|Feature type||allele||Associated gene||Dmel\drpr|
|Also Known As||draperΔ5|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
|Caused by aberration|
|Phenotype Manifest In|
The pruning of gamma neurons of larval mushroom bodies during metamorphosis is severely impaired in drpr[Δ5] mutants.
Larval hemocytes prepared from drpr[Δ5] flies less effectively phagocytose the parental S. aureus strain, compared with hemocytes of wild type flies. In contrast to wild type, phagocytosis of the mutant 'ItaS' S. aureus strain by drpr[Δ5] hemocytes is equal to that of the parental strain. In vivo assays of drpr[Δ5] flies produce the same results. A S. aureus strain lacking WTA is less effectively phagocytosed than the parental S. aureus strain by hemocytes prepared from drpr[Δ5] flies. B. subtilis and E. coli are less effectively phagocytosed by hemocytes prepared from drpr[Δ5] flies compared to wild type hemocytes. drpr[Δ5] flies infected with the parental S. aureus strain die earlier than control flies. drpr[Δ5] flies show increased growth of the bacteria compared to controls.
The level of phagocytosis occurring in hemocytes of mutant embryos is reduced compared to controls.
The number and total volume of apoptotic particles in the central nervous system (CNS) is increased about 2-fold compared to wild type. There is no significant defect in engulfment, with the fraction of untouched particles being similar to that seen in the wild type. Instead, the excess particles accumulate in the phagocytes.
Mutants show defects in glial phagocytic function; significant amounts of axonal debris remain within Or85e-innervated glomeruli and in the maxillary nerve 5 days after ablation of maxillary palps in heterozygous and homozygous animals, in contrast to control animals. Homozygous stage 14-15 embryos show a marked increase in the number of central nervous system cell corpses (38.5 cell corpses per hemisegment) compared to control embryos (24.4 cell corpses per hemisegment).
Homozygous clones grow equivalently to wild-type twin spots.
Pruning of the larval axon branches of the γ neurons is suppressed in mutants, such that many of the larval axons persist in mutant pupae at 18 hours after puparium formation (APF). The larval γ neuron branches persist in both the dorsal and medial lobes at 24 and 48 hours after puparium formation, though their total volume appears to decrease. Abnormal axon branches are seen outside of the α/β lobes in 1 week old mature adults, which appear (from analysis of marker expression) to be the remnants of the larval γ neurons. In addition, fusion of the β lobes is seen after 48 hours APF in the mutant animals. At 6 and 18 hours APF, the volume of the distal tip region of the mushroom body dorsal lobes which is infiltrated by glial processes is decreased in mutants compared to wild type. The number of glial lumps over 2 μM per mushroom body lobe is severely reduced in the mutants compared to wild type at these timepoints (these lumps are normally formed by glial processes that engulf clusters of varicosities on the axon branches), and glial lumps are observed only near the periphery of the mutant mushroom body lobes in the vicinity of the glial cell bodies.
Antennal lobe glia show no noticeable changes in morphology when the third antennal segment is ablated in drpr[Δ5] mutants. Antennal lobe morphology is grossly normal in drpr[Δ5] mutants. In wild-type controls, ablation of the maxillary palps leads to enrichment of glial membranes with maxillary palp-innervated glomeruli. However, this is blocked in drpr[Δ5] mutants. Glial processes do not accumulate in glomeruli housing severed maxillary palp ORN axons nor are they recruited at high levels to the maxillary nerve. The majority of axonal debris lingered in the CNS of drpr[Δ5] mutants after ablation of the third antennal segments. Three days after injury there is an abundance of axon fibers remaining in the antennal lobes. Five days after injury in drpr[Δ5] mutants, approximately 65% of antennal lobes retain axonal fibers. Severed axon fragmentation is not blocked in drpr[Δ5] mutants. Severed axons show signs of fragmentation as early as 5 hours after injury in drpr[Δ5] mutants.
|NOT Suppressor of|
|Phenotype Manifest In|
|NOT Suppressor of|
Expression of Atg1[Scer\UAS.cSa] in the salivary glands under the control of Scer\GAL4[fkh.PH] in drpr[Δ5] mutant animals completely suppresses the persistent salivary gland tissue phenotype.
Cell clones generated in the wing imaginal disc epithelium that are homozygous for drpr[Δ5] and overexpress fwe[Scer\UAS.cRc] driven by Scer\GAL4[Act5C.PI] still undergo apoptosis.
Glial clearance of axonal debris from the central nervous system after severing of the maxillary palp is impaired in drpr[Δ5]/+ ; Df(2R)w73-1/+ animals.
Larval hemocytes prepared from shark/+ drpr[Δ5]/+ flies show the same the level of phagocytosis of S. aureus as either single heterozygote. Larval hemocytes prepared from flies simultaneously heterozygous for drpr[Δ5], Rac1[J11] and Rac2[Δ] show a significant reduction in the level of phagocytosis of S. aureus.
The level of phagocytosis occurring in the hemocytes of prtp[Δ1] drpr[Δ5] double homozygous embryos is not significantly different from the reduction seen in each single homozygote. prtp[Δ1]/+ ; drpr[Δ5]/+ double heterozygotes show a reduced level of phagocytosis in embryonic hemocytes (neither of the single heterozygotes shows a reduction in phagocytosis compared to wild type).
drpr[Δ5]/+ ; shark/+ double heterozygotes show a striking suppression of clearance of severed axons in Or85e-innervated glomeruli and in the maxillary nerve compared to controls 5 days after ablation of maxillary palps.
When homozygous drprΔ5 clones (which are RpS17+) are induced in a background that is RpS17unspecified/+ ; drprΔ5/+, cell competition appears to be reduced, as the RpS17unspecified/+ ; drprΔ5/+ cells contribute to more of the territory and show reduced cell death compared to experiments where they are competing against +/+ cells. Ts(1Rt;2Rt)Bld/+ cells which are simultaneously homozygous for drprΔ5 are eliminated as efficiently as Ts(1Rt;2Rt)Bld/+ cells which are drpr+ when induced in a RpL36+ background.
The reduced glial infiltration phenotype and reduction in glial lumps over 2 μM per mushroom body lobe seen in animals expressing ced-6[dsRNA.Scer\UAS.cAa] under the control of Scer\GAL4[repo] at 18 hours after puparium formation is enhanced by drpr[Δ5].
|Complementation & Rescue Data|
|Stocks ( 0 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 3 )|
|Secondary FlyBase IDs|
|References ( 14 )|