mutants have wings that are significantly reduced in size and that are missing L3 and L5.
males that have been raised at 18o
C and then shifted to the restrictive temperature of 29o
C upon eclosion do not have any overt morphological abnormalities in the testes after 7 days at 29o
C and the testes contain germ cells in all stages and in quantities indistinguishable from that of controls.
Approximately 50% of eggs laid by heterozygous females have shortened and abnormally shaped respiratory appendages.
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.
The distance between veins L4 and L5 is reduced in dppd5
Embryos show cuticular holes, disorganization of the head skeleton, internalization of the seventh and eighth abdominal segments and the filzkorper and a thoracic constriction. The first and second ventral denticle belts are expanded, particularly at the tips. The filzkorper are fused into a single globular mass, reflecting the loss of dorsal fates that keeps the two anlage distinct in wild type. A significant percentage of surviving transheterozygotes between dpphr56
have a split notum.
Survival of heterozygotes is reduced if also heterozygous for certain alleles of tld
The presence of tkv7
in the mother causes dpphr27
to behave as a dominant lethal in the zygote.
Embryos display a moderately ventralised phenotype and the mutation has an haploinsufficient effect, a small fraction of heterozygous zygotes die before reaching adulthood. Maternally contributed tkv
alleles cause lethality.
Clonal analysis in the developing eye (using the FLP/FRT system) revealed nonautonomous phenotypes with large clones showing posterior-lateral eye parts missing.
Dominant lethality less than 50%. Homozygous and transheterozygous embryos were examined with respect to 25 cuticular markers, results demonstrate a graded requirement for dpp along the dorso-ventral axis.
Moderate ventralised phenotype. Rings of ventral denticle belts differentiate around the entire dorsoventral axis, almost no dorsal hairs are seen and the antennal and maxillary sense organs are missing. Defective movements of the germ band: due to loss of the amnioserosa and because the dorsalmost cells have acquired the lateral fate of the dorsal ectoderm. Dorsal cell fates are deleted and ventrolateral mitotic domains are expanded.
Heterozygotes with class I dpp
alleles have a wild type wing phenotype. Heterozygotes with class II allele dppd5
exhibit wings with a deletion of the anterior crossvein. Heterozygotes with class II allele dppd28
exhibit held out wings that are missing longitudinal and cross veins, deletion of tarsal claws, male terminalia and female analia. Heterozygotes with class III dpp
alleles display reduced held out wings that are missing longitudinal and cross veins, capitella-less halteres, reduced eyes, legs missing claws and missing or rotated male terminalia or female analia. Heterozygotes with class IV dpp
alleles display the same phenotype as class III heterozygotes with duplication of scutellar bristles, medial cleft of the dorsal notum, duplication of sex combs and partial duplication of the third antennal segment. Heterozygotes with class V dpp
alleles rarely eclose, the surviors exhibit the wing, haltere, eye and terminalia defects. At 18o
C the heterozygotes have less severe phenotypes.