Wing defects are seen in aploxP.MCP-PRE.MM/ap4 mutant flies, but they are significantly less severe than those seen in aploxP.MCP-PRE.MM homozygotes.
Wing defects are seen in Df(2R)DG-Mcp/ap4 mutant flies, but they are less severe than those seen in Df(2R)DG-Mcp homozygotes.
Wing defects are seen in Df(2R)DG/ap4 mutant flies, but they are less severe than those seen in Df(2R)DG homozygotes.
Homozygotes have reduced pre-eclosion viability and live for only about 3 days after eclosion. Homozygous females are sterile; the ovaries are poorly developed, fragile and contain no vitellogenic egg chambers.
The application of juvenile hormone III has a significant stimulatory effect on the ovary maturity index in mutant females, primarily due to a change in ovary volume.
Adults show defects in the direct flight muscles. Of the group of four muscles 51-54, only a sliver of muscle fibre develops. IFMs are reduced in width at the posterior attachment site and do not undergo complete splitting. Sometimes only a single fibre is evident. Muscle size and volume is reduced.
Homozygotes generally die 24 to 48 hours after eclosion.
Homozygotes and hemizygotes exhibit nubbin wings. Transheterozygotes with apUG-24A exhibit a much larger wing blade with deep notches.
Ultrastructure of the corpus allatum studied.
Histolysis of the larval fat body is not completed in homozygous flies and they die within 48 hours of eclosion.
Homozygous ap4 males are behaviorally sterile but have fertile gametes. For mating success ap4 is an amorph. Homozygous ap4 males showed significantly less nonwing courtship than wild type, this was a result of weakness and sluggishness, attributable to the ap locus. Homozygous ap4 males had higher immature sex appeal and rear displays component of courtship at 2--3 days old than mature wild type flies.
Blocks vitellogenesis causing an egg maturation defect. Corpora allata are defective in hormone production.
Homozygous ap4 flies have virtually no wing blade and have only 13% female receptivity to mature male ap+ flies. Female flies have a high courtship intensity, but low percentage mating: this is due to low receptivity not low 'sex appeal'. Survival of ap4/Df(2R)M41A4B is only 1% at 3 days of age.
Pleiotropic effects on the morphology and lifespan of adult flies. Mutant males spend less time courting and are less likely to perform some of the courtship behaviours than age-matched controls. Abnormalities are an indirect effect of the mutation which causes partial paralysis, lack of coordination and sluggishness.
Abnormal haemolymph.
Wings less than 10% normal length, lacking all wing blade structures. Halteres reduced to structureless remnants less than 25% normal size. Scutellar and dorsocentral bristles sometimes missing (FBrf0017003). Wing phenotype disc-autonomous in ap4/ap+ mosaic flies, although small patches of ap4 wing structures are found in ap4/ap+ mosaic wings. Haltere phenotype disc-autonomous (FBrf0036211). Adults become paralyzed about 30 hr following eclosion and die soon thereafter. Around 1% of adults are long-lived 'escapers' of this phenotype (FBrf0034522). Precocious adult-death phenotype fate-maps to proximity of Malpighian tubules and tubule malfunctioning postulated to result in this phenotype (FBrf0036211). Foregut of females swollen owing to accumulation of peritrophic membrane (FBrf0011908). Female sterile with underdeveloped ovaries; nurse cell nuclei become pycnotic after stage 7 and stage-8 oocytes are the most advanced (FBrf0011400; FBrf0034522). Ovaries develop nonautonomously when transplanted to a wild-type host (FBrf0017349). Application of juvenile hormone analog, ZR-515, to newly eclosed females results in vitellogenic oocytes (FBrf0025594). Membranes of vitellogenic oocytes lack microvilli and pinocytoxic vesicles normally present; development of these structures stimulated by administration of ZR-515 (FBrf0036874). Corpora allata from adult ap4 are juvenile-hormone deficient when bioassayed (FBrf0028948). Nonvitellogenic oocyte phenotype fate-maps to same or similar location as precocious adult death phenotype (FBrf0036211). Escaper females develop stage-14 oocytes (FBrf0011908) and are fertile (FBrf0034522). Males show immature sexual behavior and are sterile, but testes appear normal with motile sperm (FBrf0011908). Larval fat body histolysis delayed; this phenotype is nonautonomous as determined by transplantation experiments (FBrf0023756). Application of ZR-515 accelerates larval fat body histolysis in adults (FBrf0032050). Ovarian acid phosphatase level low in females and is restored after application of ZR-515 (FBrf0028948). Ovaries cultured in vitro are capable of yolk protein synthesis (FBrf0064836). ap4/Df(2R)M41A4 hemizygote has nearly normal complement of bristles but otherwise resembles ap4 homozygote (FBrf0017003). RK2.
ap4 has indirect flight muscle cell phenotype, enhanceable by sr03999/sr03999
ap4 has indirect flight muscle cell phenotype, enhanceable by sr[+]/srG11
ap4/ap4 is an enhancer of mesothoracic tergum phenotype of sr03999
ap4/ap4 is an enhancer of adult epidermis phenotype of sr03999
No wing scalloping is seen when combined with SsdpKG03600, SsdpBG01663, Ssdpneo48, Ssdp31 or Ssdp11.
ap4 is partially rescued by apUAS.cOa/Scer\GAL41151
ap4 is partially rescued by apUAS.cOa/Scer\GAL4pnr-MD237
apScer\UAS.cOa, when expressed via Scer\GAL41151, partially rescues the DFM loss phenotype of ap4 mutants (though a large single muscle mass develops as opposed to four discrete fibres) but does not rescue the IFM phenotype. When expression of apScer\UAS.cOa is driven by Scer\GAL4pnr-MD237, the DLM defects of ap4 mutants are significantly rescued (though a large single muscle mass develops as opposed to four discrete fibres) while DFM fibres remain disorganised. Muscle volume is significantly restored.
Medvedev, 15th Jan. 1932.
