Allele Dmel\drpr^Δ5

General Information
Symbol	Dmel\drpr^Δ5	Species	D. melanogaster
Name		FlyBase ID	FBal0152013
Feature type	allele	Associated gene	Dmel\drpr
Also Known As	draper^Δ5

Allele class
Mutagen	P-element activity
Recent Updates
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FB2013_03
FB2013_02
All updates	Click here to see a list of all updates to this record from FB2010_08 and on.
Nature of the Allele
Allele class
Mutagen	P-element activity (Freeman et al., 2003)
Mutations Mapped to the Genome

Type Location Additional Notes References
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name

UniProtKB/Swiss-Prot
UniProtKB/TrEMBL

Progenitor genotype	P{EP}drpr^EP522 (Freeman et al., 2003)
Nature of the lesion	Statement Reference Imprecise excision of the P{EP} element, resulting in a deletion of 1379bp that removes some drpr and some Oseg4 sequence. (Freeman et al., 2003)
Caused by aberration	Df(3L)drpr^Δ5 (Freeman et al., 2003)
Cytology
Phenotypic Data
Phenotypic Class
	immune response defective \| conditional (Hashimoto et al., 2009) neuroanatomy defective (Williams et al., 2006, MacDonald et al., 2006) neuroanatomy defective \| adult stage (Awasaki et al., 2006) neuroanatomy defective \| pupal stage (Awasaki et al., 2006, Okada et al., 2012) viable (Kurant et al., 2008)
Phenotype Manifest In
	adult mushroom body (Awasaki et al., 2006) adult olfactory receptor neuron (MacDonald et al., 2006) dendrite (Williams et al., 2006) dorsal multidendritic neuron ddaC (Williams et al., 2006) embryonic/larval salivary gland (McPhee et al., 2010) embryonic hemocyte (Kuraishi et al., 2009) gamma Kenyon cell (Awasaki et al., 2006) gamma Kenyon cell \| pupal stage (Okada et al., 2012) glial cell (Awasaki et al., 2006)
Detailed Description
	Statement Reference The pruning of gamma neurons of larval mushroom bodies during metamorphosis is severely impaired in drpr[Δ5] mutants. (Okada et al., 2012) 98% of drpr[Δ5] homozygous pupae display persistent salivary gland material. (McPhee et al., 2010) 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. (Hashimoto et al., 2009) The level of phagocytosis occurring in hemocytes of mutant embryos is reduced compared to controls. (Kuraishi et al., 2009) 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. (Kurant et al., 2008) 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). (Ziegenfuss et al., 2008) Homozygous clones grow equivalently to wild-type twin spots. (Li and Baker, 2007) 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. (Awasaki et al., 2006) 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. (MacDonald et al., 2006) In flies homozygous for drpr[Δ5], dendrite branch removal is strongly suppressed despite clear evidence of severing. (Williams et al., 2006)
External Data
Linkouts
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhancer of
Statement Reference drpr^Δ5/drpr[+] is an enhancer of neuroanatomy defective \| P-stage phenotype of Scer\GAL4^repo, ced-6^{dsRNA.Scer\UAS.cAa} (Awasaki et al., 2006)
Suppressor of
Statement Reference drpr^Δ5/drpr[+] is a suppressor of visible \| dominant phenotype of Bx¹ (Bejarano et al., 2008)
NOT Suppressor of
Statement Reference drpr^Δ5 is a non-suppressor of increased cell death \| somatic clone phenotype of Scer\GAL4^Act5C.PI, fwe^{Scer\UAS.P\T.Lose-B} (Rhiner et al., 2010)
Other
Statement Reference Oseg4^Δ5, drpr^Δ5 has lethal \| embryonic stage phenotype (Freeman et al., 2003, Freeman et al., 2003)
Phenotype Manifest In
Enhanced by
Statement Reference drpr^Δ5 has embryonic/larval salivary gland phenotype, enhanceable by Scer\GAL4^fkh.PH/BacA\p35^Scer\UAS.cHa (McPhee et al., 2010)
Suppressed by
Statement Reference drpr^Δ5 has embryonic/larval salivary gland phenotype, suppressible by Scer\GAL4^fkh.PH/Atg1^Scer\UAS.cSa (McPhee et al., 2010)
Enhancer of
Statement Reference drpr^Δ5/drpr[+] is an enhancer of glial cell phenotype of Scer\GAL4^repo, ced-6^{dsRNA.Scer\UAS.cAa} (Awasaki et al., 2006)
Suppressor of
Statement Reference drpr^Δ5/drpr[+] is a suppressor of wing margin phenotype of Bx¹ (Bejarano et al., 2008)
NOT Suppressor of
Statement Reference drpr^Δ5 is a non-suppressor of wing disc \| somatic clone phenotype of Scer\GAL4^Act5C.PI, fwe^{Scer\UAS.P\T.Lose-B} (Rhiner et al., 2010)
Other
Statement Reference Df(2R)w73-1/+, drpr^Δ5 has adult CNS glial cell phenotype (Doherty et al., 2009) drpr^Δ5/drpr[+], prtp^Δ1 has embryonic hemocyte phenotype (Kuraishi et al., 2009) Oseg4^Δ5, drpr^Δ5 has presumptive embryonic/larval central nervous system phenotype (Freeman et al., 2003, Freeman et al., 2003)
Additional Comments
Genetic Interactions
Statement Reference 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. (McPhee et al., 2010) 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. (Rhiner et al., 2010) 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. (Doherty et al., 2009) Larval hemocytes prepared from shark[1]/+ 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. (Hashimoto et al., 2009) 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). (Kuraishi et al., 2009) drpr[Δ5]/+ ; shark[1]/+ 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. (Ziegenfuss et al., 2008) When homozygous drpr^Δ5 clones (which are RpS17⁺) are induced in a background that is RpS17^unspecified/+ ; drpr^Δ5/+, cell competition appears to be reduced, as the RpS17^unspecified/+ ; drpr^Δ5/+ 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 drpr^Δ5 are eliminated as efficiently as Ts(1Rt;2Rt)Bld/+ cells which are drpr⁺ when induced in a RpL36⁺ background. (Li and Baker, 2007) 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]. (Awasaki et al., 2006) Df(3L)drpr^Δ5 homozygous embryos (which carry both Oseg4^Δ5 and drpr^Δ5) show embryonic lethality. The embryos show no defects in early central nervous system (CNS) development, but show clear defects in CNS cell corpse engulfment. (Freeman et al., 2003)
Xenogenetic Interactions
Statement Reference drpr[Δ5] mutant animals expressing BacA\p35[Scer\UAS.cHa] in the salivary glands under the control of Scer\GAL4[fkh.PH] display larger amounts of persistent salivary gland material, including multi-cell gland fragments, compared to drpr[Δ5] mutant animals. (McPhee et al., 2010)
Complementation & Rescue Data
Rescued by	drpr^Δ5 is rescued by Scer\GAL4^fkh.PH/drpr^I.Scer\UAS (McPhee et al., 2010)
Comments	Expression of drpr[I.Scer\UAS] under the control of Scer\GAL4[fkh.PH] in drpr[Δ5] mutant animals restores salivary gland degradation, and only 10% of animals display persistent gland material. (McPhee et al., 2010)
Stocks ( 0 )

Notes on Origin
Discoverer

Comments
	The drpr[Δ5] 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 drpr[Δ5] survive to adult stages. (MacDonald et al., 2006)
External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 3 )
Reported As
Symbol Synonym	draper^d5 (Bejarano et al., 2008) draper^Δ5 (Doherty et al., 2009, Ziegenfuss et al., 2008) drpr^Δ5 (Li and Baker, 2007, Kurant et al., 2008, Kuraishi et al., 2009, Okada et al., 2012, MacDonald et al., 2006, McPhee et al., 2010, Awasaki et al., 2006, Hashimoto et al., 2009)
Name Synonym	draper^Δ5 (Williams et al., 2006)
Secondary FlyBase IDs

References ( 14 )
Research paper	Okada et al., 2012, J. Biol. Chem. 287(5): 3138--3146 Apoptosis-dependent Externalization and Involvement in Apoptotic Cell Clearance of DmCaBP1, an Endoplasmic Reticulum Protein of Drosophila. [FBrf0217334] McPhee et al., 2010, Nature 465(7301): 1093--1096 Activation of autophagy during cell death requires the engulfment receptor Draper. [FBrf0211145] Rhiner et al., 2010, Dev. Cell 18(6): 985--998 Flower forms an extracellular code that reveals the fitness of a cell to its neighbors in Drosophila. [FBrf0211273] Doherty et al., 2009, J. Neurosci. 29(15): 4768--4781 Ensheathing glia function as phagocytes in the adult Drosophila brain. [FBrf0207750] Hashimoto et al., 2009, J. Immunol. 183(11): 7451--7460 Identification of lipoteichoic acid as a ligand for draper in the phagocytosis of Staphylococcus aureus by Drosophila hemocytes. [FBrf0209353] Kuraishi et al., 2009, EMBO J. 28(24): 3868--3878 Pretaporter, a Drosophila protein serving as a ligand for Draper in the phagocytosis of apoptotic cells. [FBrf0209536] Bejarano et al., 2008, Genetics 178(1): 307--323 A gain-of-function suppressor screen for genes involved in dorsal-ventral boundary formation in the Drosophila wing. [FBrf0202749] Kurant et al., 2008, Cell 133(3): 498--509 Six-microns-under acts upstream of Draper in the glial phagocytosis of apoptotic neurons. [FBrf0204720] Ziegenfuss et al., 2008, Nature 453(7197): 935--939 Draper-dependent glial phagocytic activity is mediated by Src and Syk family kinase signalling. [FBrf0205492] Li and Baker, 2007, Cell 129(6): 1215--1225 Engulfment is required for cell competition. [FBrf0201270] Awasaki et al., 2006, Neuron 50(6): 855--867 Essential role of the apoptotic cell engulfment genes draper and ced-6 in programmed axon pruning during Drosophila metamorphosis. [FBrf0192438] MacDonald et al., 2006, Neuron 50(6): 869--881 The Drosophila cell corpse engulfment receptor Draper mediates glial clearance of severed axons. [FBrf0193403] Williams et al., 2006, Nat. Neurosci. 9(10): 1234--1236 Local caspase activity directs engulfment of dendrites during pruning. [FBrf0192062] Freeman et al., 2003, Neuron 38(4): 567--580 Unwrapping glial biology: gcm target genes regulating glial development, diversification, and function. [FBrf0160527]

Allele Dmel\drprΔ5

Allele Dmel\drpr^Δ5