exd¹ homozygous mutant MARCM clones (induced using hs-FLP during the embryonic stage) in the terminal region of the female third instar larval ventral nerve cord do not have surviving doublesex-expressing larval terminal neuroblasts, similar to controls.

exd¹/exd¹ embryos lacking both maternal and zygotic contribution exhibit severe defects in Malpighian tubule migration and organization, as compared to wild type.

The T3 segment of mutant embryos acquires a mix of T1/abdominal identity, while the A1 and A2 segments resemble more posterior segments (A3-like and A4-like respectively).

Homozygous clones in the proximal leg cause the fusion of leg segments to the body wall and change the tissue to a more distal identity (bracted bristles are present). Homozygous clones in the distal leg segments do not result in a mutant phenotype.

Lack of maternal and zygotic exd function barely affects the brain by the middle of embryonic stage 12. The brain neuromeres are formed in these mutant embryos. All identifiable fiber tract founder clusters are produced, except for the D/T cluster (which shows reduced Fas2 expression in mutant embryos). Cells corresponding to the deuto- and tritocerebrum anlagen are clearly produced. The mutant brain starts to show marked abnormalities as axogenesis begins. By stage 14, significant perturbation of growing axonal tracts is seen in all the fiber tract founder clusters in both the supra- and subesophageal ganglia. The D/T cluster is largely missing. Axogenesis is abnormal in the procephalic clusters. The formation of the supraesophageal commissure (brain commissure) is significantly delayed. Severe disruption of the axonal scaffolds in both the supra- and subesophageal ganglia is seen in stage 16 embryos. The cervical longitudinal tracts are missing and the supra- and subesophageal ganglia remain separated. In the supraesophageal ganglia, all the axonal fibres are clumped around the brain commissure which is formed in this stage but posteriorly shifted. The tritocerebral commissure is missing. The Bolwig's organ and Bolwig's nerve are not formed. The optic lobe primordia are strongly reduced. Components of the stomatogastric nervous system are missing or severely disrupted. The salivary glands are missing.

Hemizygotes show perturbations in structures derived from all head segments except the antennal and hypopharyngeal lobes. The cirri are normal. The lateralgraten are short and thick. The hypostomal sclerite is elongated and perhaps fused to the ectostomal sclerite. The median tooth, epistomal sclerite and dorsal bridge were disrupted or fused. The dorsal phenotypes may be caused by defects in dorsal head involution.

Null allele.

Homozygous embryos which lack zygotic exd function appear normal and do not show any obvious defects in the PNS. Embryos derived from homozygous female germ line clones and lacking maternal exd function but not zygotic exd function show a "dorsal chordotonal" phenotype in approximately 5% of abdominal segments, with LCh5 neurons being positioned more dorsally than normal. Embryos lacking both maternal and zygotic exd function show a stronger phenotype, with the Lch5 neurons positioned in the dorsal PNS cluster in more than 65% of abdominal segments, and a reduction in the number of LCh5 neurons. A reduction in the number of other PNS neurons and axonal pathway defects are also seen in these embryos.

Clones of exd¹ proboscis cells induced during first/second larval stage are wild type.

Clones in the trochanter exhibit transformation towards a more distal, tibia-like pattern (bracted bristles). Clones in proximal femur regions differentiate inappropriate structures featured in more distal leg segments. Proximal femur is reduced and fused to coxa and ventral body wall or sternopleura. Some medial femur clones develop abnormally, the remaining normally. Distal femur clones are normal.

exd^- clones in the metanotum produce a transformation to the mesonotum, similar to that produced by Ubx^- clones. exd^- clones in the antenna show a transformation into the distal leg resembling those produced by the ss^a or Antp mutations. exd^- clones in the dorsal posterior head differentiate thoracic tissue, resembling the transformation produced by lab. Some of these clones extend to the eye where they differentiate normally. The majority of these clones appear in the posterior head capsule, from the ocellar region towards the occipital region. Anterior to the ocellus, exd^- clones are nearly always absent. Clones in the A1-A4 abdominal tergites present a pattern similar to the A5 tergite. Clones appearing in the ventral head regions, many of which extend to the antenna, exhibit novel homeotic transformations. Clones appearing in the rostral membrane differentiate ectopic eyes. If they extend to the ptilinum they differentiate proximal and medial leg structures of midleg identity. exd^- clones eliminate the dorsoventral difference in the abdomen. exd^- clones in the mesonotum differentiate bristles arranged in an abnormal pattern. Clones in the wing hinge region produce unusual bristle patterns and outgrowth. Clones in the distal part of the legs differentiate normally, but those in the proximal part differentiate innapropriate patterns.

Homozygous mutants display transformation of abdominal segment 1 to A2 identity. The survival of gynandromorph mosaic individuals is 18%. Clones in abdominal segments 1 to 4 are transformed posteriorly toward abdominal segment 5 or 6, evidenced by the darker cuticle pigmentation and trichome density. Clones in abdominal segments 6 and 7 are transformed anteriorly, clones within A6 are transformed toward abdominal segment 5, evidenced by the presence of trichomes. The ectopic A7 tergites have a morphology characteristic of A5 or A6. Clones in female genitalia also show anterior-ward transformation, clones in the male genitalia have subtle effects. Clones in the head could only be recovered in limited regions. Clones in the third antennal segment and arista are transformed to leg-type structures, evidenced by the presence of bracted bristles and tarsal claws. Clones in the proboscis also show transformation to leg identity, evidenced by the presence of bracted bristles. Cells within a head clone never gave rise to recognisable vibrissae, orbital, postorbital or palp bristles. Mitotic clones in the distal tarsal regions of the leg survive and participate in normal patterning. Clones located in the proximal regions either do not survive, grossly distort pattern and reduce leg segment size or make ectopic clusters of bristles in regions of leg usually devoid of bristles. The segment identities of mutant legs are not affected.

Dorsally, pT3 and pT2 are transformed posteriorly, and T1, aT2 and aT3 are normal. exd¹ embryos lacking maternal as well as zygotic exd function have a more severe phenotype. The head skeleton is completely eliminated, with ventral gnathal and thoracic segments being replaced by smooth cuticle. Ventrally, abdominal segments are fused in a pair-rule pattern and denticles are poorly differentiated. Dorsally, the thoracic segments are relatively well formed, although dorsal closure is not complete.

homozygous lethal resemble prothorax; first abdominal like posterior abdominal segments. In combination with Pc-like mutants shows abdominal transformations. meso- and metathoracic segments

exd[+]/exd¹ is an enhancer of partially lethal - majority die phenotype of Dfd¹³/Dfd³

exd¹ is an enhancer of partially lethal phenotype of Dfd¹³/Dfd³

exd[+]/exd¹ is a non-enhancer of eye disc | somatic clone phenotype of L²

exd[+]/exd¹ is a non-enhancer of eye | somatic clone phenotype of L²

exd[+]/exd¹ is a non-suppressor of eye disc | somatic clone phenotype of L²

exd[+]/exd¹ is a non-suppressor of eye | somatic clone phenotype of L²

Scr², exd¹, pb²⁷ has arista phenotype

Scr², exd¹, pb²⁷ has antenna phenotype

Scr², exd¹, pb²⁷ has proboscis phenotype

exd¹, pb²⁷ has proboscis phenotype