Clones of homozygous Dl^M1 mutant ovarian follicle cells tend to have larger nuclei than surrounding wild-type cells.

Homozygous mutant germ-line clones produces severe encapsulation defects leading to the fusion of adjacent egg chambers into a single large compound egg chamber that contains multiple germ-line cysts. When germ cells of an single egg chamber are made mutant for Dl^M1 (by germ-line clone induction), the wild-type follicle cells that surround them continue to divide well beyond stage 6. These egg chambers show a strong and highly penetrant oocyte polarity defect, as the oocyte nucleus remains at the posterior pole of the cell almost all cases. Individual egg chambers bearing mutant germ-line clones usually fuse with an adjacent wild-type one to form a mosaic egg chamber in which a single follicular epithelium surrounds both wild-type and mutant germ-cells. The anterior posterior axis is also not polarised in these egg chambers. Homozygous mutant somatic clones in the follicle cells leads to occasional partial fusions between the adjacent egg chambers. The cysts are still surrounded by follicle cells, but the stalk between them is completely absent. No other obvious defects are seen.

Heterozygotes show thickening of the wing veins, mainly in the distal part of the veins.

Wing veins L2 and L5 are irregularly broader than wild-type veins in heterozygous flies, with the effect being most obvious at the distal tips of the veins.

Wing veins are thickened.

Homozygous clones in the tarsi result in fusion between tarsal segments. The remnants of some joints are still recognisable.

Mitotic clones in the dorsal LIII and ventral LIV wing veins induce vein differentiation in the adjacent one or two wild type cells. Clones induced in a rho^ve-1 vn¹ mutant background differentiate extra-sensilla associated with the remnants of the vein, most cells in the clone differentiate as intervein cells.

Homozygous clones including dorsal and ventral clones cause extensive wing scalloping. Clones in the ventral compartment cause small nicks or loss of margin sensory elements. Clones in the dorsal compartment cause only loss of sensory elements.

Dominant increase-in-chaetae-density phenotype.

Dominant by haplo-insufficiency causing notum phenotypes of evenly spaced macrochaetae.

Heterozygote have thickened veins and terminal deltas.

Delta^M1/Dl[+] is an enhancer of visible | dominant phenotype of amos^Tft

Delta^M1/Dl[+] is an enhancer of visible | somatic clone phenotype of emc¹

Delta^M1 has wing phenotype, suppressible by N[+]/N^55e11

Delta^M1 has wing vein phenotype, suppressible by N[+]/N^55e11

Delta^M1 has phenotype, suppressible by Egfr^t1/Egfr^f11

Delta^M1/Dl[+] is an enhancer of macrochaeta | ectopic phenotype of amos^Tft

Delta^M1/Dl[+] is an enhancer of wing vein | somatic clone phenotype of emc¹

Delta^M1/Dl[+] is a suppressor of wing phenotype of N^55e11

Delta^M1/Dl[+] is a suppressor of wing vein phenotype of N^55e11

Delta^M1/Dl[+] is a suppressor of phenotype of Egfr^t1/Egfr^f11