fng¹³ embryos, lacking maternal contribution, do not show a neurogenic phenotype at either 25[o]C or 30[o]C.

The contact area between fng¹³ mutant female germline stem cells and the niche is greater than in wild type controls at two weeks after clone induction.

Specification and terminal differentiation of intestinal stem cells is indistinguishable from wild type in homozygous clones in the adult intestine.

The overall number and positioning of the longitudinal glia in fng^L73/fng¹³ embryos is normal.

fng¹³ mutant follicle cell clones at the egg chamber termini result in defective egg chambers that degenerate in midoogenesis. fng¹³ mutant clones in the main body of the follicular epithelium do not affect egg chamber development and can be analysed for patterning defects. Ventral and lateral fng¹³ clones do not exhibit changes in cell shape, or production of ectopic appendage materal, indicating that a fngexpression boundary is not sufficient to induce an appendage-producing fate.

Stage 14 fng¹³ embryos show defects in the denticle field primordium cells. The actin-based protrusions that precede the formation of denticles can be misplaced, being located at anterior cell edges, or mid-face, rather than at the posterior cell edge. fng¹³ larval cuticle shows ectopic denticles and denticle rows that show a less regular alignment than in control larvae.

fng¹³ larvae have extra denticles anterior to, or within, the denticle field.

In fng¹³ homozygous embryos, the early steps of proventricular development including the formation of the ball-like evagination at the ectoderm/endoderm boundary occur normally. However, at stage 14, the anterior boundary cells of the keyhole region fail to invaginate into the endodermal cell layer. In addition, the posterior boundary cells of the endodermal component of the proventriculus rim collapses in these animals.

fng¹³/fng^M69 animals that survive to adulthood when grown at 18^oC exhibit a strong wing phenotype. fng¹³/fng⁵² animals that survive to adulthood exhibit a moderate wing phenotype. fng¹³/fng² animals that survive to adulthood exhibit a moderate wing phenotype.

When homozygous somatic clones are made in the eye, photoreceptor cell R8 specification appears unaffected, Though aberrations in R8 spacing pattern are seen.

When clones are made in the dorsal compartment of the wing disc, they are rounder than wild-type clones, though their borders are irregular and highly indented.

When the cells that would ordinarily form polar cells are mutant for fng in mosaic follicles, the polar cells do not form. The majority of these mosaic follicles lacking polar cells either form compound egg chambers or fail to develop to stages late enough to examine the patterning of terminal follicle cells. Mosaic follicles that lack fng⁺ follicle cells at the anterior that develop to stage 9 do not form anterior polar cells and no border cells are specified. No stretched follicle cells are specified in stage 9 mosaic follicles of this type, but the anterior follicular cells continue to migrate over the oocyte, so that many nurse cells are no longer covered by a follicular epithelium. No centripetal cells are specified in stage 9 mosaic follicles of this type. Polar and outer border follicle cells are specified and migrate properly in stage 10A mosaic follicles in which all of the most anterior follicle cells, including the outer cells, are fng^-, except for the two polar cells which are fng⁺. The polar and stretched follicle cells are specified properly in stage 10B mosaic follicles which have only a few fng⁺ follicle cells (including the polar cells) at the anterior. Polar and centripetal follicle cells are specified and migrate properly in stage 10A mosaic follicles in which all of the most anterior follicle cells, including the outer cells, are fng^-, except for the two polar cells which are fng⁺. Mosaic follicles that lack posterior polar cells have the oocyte abnormally localised to the anterior of the follicle, in contact with the anterior polar cells. fng mosaic follicles which lack posterior polar cells, but which have two polar cells along the lateral side of the follicle can be recovered. The oocyte is in contact with these mislocalised polar cells in each case. Mosaic follicles with these ectopic lateral polar cells, which lack both the normal anterior and posterior polar cells tend to be round or even elongated perpendicular to the axis of the ovariole.

Transheterozygous fng²/fng¹³ females have ovaries showing 0% compound follicles, 12% with long stalks 42% of follicles have abnormal epithelium. The long stalk phenotype is sometimes accompanied by a stalk disorganization phenotype. In somatic mosaics most follicles have multiple 16 cell cysts, and for these fng⁺ cells are always located at both ends of the egg chamber with fng^- cells contributing to non-terminal regions. In the remaining mosaic follicles the separation of the follicles is defective - stalk cells do not separate the adjacent follicles, between which lie a bilayer of fng^- (from the older follicle) and both fng^- and fng⁺ (from the younger follicle) follicle cells. Polar-stalk precursor cells that are mutant for fng are unable to develop into polar cells. Mosaic follicles where all of the main-body follicle cells are fng^- but the polar and stalk cells are fng⁺ appear normal. Cases of stalks occur where all the stalk cells are fng^- but the polar cells at each end of the stalk are fng⁺. Mosaic follicles where all of the main-body follicle cells are fng⁺ but the polar and stalk cells are fng^- usually have elongated and/or disorganised stalks. The genotype of the polar cells dictates how well the stalk cells form a stalk, irrespective of the genotype of the stalk cells.

Dorsal clones in the wing induced in the second larval instar stage induce ectopic wing margin tissue and induce outgrowth of the of the wing. Ventral clones located near the second longitudinal wing vein autonomously induce an ectopic vein. Dorsal clones in the wing induced in early third larval instar stage (72 hours after egg laying) at or near the endogenous margin induce ectopic wing margin tissue. Clones at a distance from the wing margin do not show any phenotype. Clones induced in the mid third larval instar stage do not produce any phenotype in the adult wing.

Many egg chambers containing homozygous clones degenerate during stages 6-10. Many compound egg chambers are formed, which then degenerate. Egg chambers that survive beyond stage 6 have a disrupted follicle cell epithelium; the follicle cells are rounded and delaminate from the oocyte, often forming multilayers. Clones at more posterior locations of the egg chamber tend to be more deleterious. Some anterior/dorsal clones have no effect on egg development. Some egg chambers that have only small clonal patches progress to the end of oogenesis. Three distinct dorsal appendage phenotypes are seen in eggs laid by female flies containing homozygous follicle cell clones. In the time period 13-24 hours after induction of the clones, approximately 8% of eggs have dorsal appendages that are fused along the base. Approximately 9% of eggs laid between 13-36 hours after clone induction have dorsal appendages that have a narrower dorsal gap between them than normal. 8-9% of eggs laid between 25-36 hours after clone induction have dorsal appendages that are fused at their tips. Subsequent to 36 hours after clone induction, the percentage of mutant eggs drops. In all cases, the dorsal appendage phenotypes do not appear to affect the embryos, as more than 87% hatch normally.

Homozygous clones in the leg result in fused joints and shortened legs. All joints except the tibia-tarsal1 joint are affected. In most cases, the failure to form joints is an autonomous property of the mutant cells in the clone, although occasionally joint formation is also inhibited in wild-type cells that border a clone. Homozygous clones in the antenna can be associated with segmental fusions.

Dorsal somatic clones in the wing disc fail to respect the dorsal-ventral border.

One to three ommatidia of ventral polarity are often generated at the polar boundaries of homozygous clones in the dorsal region of the eye, producing an ectopic "mini-equator". No dramatic difference in clone shapes is seen between homozygous and wild-type clones in the ventral part of the eye.

Mutant clones induced in the equator or dorsal region of the developing eye do not show significant polarity changes either inside or outside the clone boundary. Mutant clones induced in the ventral domain (close to or far from the equator) caused polarity reversals extending up to four ommatidia from the clone boundary. The shift in chirality is observed only outside the clone boundaries towards the normal equator. Photoreceptor numbers are affected in 24% of ommatidia.

Mutant clones in the eye that fall close to the equatorial region repolarize adjacent ommatidia over a short distance. Clones in more ventral regions cause a bulge in the eye and long range repolarizing effects. Clones of fng⁺/fng⁺ next to fng⁺/fng¹³ also cause repolarization.

fng⁵²/fng¹³ flies have small eyes. Tissue loss in the ocellar region is also seen. Homozygous clones in the ventral part of the eye can be associated with reversals of ommatidial chirality which can be nonautonomous, whereas clones that cross the dorsal-ventral midline disrupt the normal equator.

Homozygous clones spanning the boundary between the femur and tibia result in the fusion of these two segments and a shortening of the leg. In more distal leg segments, homozygous clones only cause detectable defects in the joint between the proximal two tarsal segments.

Clonal analysis demonstrates fng¹³ cells cannot be rescued by adjacent fng⁺ cells.

Mutant clones in the wing reveal ectopic wing margins along clone borders, composed of both wild type and mutant cells. Ectopic margins are composed of a mirror image duplication of dorsal-type bristles. Clone boundaries farther from the normal margin often partially or completely fail to induce ectopic margins. Clones contained with the dorsal surface can be associated with an expansion of the dorsal wing surface. The size of distal outgrowths varies with their location in the wing. Some clones are associated with loss of tissue from the wing margin and reduction in size of the wing. fng⁺ is not autonomously required for wing cell viability.

fng[+]/fng¹³ is an enhancer of visible | dominant phenotype of N^Ax-E2

fng[+]/fng¹³ is an enhancer of visible | recessive phenotype of Bx^hdpR590

fng[+]/fng¹³ is an enhancer of wing vein phenotype of N^Ax-E2

fng[+]/fng¹³ is an enhancer of wing phenotype of Bx^hdpR590