Table 1.

sog interacts genetically with genes coding ECM molecules

Interaction with
Gene/allelesog (EP7)sog (EP11)Molecule encodedWing expression pattern
LamA(25) EE EE Laminin All wing, veins after apposition 
LamA(6-36) EEE EEE   
LamA(9-32) EEE EEE   
LamA(216) EE EE   
DCgl(234) Collagen IV a1 All wing, veins after apposition 
Cg25c(GDB)   
vkg(BLK) Collagen IV a2 ND 
vkg(SAC)   
vkg(ICO)   
vkg(228)   
vkg(177)   
mys(1) EE EE βPS integrin Both wing surfaces; interveins 
mys(XB87) EE EE   
mys(nj42)   
mys(nj42)/mys(nj42) EE EE   
mys(XR04)   
hs-βPS* βPS under control of a hs promoter NA 
mew(498) αPS1 integrin Dorsal wing surface; interveins 
mew(M6)   
if(k27e) αPS2 integrin Ventral wing surface; interveins 
if(B2)   
if(3)   
scb(1) EE EE αPS3 integrin Pupal wing (this report) 
scb(2) EE EE   
vol(1)   
vol(2)   
ds(33k) Cadherin ND 
ds(1)   
dally(Gem) Proteoglycan Imaginal wing disc 
dally(P2)   
dally(ΔP527)   
sas(15) Fibronectin type III repeats Imaginal discs 
fw(1) Selectin ND 
tig(X) Ligand for if ND 
tig(A1)   
tld(68-62) Metalloprotease Imaginal wing disc 
Df3R slo(3) EE EE   
tok(Δ41) Metalloprotease Imaginal wing disc 
tkv(1) EE EE Bmp receptor All wing, stronger at vein border 
tkv(8)   
sax(8) Bmp receptor Imaginal wing disc 
dpp(shv) EE EE Bmp family member Pupal wing veins 
gbb(1) Bmp family member Imaginal wing disc 
gbb(4)   
rho (ve) EE EE Membrane protein, Egfr signalling Pupal wing veins 
Interaction with
Gene/allelesog (EP7)sog (EP11)Molecule encodedWing expression pattern
LamA(25) EE EE Laminin All wing, veins after apposition 
LamA(6-36) EEE EEE   
LamA(9-32) EEE EEE   
LamA(216) EE EE   
DCgl(234) Collagen IV a1 All wing, veins after apposition 
Cg25c(GDB)   
vkg(BLK) Collagen IV a2 ND 
vkg(SAC)   
vkg(ICO)   
vkg(228)   
vkg(177)   
mys(1) EE EE βPS integrin Both wing surfaces; interveins 
mys(XB87) EE EE   
mys(nj42)   
mys(nj42)/mys(nj42) EE EE   
mys(XR04)   
hs-βPS* βPS under control of a hs promoter NA 
mew(498) αPS1 integrin Dorsal wing surface; interveins 
mew(M6)   
if(k27e) αPS2 integrin Ventral wing surface; interveins 
if(B2)   
if(3)   
scb(1) EE EE αPS3 integrin Pupal wing (this report) 
scb(2) EE EE   
vol(1)   
vol(2)   
ds(33k) Cadherin ND 
ds(1)   
dally(Gem) Proteoglycan Imaginal wing disc 
dally(P2)   
dally(ΔP527)   
sas(15) Fibronectin type III repeats Imaginal discs 
fw(1) Selectin ND 
tig(X) Ligand for if ND 
tig(A1)   
tld(68-62) Metalloprotease Imaginal wing disc 
Df3R slo(3) EE EE   
tok(Δ41) Metalloprotease Imaginal wing disc 
tkv(1) EE EE Bmp receptor All wing, stronger at vein border 
tkv(8)   
sax(8) Bmp receptor Imaginal wing disc 
dpp(shv) EE EE Bmp family member Pupal wing veins 
gbb(1) Bmp family member Imaginal wing disc 
gbb(4)   
rho (ve) EE EE Membrane protein, Egfr signalling Pupal wing veins 

Alleles of genes coding for ECM molecules or their receptors were tested for genetic interactions with sog misexpression lines. Among the Drosophila genes encoding ECM proteins, we tested those for which a wing phenotype and/or expression in the wing had been previously reported. Interactions were scored against the enhancer piracy sog lines EP7 and EP11 (Yu et al., 1996),and classified as no interaction (0), enhancement (E) or suppression (S) of the sogEP vein truncation phenotype. In the case of enhancer mutations, the number of Es indicates the strength of the interaction. sogEP7 induces ectopic expression of sog in vein domains during pupal development. Interacting alleles were also crossed to enhancer piracy lines EP9, EP8, EP2 and EP3. In all such cases, we observed consistent types of interactions. Unless cited,modifications of the sogEP phenotype were similar for both the L4/L5 truncation and L2 wandering phenotypes.

*

The strongest effects were observed when pupae were heat shocked at 4-8 hours after fertilization and 20-28 hours after fertilization, which coincide with periods of apposition between wing surfaces(Fristrom et al., 1993). Phenotypes were compared with those observed in sogEP7/+flies heat shocked under the same conditions.

scb only enhances the vein truncation phenotype.

The deficiency Df 3R slo3 uncovers tld and tok.

NA, not applicable; ND, not determined or not analyzed through all stages.

Close Modal

or Create an Account

Close Modal
Close Modal