FlyBase Allele Report: Dmel\drpr[Δ5]

drpr^Δ5 third instar larvae exhibit decreased crawling ability, namely a severe decrease in linear movement, and adults show decreased climbing ability. Larval macrophages show decreased binding and phagocytosis of apoptotic cells

(Petrignani et al., 2021)

drpr^Δ5 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.

(Santoso et al., 2018)

drpr^Δ5 mutants do not display any significantly reduced survival when infected with Leishmania amastigotes, as compared to wild type.

(Okuda et al., 2016)

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.

(Draper et al., 2014)

drpr^Δ5/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, drpr^Δ5/Df(3L)BSC181 mutant larvae in which the dendrites have been injured (severed with an infrared laser) exhibit defects in debris clearance.

(Han et al., 2014)

Homozygous drpr^Δ5 mutant flies are unable to clear axonal debris from L1 wing vein neurons following axotomy.

(Neukomm et al., 2014)

In the posterior abdominal region of the ventral nerve cord at 6 hours after pupal formation, drpr^Δ5 mutants exhibit similar numbers of astrocytic vacuoles compared with controls, although vacuole size is significantly reduced (by ~50% compared to controls).

drpr^Δ5 mutants exhibit a significant amount of brp[+] debris in the abdominal region of the ventral nerve cord.

drpr^Δ5 mutants exhibit a strong suppression of mushroom body γ neuron pruning at 18 hours after pupal formation and a mild phenotype in adults.

(Tasdemir-Yilmaz and Freeman, 2014)

Under normal nutritional conditions drpr^Δ5 mutant egg chambers develop normally through mid-oogenesis. However, when degenerating egg chambers are induced by starvation drpr^Δ5 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 drpr^Δ5 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.

(Etchegaray et al., 2012)

Dispersed hemocytes derived from drpr^Δ5 embryos show a significantly reduced level of phagocytosis of apoptotic cells compared to wild type.

(Fujita et al., 2012)

Axonal debris from severed ORN axons is not cleared in drpr^Δ5 mutants, indicating a defect in glial engulfment.

(Logan et al., 2012)

The pruning of gamma neurons of larval mushroom bodies during metamorphosis is severely impaired in drpr^Δ5 mutants.

(Okada et al., 2012)

drpr^Δ5 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.

(Nagaosa et al., 2011)

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 genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

drpr^Δ5 has increased cell number | spermatogenesis phenotype, enhanceable by Scer\GAL4^C587/Ced-12^KK102788

(Zohar-Fux et al., 2022)

drpr^Δ5 has increased cell number | spermatogenesis phenotype, enhanceable by crq^GD784/Scer\GAL4^C587

(Zohar-Fux et al., 2022)

drpr^Δ5 has abnormal neuroanatomy phenotype, enhanceable by Ced-12^KK102788/Scer\GAL4^alrm.PD

(Tasdemir-Yilmaz and Freeman, 2014)

drpr^Δ5 has abnormal neuroanatomy phenotype, enhanceable by Crk^GD8583/Scer\GAL4^alrm.PD

(Tasdemir-Yilmaz and Freeman, 2014)

NOT Enhanced by

Statement

Reference

drpr^Δ5 has abnormal neuroanatomy | P-stage phenotype, non-enhanceable by ctg^wgd/galectin^wgv

(Sung et al., 2024)

drpr^Δ5 has increased cell number | spermatogenesis phenotype, non-enhanceable by Scer\GAL4^C587/Lamp1^GD1798

(Zohar-Fux et al., 2022)

Suppressed by

Statement

Reference

drpr^Δ5 has abnormal cell death | nutrition conditional phenotype, suppressible by hep^CA.UAS/Scer\GAL4^GR1

(Etchegaray et al., 2012)

NOT suppressed by

Statement

Reference

drpr^Δ5 has abnormal neuroanatomy | P-stage phenotype, non-suppressible by ctg^wgd/galectin^wgv

(Sung et al., 2024)

Enhancer of

Statement

Reference

drpr^Δ5 is an enhancer of increased cell number | spermatogenesis phenotype of Ced-12^KK102788, Scer\GAL4^C587

(Zohar-Fux et al., 2022)

drpr^Δ5/drpr[+] is an enhancer of abnormal neuroanatomy | P-stage phenotype of Scer\GAL4^repo, ced-6^RNAi.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^UASp.Lose-B

(Rhiner et al., 2010)

Other

Statement

Reference

Pez^CB-5380-3, drpr^Δ5 has abnormal wound healing | embryonic stage phenotype

(Campbell et al., 2021)

Itgbn², drpr^Δ5 has abnormal developmental rate phenotype

(Nagaosa et al., 2011)

Oseg4^Δ5, drpr^Δ5 has lethal | embryonic stage phenotype

(Freeman et al., 2003)

Phenotype Manifest In

Enhanced by

Statement

Reference

drpr^Δ5 has spermatogonium | increased number phenotype, enhanceable by Scer\GAL4^C587/Ced-12^KK102788

(Zohar-Fux et al., 2022)

drpr^Δ5 has spermatogonium | increased number phenotype, enhanceable by crq^GD784/Scer\GAL4^C587

(Zohar-Fux et al., 2022)

drpr^Δ5 has astrocyte-like glial cell phenotype, enhanceable by Ced-12^KK102788/Scer\GAL4^alrm.PD

(Tasdemir-Yilmaz and Freeman, 2014)

drpr^Δ5 has gamma Kenyon cell phenotype, enhanceable by Ced-12^KK102788/Scer\GAL4^alrm.PD

(Tasdemir-Yilmaz and Freeman, 2014)

drpr^Δ5 has astrocyte-like glial cell phenotype, enhanceable by Crk^GD8583/Scer\GAL4^alrm.PD

(Tasdemir-Yilmaz and Freeman, 2014)

drpr^Δ5 has gamma Kenyon cell phenotype, enhanceable by Crk^GD8583/Scer\GAL4^alrm.PD

(Tasdemir-Yilmaz and Freeman, 2014)

drpr^Δ5 has embryonic/larval hemocyte phenotype, enhanceable by Itgbn²

(Nagaosa et al., 2011)

drpr^Δ5 has embryonic/larval salivary gland phenotype, enhanceable by Scer\GAL4^fkh.PH/BacA\p35^UAS.cHa

(McPhee et al., 2010)

NOT Enhanced by

Statement

Reference

drpr^Δ5 has dendrite | P-stage phenotype, non-enhanceable by ctg^wgd/galectin^wgv

(Sung et al., 2024)

drpr^Δ5 has larval dorsal multidendritic neuron ddaC | P-stage phenotype, non-enhanceable by ctg^wgd/galectin^wgv

(Sung et al., 2024)

drpr^Δ5 has spermatogonium | increased number phenotype, non-enhanceable by Scer\GAL4^C587/Lamp1^GD1798

(Zohar-Fux et al., 2022)

drpr^Δ5 has nurse cell phenotype, non-enhanceable by Eato^MI14571/Eato^MI14571

(Santoso et al., 2018)

drpr^Δ5 has egg chamber phenotype, non-enhanceable by Eato^MI14571/Eato^MI14571

(Santoso et al., 2018)

Suppressed by

Statement

Reference

drpr^Δ5 has lysosome | increased number phenotype, suppressible by Scer\GAL4^C587/Lamp1^GD1798

(Zohar-Fux et al., 2022)

drpr^Δ5 has egg chamber | nutrition conditional phenotype, suppressible by hep^CA.UAS/Scer\GAL4^GR1

(Etchegaray et al., 2012)

drpr^Δ5 has follicle cell | nutrition conditional phenotype, suppressible by hep^CA.UAS/Scer\GAL4^GR1

(Etchegaray et al., 2012)

drpr^Δ5 has embryonic/larval salivary gland phenotype, suppressible by Scer\GAL4^fkh.PH/Atg1^UAS.cSa

(McPhee et al., 2010)

NOT suppressed by

Statement

Reference

drpr^Δ5 has dendrite | P-stage phenotype, non-suppressible by ctg^wgd/galectin^wgv

(Sung et al., 2024)

drpr^Δ5 has larval dorsal multidendritic neuron ddaC | P-stage phenotype, non-suppressible by ctg^wgd/galectin^wgv

(Sung et al., 2024)

Enhancer of

Statement

Reference

drpr^Δ5 is an enhancer of spermatogonium | increased number phenotype of Ced-12^KK102788, Scer\GAL4^C587

(Zohar-Fux et al., 2022)

drpr^Δ5 is an enhancer of embryonic/larval hemocyte phenotype of Itgbn²

(Nagaosa et al., 2011)

drpr^Δ5/drpr[+] is an enhancer of glial cell phenotype of Scer\GAL4^repo, ced-6^RNAi.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^UASp.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/larval hemocyte phenotype

(Kuraishi et al., 2009)

Oseg4^Δ5, drpr^Δ5 has presumptive embryonic/larval central nervous system phenotype

(Freeman et al., 2003)

Additional Comments

Genetic Interactions

Statement

Reference

The nurse cell clearance defect observed in drpr^Δ5 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 Eato^MI14571 in homozygous state and both drpr^Δ5 single and Eato^MI14571;drpr^Δ5 double mutant egg chambers display on average ~9 persistent nuclei.

(Santoso et al., 2018)

Knockdown of Ced-12 in a drpr^Δ5 background, through the expression of Ced-12^KK102788 under the control of Scer\GAL4^alrm.PD, leads to a near-complete loss of astrocytic vacuole formation.

Knockdown of Crk in a drpr^Δ5 background, through the expression of Crk^GD8583 under the control of Scer\GAL4^alrm.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 drpr^Δ5 background, through the expression of Ced-12^KK102788 under the control of Scer\GAL4^alrm.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 drpr^Δ5 background, through the expression of Crk^GD8583 under the control of Scer\GAL4^alrm.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.

(Tasdemir-Yilmaz and Freeman, 2014)

Expression of hep^CA.Scer\UAS under the control of Scer\GAL4^GR1 partially rescues the cell death defects seen in drpr^Δ5 mutant starvation-induced degenerating egg chambers. Many abnormal egg chambers are still seen but, unlike in drpr^Δ5 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.

(Etchegaray et al., 2012)

Itgbn², drpr^Δ5 double mutants show a significant delay in development to adulthood, as compared to wild-type controls and either single mutants.

(Nagaosa et al., 2011)

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 shark¹/+ 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/+ ; 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.

(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 and Rescue Data

Rescued by

drpr^Δ5 is rescued by drpr^UAS.cSa.EGFP/Scer\GAL4^A58

(Sung et al., 2024)

drpr^Δ5 is rescued by Scer\GAL4^C587/drpr^I.UAS

(Zohar-Fux et al., 2022)

drpr^Δ5 is rescued by drpr^I.UAS/Scer\GAL4^GR1

(Etchegaray et al., 2012)

drpr^Δ5 is rescued by drpr^UAS.cFa/Scer\GAL4^srp.Hemo

(Fujita et al., 2012)

drpr^Δ5 is rescued by Scer\GAL4^srp.Hemo/drpr^Y949F.UAS

(Fujita et al., 2012)

drpr^Δ5 is rescued by drpr^I.UAS/Scer\GAL4^repo

(Logan et al., 2012)

drpr^Δ5 is rescued by Scer\GAL4^repo/drpr^{IIex.Iintra.UAS}

(Logan et al., 2012)

drpr^Δ5 is rescued by Scer\GAL4^fkh.PH/drpr^I.UAS

(McPhee et al., 2010)

Not rescued by

drpr^Δ5 is not rescued by drpr^NQ4.UAS.EGFP/Scer\GAL4^A58

(Sung et al., 2024)

drpr^Δ5 is not rescued by Scer\GAL4^srp.Hemo/drpr^Y858F.UAS

(Fujita et al., 2012)

drpr^Δ5 is not rescued by drpr^II.UAS/Scer\GAL4^repo

(Logan et al., 2012)

drpr^Δ5 is not rescued by Scer\GAL4^repo/drpr^III.UAS

(Logan et al., 2012)

drpr^Δ5 is not rescued by Scer\GAL4^repo/drpr^{Iex.IIintra.UAS}

(Logan et al., 2012)

drpr^Δ5 is not rescued by drpr^{Iex.IIIintra.UAS}/Scer\GAL4^repo

(Logan et al., 2012)

Comments

Expression of drpr^I.Scer\UAS in the follicle cells under the control of Scer\GAL4^GR1 rescues the enlargement and nurse cell debris uptake defects seen in starvation-induced degenerating egg chambers in drpr^Δ5 mutant flies. Unlike in drpr^Δ5 alone, no premature follicle cell death is seen.

(Etchegaray et al., 2012)

Expression of drpr^Scer\UAS.cFa under the control of Scer\GAL4^srp.Hemo rescues the reduced level of phagocytosis of apoptotic cells seen in dispersed hemocytes derived from drpr^Δ5 embryos.

Expression of drpr^{Y858F.Scer\UAS} under the control of Scer\GAL4^srp.Hemo fails to rescue the reduced level of phagocytosis of apoptotic cells seen in dispersed hemocytes derived from drpr^Δ5 embryos.

(Fujita et al., 2012)

Glial expression of drpr^I.Scer\UAS rescues the engulfment defects found in degenerating ORN axons in drpr^Δ5 mutants.

(Logan et al., 2012)

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)

Images (0)

Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

The 'drpr^Δ5 rec8' chromosome harbours a lethal mutation that is separable from drpr^Δ5.

(Boulanger et al., 2021)

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 and Linkouts ( 0 )

Synonyms and Secondary IDs (12)

Reported As

Symbol Synonym

Draper^Δ5rec9

(Purice et al., 2017)

draper null

(Nelson et al., 2024)

draper^d5

(Bejarano et al., 2008)

draper^Δ5

(Nelson et al., 2024, Campbell et al., 2021, Petrignani et al., 2021, Vita et al., 2021, Nakano et al., 2019, Meehan et al., 2016, Purice et al., 2016, Timmons et al., 2016, Doherty et al., 2014, Doherty et al., 2009, Ziegenfuss et al., 2008)

drpr null

(Zohar-Fux et al., 2022)

drpr^</up>Δ5

(Chakrabarti and Visweswariah, 2020)

drpr^recΔ5

(Van Goethem et al., 2012)

drpr^Δ5rec8

(Boulanger et al., 2021)

drprD5

(Davis et al., 2024)

drprΔ5

(Zohar-Fux et al., 2022, Okuda et al., 2016, Pearce et al., 2015)

drprΔ5rec9

(Ray et al., 2017)

Name Synonyms

draperΔ5

(Williams et al., 2006)

Secondary FlyBase IDs

References (58)

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