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. 2005 Nov;171(3):1057–1081. doi: 10.1534/genetics.104.038018

TABLE 2.

Deficiencies suppress GMR-dRetWT, GMR-dRetMEN2A, and GMR-dRetMEN2B

Deficiency Breakpoints GMR-dRetWT GMR-dRetMEN2A GMR-dRetMEN2B Candidate gene, alleles tested Interaction
Df(2L)net-PMF 21A1;21B8 WS(100) WS(86) WS(83) kismet: kisk10237, kisk13416 WS
Df(2L)al 21B8;21D1 SS(100) MS(100) SS(100) ebi: ebik16213 WS
Df(2L)TW161 38A6;40B1 WS(75) SS(96) SS(100) diaphanousa: diak07135 N
dRet
Df(2R)X58-12 58D1;59A MS(80) SS(100) SS(100) plexus: pxk08316 WS
Df(2R)59AD 59A1;59D4 WS(78) SS(100) SS(100)
Df(3L)Pc-2q 78C5;79A1 MS(100) WS(100) WS(100) SAKb: SAKc06612 N
Df(3R)ME15 81F3;82F7 MS(90) SS(97) SS(100) Gelsolinc
Df(3R)Antp17 84A5;84D14 WS(67) SS(100) MS(100)
Df(3R)Hu 84A6;84B6, 84D4;84F2 WS(76) MS(100) MS(82)
Df(3R)by10 85D8;85F1 nt WS(97) WS(77) Ras85D: Ras85D06677, Ras85DΔc40b WS-MS
Df(3R)DG2 89E1;91B2 SS(100) SS(100) SS(100) glass: gl2 SS
Df(3R)Cha7 90F1;91F5 WS (89) WS(100) WS(100) glass: gl2 SS

Each deficiency is listed by name. The cytological breakpoints for each are derived from the FlyBase and Bloomington Stock Center online databases. Genetic interactions are indicate according to strength of phenotype: W, weak; M, moderate; S, strong; and type of interaction: S, suppressor; N, no interaction; nt, not tested. Therefore, SS is a strong suppressor. Parentheses indicate the penetrance of the interaction calculated as a percentage. See text for details on candidate genes. —, indicates that there were no mutants in the candidate gene available for testing.

a

dia encodes a formin homology protein involved in cytoskeleton remodeling and Rho signaling (Prokopenko et al. 1999).

b

Encodes a serine/threonine kinase, which is a putative effector of Src signaling (Yamashita et al. 2001).

c

Gelsolin encodes an actin-binding protein linked to Src signaling (Chellaiah et al. 2000).