No wing phenotypes are seen in dppd6 heterozygotes.
dppd6 mutant embryos display an increased number of hematopoietic cells in the lymph gland of embryos compared to wild-type, and the lymph gland is still hypertrophic in third instar larvae and there is an overabundance of plasmatocyte precursors. There is no significant difference in the number of crystal cell precursors in these larvae.
dppd6 mutant larvae fed on S. typhimurium experience a developmental delay of 1 full day from hatching to pupation, and infection results in eventual lethality of these animals. Under normal conditions, dppd6 mutant larvae generate 38% more blood cells per larvae compared to wild-type. There is significantly more (74%) blood cells observed in 3-day fed infected mutant larvae than in non-infected mutant larvae. There is no significant difference in the number of crystal cells between infected mutant and wild-type larvae. In the absence of infection 48% of blood cells in mutant larve are new plasmatocytes, compared to 31% in controls. Within 1 day of infection, the level of new plasmatocytes decreases to 23% and continues to decrease over subsequent days, reduced compared to levels in wild-type infected larvae. Infected dppd6 mutant larvae are significantly impaired in their ability to produce lamellocytes, whereas infected wild-type larvae show >10-fold increase in the percentage of circulating lamellocytes.
Stage 15 dppd6 embryos contain a significantly greater number of zfh1-expressing pericardial cells than normal, but show no change in the number of Mef2 expressing cardiac cells. Hyperplasia of the zfh1-expressing pericardial cells is still seen in stage 17 mutant embryos.
dppd6 embryos show expanded cell proliferation in the dorsal mesoderm during stage 12 compared to wild-type embryos, and cell division in the dorsal mesoderm persists in dppd6 embryos throughout stage 13 (in contrast to wild type, where cell division is absent in the dorsal mesoderm in stage 13).
In the anterior region of the heart (the aorta), mutant first instar larvae show no difference in heart rate or pulse distance compared to controls. However, in the posterior region (the heart proper), the mutant larvae show a considerable reduction in the systolic distance (mutant cells do not approach each other as closely as wild-type cells do) and the diastolic distance (mutant cells do not separate from each other as far as wild-type cells do). The mutant larvae have a 44% reduction in the average pulse distance per beat, an indication that the beat volume is significantly reduced. The heart rate in the posterior region of the heart is comparable to wild type.
Heterozygotes do not have an ectopic wing vein phenotype.
dppd6/dpphr4 wings have only two veins, L3 and L5 and are missing L2 and L4 completely. dppd6/dpphr27 mutants have wings that are significantly reduced in size and that are missing L3 and L5. The wings of dppd5/dppd6 mutants are so small that the identification of patterning defects is obscured.
dppd12/dppd6 flies show a considerable loss of taste bristles but do not show a loss of pseudotrachae or a significant change in gross mediproboscis morphology.
Approximately 50% of eggs laid by heterozygous females have shortened and abnormally shaped respiratory appendages.
dppd6/dpphr27 flies show partial fusions of the L2 and L3 and the L4 and L5 wing veins. The wing is compressed along the A/P axis compared to wild type.
dppd6/dppd12 flies have a reduced number of ommatidia. The adults are weak, short-lived (live for 2-3 days) and have abnormalities in the wing, leg, antenna and external genitalia. The tarsal and meta-tarsal segments of all legs are abnormal in dppd6/dppd12 flies, due to loss of claws and fusion of the tarsal segments. The dorsal parts of the leg are sometimes ventralised. The tibia and femur are progressively less affected, while the trochanter and coxa are almost wild type. The number of sex comb bristles is generally higher than normal. dppd6/dppd12 flies have defects in the distal segments of the antenna. The arista is usually absent and a conical projection is present on the third segment (which presumably represents the fused 4th, 5th and 6th antennal segments). Most dppd6/dppd12 males completely lack external genitalia while some have abnormal external genitalia. There is little effect on the female genitalia. The leg and antennal discs of dppd6/dppd12 larvae are deformed.
The external genitalia of dppd6/dppd12 males are reduced to a small ring like structure. dppd6/dppd12 females show duplication of the thorn bristles accompanied by an absence of long bristles.
Heterozygotes are phenotypically wild-type. Wings derived from dppd6/dpps4 animals lack only the anterior crossvein.
dppd6/dppd8 transheterozygotes have defects in both wing and leg development. Mutants can produce ventral wing hinge structures in transdetermined legs.
70 to 100% of homozygous males show loss of tarsi and claws and have small wings and eyes. 35 to 70% of homozygous males show duplication of leg structures, and 10 to 35% of homozygous males have duplicated antennal structures.
dpphr4/dppd6 transheterozygotes exhibit reduced wings to approximately half wild type size and no defects in eyes or legs.
Homozygotes exhibit greatly reduced wings and eyes and loss of tarsal claws at the tips of the legs. Transheterozygotes with dpphr4 have wings approximately half size and normal legs and eyes. When in combination with Df(2L)C28/Mad+ the transheterozygotes exhibit more severe phenotype, further reduction in wing blade, slight reduction in the eye and loss of tarsal claws. Trisomy for Mad (Dp(2;3)JS20) partially ameliorates transheterozygote phenotype, wings are of normal size and show residual vein fusions.
dppd6/dpphr4 individuals have a nearly full size wing, except for the absence of the anterior crossvein, a reduction in the distance between L4 and L5 and a small amount of ectopic vein between L2 and L3.
The medulla neuropil is reduced to a size similar to that produced by inactivating wg prior to 44hr AEL. The number of ommatidia is correspondingly reduced. The number of outer proliferative center cells incorporating BrdU is markedly decreased in the Fas2 expressing domain of wg and dpp early third instar brains.
dppd6/dppd14 clones are associated with defects in the wing, but not the notum. dppd6/dppd14 clones in the posterior compartment are associated with normal venation.
Adults lack distal portion of appendages.