Deletion of drk.
drkΔP24 mosaic clones are made in the antenna and the eye by using the eyFLP system.
partially lethal (with drk6)
Adults bearing whole-eye/antenna drkΔP24 clones have severely reduced climbing activity, suggesting defects in gravity sensing. These individuals exhibit disorganized scolopidia (as revealed by phalloidin staining, which labels cap rods, scolopale rods, and the actin bundles within the cilia of the mechanosensory neurons) and significantly smaller antennal mechanosensory motor center, indicating loss of sensory nerve terminals in the brain.
Olfactory association learning is lower in drkΔP24 heterozygotes compared to controls. There is a 20% decrease in learning after training with 6 or less pairings.
Histological and immunohistochemical examination of drke0A heterozygous heads with multiple antigenic markers does not reveal and gross structural anomalies in the brain. Avoidance of odors used as CS and electroshock (US) are no different from that of controls. Heterozygous mutants exhibit normal odor avoidance after pre-exposure to electric shock.
drkΔP24 homozygous clones in the dorsal air sac primordium are found at the tip of the primordium at a significantly lower frequency than wild-type clones.
The initiation of mesoderm spreading is unaffected in embryos derived from homozygous female germline clones.
Mutants exhibit no defects in hemocyte migration.
When mutant somatic clones are made in the border cells no effect is seen.
drkΔP24 has abnormal gravitaxis | somatic clone phenotype, suppressible by Scer\GAL4elav.PU/Hsap\GRAP311.UAS.Tag:HA
drkΔP24 has abnormal learning phenotype, suppressible by Scer\GAL4c747/Ras85DV12.S35.UAS
drkΔP24 has abnormal learning phenotype, suppressible by Scer\GAL4c747/RafUAS.F179
drkΔP24 has abnormal gravitaxis | somatic clone phenotype, non-suppressible by Scer\GAL4elav.PU/Hsap\GRAPUAS.Tag:HA
drkΔP24 has abnormal learning phenotype, non-suppressible by Scer\GAL4c747/Scer\GAL80ts.αTub84B/Ras85DV12.S35.UAS
drkΔP24 has abnormal learning phenotype, non-suppressible by Scer\GAL4c747/RafUAS.F179/Scer\GAL80ts.αTub84B
drkΔP24 has abnormal memory phenotype, non-suppressible by Scer\GAL4c747/RafUAS.F179
drkΔP24 has abnormal memory phenotype, non-suppressible by Scer\GAL4c747/Raffl.UAS
drk[+]/drkΔP24 is a suppressor of phenotype of Src42ASu(Raf)1-1
Expression of Ras85DV12.S35.Scer\UAS alone, or combined with the Scer\GAL4c747 driver but kept silent by Scer\GAL80ts.αTub84B does not suppress the learning deficit of drkΔP24/+ animals. In contrast, expression of Ras85DV12.S35.Scer\UAS by inactivation of the Scer\GAL80ts.αTub84B suppressor restores normal learning to drkΔP24 heterozygotes, while it does not appear to affect learning in control animals.
Expression of phlScer\UAS.F179 alone, or combined with the Scer\GAL4c747 driver but kept silent by Scer\GAL80ts.αTub84B does not suppress the learning deficit of drkΔP24/+ animals. Conditional expression of phlScer\UAS.F179 in adult mushroom bodies reverse the learning deficit of drkΔP24 heterozygotes.
Expression of phlScer\UAS.F179 under the control of Scer\GAL4c747 does not rescue 90 minute memory in drkΔP24/+ animals.
Dominantly suppresses the ability of Src42ASu(phl)1-1 to suppress the lethality of phl1/Y flies.
drkΔP24 is partially rescued by Scer\GAL4elav.PU/drkUAS.cUa
T. Raabe and E. Hafen.