S1 Not tested
CG11779 91F6-7 1123 Big S2 Df(3R)Cha9 91C7-D1; 92A2 0 +
Novel genes with unknown function
CG3600 2C1 1232 Wild type S1 Df(1)sc8 1B; 3A3-C2 Lethal + Tseng and Hariharan (2002)
CG12462 3,F4 1413 Little small E2 Df(1)GA102 3D4-5; 3F7-8 E1 +
CG11068 12D1-2 1595 Little big E3/4 Df(1)HA92 12A6-7; 12D3 S1 Not tested Tseng and Hariharan (2002)
CG32521 19F2-3 555 Little big S1 Df(1)Q359 19E7; 19F6 E1 +
CG17223 23C5 797 Wild type E2 Df(2L)JS32 23C3-5; 23D1-2 S1 Not tested
Df(2L)JS17 23C1-2; 23E1-2 S1
l(2)k10113 27F4-5 1221 Little big S1 Df(2L)spd 27D-E; 28C 0 + Abdelilah-Seyfried et al. (2000); Peña-Rangel et al. (2002)
CG8788 45A11-12 2301 Little small E1 Df(2R)w45 45A6-7; 45E2-3 S1 —
l(2)05510 57A6 2356; 2587 Pupal lethal E4 Df(2R)AA21 56F9-17; 57D11-12 S1 — Abdelilah-Seyfried et al. (2000); Peña-Rangel et al. (2002); Tseng and Hariharan (2002)
CG17180 61C3 3104 Little big E2 Df(3L)emc-E12 61A; 61D3 0 Not tested Bidet et al. (2003)
CG14959j 63C2-3 3139 Wild type S1 Df(3L)Awh2 63B10-11; 63E4-9 0 — Peña-Rangel et al. (2002); Tseng and Hariharan (2002)
CG7752 78C5-6 756 Wild type S2 Df(3L)Pc-Mk 78A2; 78C9 E1 +
CG7552 88D1 666 Little big E1 Df(3r)red-1 88B1; 88D3-4 S1 Not tested Peña-Rangel et al. (2002); Tseng and Hariharan (2002)
CG5720 95F11-12 3716 Little big E1 Df(3R)crb-F89 95D7-11; 95F15 0 Not tested Abdelilah-Seyfried et al. (2000); Bidet et al. (2003); Peña-Rangel et al. (2002)
CG15507 99B10 3084 Wild type E1 Df(3R)01215 99A6; 99AC1 S1 Not tested

The identified modifiers were grouped according to their predicted molecular function and arranged by localization. Only those in which the EP element is inserted in sense orientation relative to the transcription unit are listed.

a

Genes are listed with their full names. Gene names are underlined if gain- and loss-of-function mutations showed the opposite genetic interaction with GMR>H.

b

EP lines are listed with their numbers. In some cases, a dominant-negative form (UASDN) of the respective gene was used.

c

Short description of the eye phenotype obtained after overexpression of EP or UASDN lines with GMR-Gal4.

d

Categories of phenotypes according to Figure 2; S, Suppressor; E, Enhancer. All crosses were maintained at 25°.

e

Name of deficiencies and loss-of-function alleles of candidate genes crossed with GMR>H. Deficiencies underlined in this column were also identified in the LOF screen.

f

Breakpoints of deficiencies according to FlyBase.

g

Phenotype of respective deficiency or mutant allele in trans over GMR>H categorized according to Figure 2; S, Suppressor; E, Enhancer; 0, no interaction. All crosses were maintained at 25°.

h

Modifiers were assayed for their influence on cell death processes. Suppressors of GMR>H were tested for their ability to rescue the eye phenotype caused by misexpression of p53 or proapoptotic genes. Enhancers of GMR>H as well as lines that caused lethality were subjected to a rescue experiment by simultaneously overexpressing DIAP1. Factors that showed modification are marked with (+) and with (−) for no interaction. For detailed results, see Table 2.

i

EP lines identified in other gain-of-function screens.

j

For EP(3)3139 and EP(3)3560 we were unable to identify the sequences responsible for the interaction. In situ hybridizations on chromosomes revealed that these lines have multiple insertions.