endosome & embryonic nervous system
Rab52 larval fat body clone cells are slightly but significantly larger than control cells.
Fat body cells in Rab52 mutant somatic clones in starved third instar larvae are larger than the surrounding control cells but show similar number and size of autophagic structures and acidic autolysosomes (detected by LysoTracker staining).
Rab52 heterozygotes do not exhibit a discernible phenotype in the adult brain.
Homozygous single-cell DL1 PN clones show defects in both the axons and dendrites. The axon fails to exit the antennal lobe in 47.6% of cases. The dendrites have an additional branch appearing from the proximal side of the dendrite shaft (85.7% penetrance), and sometimes target two glomeruli instead of a single glomerulus.
Rab52 mutant cells display seamless tracheal tube cysts and disorganized tube termini. They also show reduced terminal branching, failure in gas filling, increased tube diameter, and extreme disorganization of the apical membrane.
Mutant egg chambers in females containing homozygous germline clones show normal accumulation of intracellular lipid droplets.
The cortical F-actin layer at the posterior pole of stage 10b oocytes is disrupted in females carrying homozygous germline clones.
Homozygous mutant Rab52 eye disc clones do not undergo R-cell differentiation, leading to the overgrowth of the eye imaginal discs.
Eggs derived from Rab52 germ-line clones are flaccid, and they collapse. In Rab52 germ line clones, no condensed yolk granules are observed in the oocyte cytoplasm. Clathrin coated pits are still present at the oocyte plasma membrane. Below the plasma membrane, the density of early endocytic vesicles is increased compared to controls.
Oocytes derived from homozygous germline clones lack yolk granules.
Homozygous Rab52 mutant neurons extend axons and major dendritic branches, however, they display greatly simplified dendritic arbors and decreased number of terminal branches compared with that found for wild-type neurons.
Mutant eye discs (generated using the eyFLP-cell lethal system) show disorganised cellular architecture and reduced differentiation compared to wild type.
Larvae containing mutant eye discs generated using the eyFLP-cell lethal system are increased in size compared to control larvae when examined as pupariation commences. The animals do not develop into adults.
Wing discs contain regions of neoplastic overgrowth in animals in which clones have been induced in the wing, haltere and leg discs (using the UbxFLP-cell lethal system). Eye discs are normal in these animals.
Zygotic loss of Rab52 results in the disruption of endosomes in the embryonic nervous system. In control embryos, the Avic\GFPScer\UAS.T:Hsap\MYC,T:Mmus\2xFYVE-positive endosomes appear as punctate structures within the cell bodies of the central nervous system, peripheral nervous system and neuromuscular junctions. Avic\GFPScer\UAS.T:Hsap\MYC,T:Mmus\2xFYVE-positive endosomes are disrupted in the nervous system and neuromuscular junctions of Rab52 mutant embryos.
Df(1)rush4, Rab52, sta+t4.4 has partially lethal - majority live phenotype, suppressible | partially by rushUAS.GFP/Scer\GAL4arm.PS
Rab52 has abnormal cell size | somatic clone | third instar larval stage phenotype, non-suppressible by Mon1mut4/Mon1mut4
Rab52 is a suppressor | partially of decreased cell number | adult stage | progressive phenotype of Hsap\BIN1UAS.1, Scer\GAL4ninaE.PT
Rab52/Rab5[+] is a suppressor of abnormal neuroanatomy phenotype of vap2
Df(1)rush4, Rab52, sta+t4.4 has partially lethal - majority live phenotype
Rab52/Rab5[+], Scer\GAL4en-e16E, Vps45RNAi.UAS.WIZ has visible phenotype
Rab52 has embryonic/larval fat body | somatic clone | third instar larval stage phenotype, non-suppressible by Mon1mut4/Mon1mut4
Rab52/Rab5[+] is an enhancer of eye phenotype of RN-treUAS.cHa, Scer\GAL4GMR.long
Rab52 is a suppressor | partially of outer photoreceptor cell | adult stage | decreased number phenotype of Hsap\BIN1UAS.1, Scer\GAL4ninaE.PT
Rab52/Rab5[+] is a suppressor of adult brain phenotype of vap2
Rab52 is a suppressor of wing vein L5 phenotype of Df(3L)ru-22/rhove-1
Rab52 is a suppressor of wing vein L5 phenotype of rhove-1
Rab52/Rab52 is a non-suppressor of embryonic/larval fat body | somatic clone | third instar larval stage phenotype of Mon1mut4
Rab52/Rab52 is a non-suppressor of autolysosome | somatic clone | third instar larval stage phenotype of Mon1mut4
Rab52/Rab5[+], Scer\GAL4en-e16E, Vps45RNAi.UAS.WIZ has wing phenotype
Somatic clones of fat body cell double mutant for both Rab52 and Mon1mut4 are larger than their neighboring control cells (as are Rab52 single mutant cells) but display similar abnormal accumulation of autophagosomes and lack of acidic autolysosomes as Mon1mut4 mutant cells in starved third instar larvae.
While Df(1)rush4, sta+t4.4 homozygous fies and Rab52heterozygotes are viable, their combination decreases viability at embryonic and pupal stages. This decreased survival is partially rescued by expression of rushScer\UAS.T:Avic\GFP under the control of Scer\GAL4arm.PS.
Reducing the dosage of Rab5 through a Rab52 heterozygous background significantly enhances the RN-treScer\UAS.cHa-induced rough eye phenotype.
Expression of Vps45dsRNA.Scer\UAS.WIZ under the control of Scer\GAL4en-e16E in a Rab52/+ background results in defects in the wing.
Expression of Rab5Scer\UAS.P\T.T:Avic\GFP-YFP under the control of Scer\GAL4GH146 rescues the defects seen in homozygous Rab52 single-cell DL1 olfactory projection neuron clones.