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General Information
Symbol
Dmel\drprΔ5
Species
D. melanogaster
Name
FlyBase ID
FBal0152013
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
draperΔ5, drprΔ5
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

drprΔ5 has a deletion of 1380bp in the promoter and first (non-coding) exon of the drpr locus.

Imprecise excision of the P{EP} element, resulting in a deletion of 1379bp that removes some drpr and some Oseg4 sequence.

Caused by aberration
Expression Data
Reporter Expression
Additional Information
Statement
Reference
 
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 1 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

drprΔ5 homozygous mutant stage 14 egg chambers show nurse cell clearance defect and contain persistent nurse cell nuclei, while in wild-type egg chambers all the germ-line derived nurse cells have undergone programmed cell death and been cleared by this stage.

drprΔ5 mutants do not display any significantly reduced survival when infected with Leishmania amastigotes, as compared to wild type.

Homozygous adults are short lived and show an age-dependent decline in locomotor activity in a negative geotaxis assay, as compared to age-matched controls.

30 day old homozygous adults sometimes show defects in the jump muscle of the thorax, including hyalinization with loss of striation, vacuolisation and variable muscle fiber size. The flight muscles appear normal. Degeneration is also seen in the brain and retina.

drprΔ5/Df(3L)BSC181 mutant pupae exhibit defects in phagocytic clearance of ddaC neuron dendrite debris following pupal stage dendritic pruning. Similarly, unlike in wild type, drprΔ5/Df(3L)BSC181 mutant larvae in which the dendrites have been injured (severed with an infrared laser) exhibit defects in debris clearance.

Homozygous drprΔ5 mutant flies are unable to clear axonal debris from L1 wing vein neurons following axotomy.

In the posterior abdominal region of the ventral nerve cord at 6 hours after pupal formation, drprΔ5 mutants exhibit similar numbers of astrocytic vacuoles compared with controls, although vacuole size is significantly reduced (by ~50% compared to controls).

drprΔ5 mutants exhibit a significant amount of brp[+] debris in the abdominal region of the ventral nerve cord.

drprΔ5 mutants exhibit a strong suppression of mushroom body γ neuron pruning at 18 hours after pupal formation and a mild phenotype in adults.

Under normal nutritional conditions drprΔ5 mutant egg chambers develop normally through mid-oogenesis. However, when degenerating egg chambers are induced by starvation drprΔ5 mutant flies show significant defects in the normal engulfment of dying germline cells. Unlike in wild type, the follicle cells fail to enlarge as nurse cell chromatin condenses, and minimal uptake of nuclear fragments is seen. As egg chamber death progresses, the follicle cells die without clearing most of the nurse cell debris.

The majority of drprΔ5 mutant germline clones in starvation-induced degenerating egg chambers are able to undergo proper follicle cell engulfment of germline debris, although some do show some aberrant engulfment.

Dispersed hemocytes derived from drprΔ5 embryos show a significantly reduced level of phagocytosis of apoptotic cells compared to wild type.

Axonal debris from severed ORN axons is not cleared in drprΔ5 mutants, indicating a defect in glial engulfment.

The pruning of gamma neurons of larval mushroom bodies during metamorphosis is severely impaired in drprΔ5 mutants.

drprΔ5 mutant embryonic hemocytes show decreased competence to undertake phagocytosis of apoptotic cells, as compared to controls. These mutants do not show a delay in development to adulthood, as compared to controls.

98% of drprΔ5 homozygous pupae display persistent salivary gland material.

Larval hemocytes prepared from drprΔ5 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 drprΔ5 hemocytes is equal to that of the parental strain. In vivo assays of drprΔ5 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 drprΔ5 flies.

B. subtilis and E. coli are less effectively phagocytosed by hemocytes prepared from drprΔ5 flies compared to wild type hemocytes.

drprΔ5 flies infected with the parental S. aureus strain die earlier than control flies. drprΔ5 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 drprΔ5 mutants. Antennal lobe morphology is grossly normal in drprΔ5 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 drprΔ5 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 drprΔ5 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 drprΔ5 mutants, approximately 65% of antennal lobes retain axonal fibers. Severed axon fragmentation is not blocked in drprΔ5 mutants. Severed axons show signs of fragmentation as early as 5 hours after injury in drprΔ5 mutants.

In flies homozygous for drprΔ5, dendrite branch removal is strongly suppressed despite clear evidence of severing.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Suppressed by
Statement
Reference

drprΔ5 has cell death defective | nutrition conditional phenotype, suppressible | partially by hepCA.UAS/Scer\GAL4GR1

Enhancer of
Statement
Reference
Suppressor of
Statement
Reference

drprΔ5/drpr[+] is a suppressor of visible | dominant phenotype of Bx1

NOT Suppressor of
Statement
Reference
Other
Phenotype Manifest In
Enhanced by
NOT Enhanced by
Statement
Reference
Suppressed by
Statement
Reference

drprΔ5 has egg chamber | nutrition conditional phenotype, suppressible | partially by hepCA.UAS/Scer\GAL4GR1

drprΔ5 has follicle cell | nutrition conditional phenotype, suppressible | partially by hepCA.UAS/Scer\GAL4GR1

Enhancer of
Statement
Reference

drprΔ5 is an enhancer of embryonic hemocyte phenotype of Itgbn2

Suppressor of
Statement
Reference

drprΔ5/drpr[+] is a suppressor of wing margin phenotype of Bx1

NOT Suppressor of
Statement
Reference
Other
Additional Comments
Genetic Interactions
Statement
Reference

The nurse cell clearance defect observed in drprΔ5 mutant stage 14 egg chambers (which contain persistent nurse cell nuclei, while in wild-type egg chambers all the germ-line derived nurse cells have undergone programmed cell death and been cleared by this stage) is not significantly exacerbated by combination with EatoMI14571 in homozygous state and both drprΔ5 single and EatoMI14571;drprΔ5 double mutant egg chambers display on average ~9 persistent nuclei.

Knockdown of Ced-12 in a drprΔ5 background, through the expression of Ced-12KK102788 under the control of Scer\GAL4alrm.PD, leads to a near-complete loss of astrocytic vacuole formation.

Knockdown of Crk in a drprΔ5 background, through the expression of CrkGD8583 under the control of Scer\GAL4alrm.PD, leads to the loss of astrocytic vacuole formation. These animals also exhibit a significant accumulation of brp[+] debris in the SOG and the abdominal region of the ventral nerve cord.

Knockdown of Ced-12 in a drprΔ5 background, through the expression of Ced-12KK102788 under the control of Scer\GAL4alrm.PD, results in an additive phenotype, with these animals exhibiting a stronger suppression of mushroom body γ axon pruning at 48 hours after pupal formation and into adult stages.

Knockdown of Crk in a drprΔ5 background, through the expression of CrkGD8583 under the control of Scer\GAL4alrm.PD, results in an additive phenotype, with these animals exhibiting a stronger suppression of mushroom body γ axon pruning at 48 hours after pupal formation and into adult stages.

Expression of hepCA.Scer\UAS under the control of Scer\GAL4GR1 partially rescues the cell death defects seen in drprΔ5 mutant starvation-induced degenerating egg chambers. Many abnormal egg chambers are still seen but, unlike in drprΔ5 mutants alone, enlargement of the follicle cells occurs and germline engulfment takes place. Hyper-engulfment, where follicle cells engulf intact nurse cells, takes place in some egg chambers.

Itgbn2, drprΔ5 double mutants show a significant delay in development to adulthood, as compared to wild-type controls and either single mutants.

Expression of Atg1Scer\UAS.cSa in the salivary glands under the control of Scer\GAL4fkh.PH in drprΔ5 mutant animals completely suppresses the persistent salivary gland tissue phenotype.

Cell clones generated in the wing imaginal disc epithelium that are homozygous for drprΔ5 and overexpress fweScer\UAS.cRc driven by Scer\GAL4Act5C.PI still undergo apoptosis.

Glial clearance of axonal debris from the central nervous system after severing of the maxillary palp is impaired in drprΔ5/+ ; Df(2R)w73-1/+ animals.

Larval hemocytes prepared from shark1/+ drprΔ5/+ flies show the same the level of phagocytosis of S. aureus as either single heterozygote.

Larval hemocytes prepared from flies simultaneously heterozygous for drprΔ5, Rac1J11 and Rac2Δ show a significant reduction in the level of phagocytosis of S. aureus.

The level of phagocytosis occurring in the hemocytes of prtpΔ1 drprΔ5 double homozygous embryos is not significantly different from the reduction seen in each single homozygote.

prtpΔ1/+ ; drprΔ5/+ 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).

drprΔ5/+ ; shark1/+ 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-6dsRNA.Scer\UAS.cAa under the control of Scer\GAL4repo at 18 hours after puparium formation is enhanced by drprΔ5.

Df(3L)drprΔ5 homozygous embryos (which carry both Oseg4Δ5 and drprΔ5) show embryonic lethality. The embryos show no defects in early central nervous system (CNS) development, but show clear defects in CNS cell corpse engulfment.

Xenogenetic Interactions
Statement
Reference

drprΔ5 mutant animals expressing BacA\p35Scer\UAS.cHa in the salivary glands under the control of Scer\GAL4fkh.PH display larger amounts of persistent salivary gland material, including multi-cell gland fragments, compared to drprΔ5 mutant animals.

Complementation and Rescue Data
Comments

Expression of drprI.Scer\UAS in the follicle cells under the control of Scer\GAL4GR1 rescues the enlargement and nurse cell debris uptake defects seen in starvation-induced degenerating egg chambers in drprΔ5 mutant flies. Unlike in drprΔ5 alone, no premature follicle cell death is seen.

Expression of drprScer\UAS.cFa under the control of Scer\GAL4srp.Hemo rescues the reduced level of phagocytosis of apoptotic cells seen in dispersed hemocytes derived from drprΔ5 embryos.

Expression of drprY858F.Scer\UAS under the control of Scer\GAL4srp.Hemo fails to rescue the reduced level of phagocytosis of apoptotic cells seen in dispersed hemocytes derived from drprΔ5 embryos.

Glial expression of drprI.Scer\UAS rescues the engulfment defects found in degenerating ORN axons in drprΔ5 mutants.

Expression of drprI.Scer\UAS under the control of Scer\GAL4fkh.PH in drprΔ5 mutant animals restores salivary gland degradation, and only 10% of animals display persistent gland material.

Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
Comments
Comments

The drprΔ5 allele used in FBrf0160527 was found to have an unlinked lethal mutation which was removed by standard mitotic recombination over a wild-type chromosome. Animals bearing this version of drprΔ5 survive to adult stages.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (6)
References (38)