The class IV dendritic arborization neurons in Pka-C1H2 mutant clones show a significant decrease in the complexity of dendritic arbors in respect to the total dendritic length. The total number of dendritic branching points is also decreased.
Pka-C1H2 heterozygotes do not exhibit an effect on immediate memory and long-term memory.
No change in wing area is seen in heterozygous Pka-C1H2 mutant flies raised at 27[o]C.
Pka-C1H2/+ heterozygotes have dramatically improved memory retention curves compared with wild-type flies. Avoidance of naive flies to the odors odors and electrical shocks used during training is not significantly different between wild-type and Pka-C1H2 heterozygous mutants, indicating that the observed increases in memory are not caused by increased sensitivity to these stimuli. Memory retention curves of Pka-C1H2 /+ heterozygotes indicate that early forms of memory, including memory tested immediately after training (3-min memory) and short forms of memory (1-h memory) are not greatly affected. However, memory at later time points, 3 h and 7 h after training, progressively increases relative to wild-type, such that at 7h, memory is approximately double that of wild-type.
Pka-C1H2/+ flies have improved cold shock-resistant 3-h memory, indicating that anesthesia-resistant memory is increased in these flies. Pka-C1H2/+ heterozygote show increased 24-h memory after massed training, indicating increased ARM production.
Compared to wild-types, long-term memory is not altered in Pka-C1H2/+ heterozygotes.
Memory enhancement in Pka-C1H2/+ flies begins between 1 and 3 h after single cycle training and reverts to normal within 4 days after spaced training.
Heterozygotes show normal one-day memory after spaced training in a Pavlovian olfactory learning assay.
Pka-C1H2 germline clones show over 90% penetrance of mid-oogenesis AP polarity defects and fusion of nurse cell membranes. The polarity defects are in least in part due to a defect in microtubule organization; microtubules emanate from along the entire cortex in stage 8-10 oocytes, instead of emanating from multiple sites at the anterior cortex only as in wild-type oocytes. Additionally, a strong focus of microtubules is sometimes seen at the posterior pole of these clones, indicating that these oocytes aberrantly retain a discrete posterior microtubule organizing center. However, movement of the oocyte nucleus from the posterior to the anterior cortex is not affected and dorsal follicle cell fate is specified correctly.
When mutant clones are made in the legs of female adults, slightly thickened bristles are seen, indicating a weak transformation to male.
Egg chambers containing homozygous follicle cell clones contain ectopic polar cells.
Germ cells in embryos lacking maternal Pka-C1 function (derived from females carrying Pka-C1H2 germline clones and fertilised with a wild-type sperm) associate prematurely into clumps at stage 11 and remain in clumps at the centre of the embryo at later stages. There is an increase in germ cell number indicative of a failure to maintain cell cycle arrest. These embryos do not hatch.
Homozygous somatic stem cell clones in the ovary induce ectopic polar and border cells, but cause only mild over-proliferation of follicle cells and do not affect oocyte positioning or oocyte polarity (as indicated by normal migration of the oocyte nucleus to the dorsal anterior corner). Mutant ovarioles include follicle cells that proliferate beyond stage 6 (in contrast to wild type), although rarely beyond stage 8.
Heterozygotes show increased sensitivity to ethanol in an inebriometer assay.
Clones in the eye that lack both Pka-C1 and smo behave like loss of function Pka-C1 clones. Clones show ectopic photoreceptor differentiation and eventually merge with the endogenous field of differentiation, show no retardation of the furrow, pass through a furrow fate and induce non-autonomous ectopic photoreceptor differentiation outside the clone.
Homozygous clones produce anterior duplications of the normal pattern in the wing. Reduction or elimination of protein kinase A activity has no effect on the phenotype generated when the G-sα60A pathway is activated in wing epithelial cells; wing duplications that contain blisters are formed when G-sα60AQ215L.Scer\UAS is expressed in a Pka-C1H2 background using Scer\GAL4OK10.
Border follicle cells sometimes do not migrate or show incomplete migration in Pka-C1H2/Pka-C1Tw2 females.
Pka-C1H2 clones cause pattern defects in the wing, notum, halteres, antennae and leg.
Homozygous germline clones generate egg chambers with numerous nurse cell fusions.
Hemizygotes are larval lethal. Mature oocytes are smaller than wild type and nurse cells are multinucleate.