Allele Dmel\Eph^x652

General Information
Symbol	Dmel\Eph^x652	Species	D. melanogaster
Name		FlyBase ID	FBal0196836
Feature type	allele	Associated gene	Dmel\Eph

Allele class	loss of function allele
Mutagen	Delta2-3
Recent Updates
Description	What does this section display? This section contains items that were added to this record for each release. It currently only tracks new links between this FlyBase report and other FlyBase data classes (e.g. genes, references, stocks) or controlled vocabulary terms (e.g. GO, anatomy terms). What does this section not display? This section does not currently display links that were removed or gene model changes.
Update Feed	Click the icon below to subscribe to this FlyBase record and receive updates automatically through your feed reader.
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	loss of function allele (Boyle et al., 2006)
Mutagen	Delta2-3 (Boyle et al., 2006)
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{hsp26-pt-T}P114 (Boyle et al., 2006)
Nature of the lesion	Statement Reference Imprecise excision of the P{hsp26-pt-T} element that results in deletion of the first three exons of Eph (up to amino acid residue 79 of the expressed protein) and 5' sequences of the onecut gene (up to 368bp from its translation start site). (Boyle et al., 2006)
Caused by aberration	Df(4)Eph^x652 (Boyle et al., 2006)
Cytology
Phenotypic Data
Phenotypic Class
	fertile \| recessive (Boyle et al., 2006) immune response defective \| larval stage (Howell et al., 2012) neuroanatomy defective (Boyle et al., 2006) viable \| recessive (Boyle et al., 2006)
Phenotype Manifest In
	mushroom body medial lobe (Boyle et al., 2006) mushroom body vertical lobe (Boyle et al., 2006) mushroom body vertical lobe \| somatic clone (Boyle et al., 2006)
Detailed Description
	Statement Reference Mutant larvae fail to encapsulate eggs when parasitised by the avirulent L. boulardi wasp strain G486 (no melanisation is seen). Plasmatocytes fully cover the egg, while lamellocytes partially cover it. (Howell et al., 2012) The Eph[x652] mutation has only a minor effect on baseline synaptic transmission at the neuromuscular junction (NMJ). (Frank et al., 2009) Eph^x652 flies have no obvious morphological defects. Eph^x652 embryos show no obvious defect in overall axon tract organization. Eph^x652 mutants show defects in the formation of the dorsal lobe of the mushroom body throughout development. Both Eph^x652 embryos and pupae show reduced dorsal projections. In 60% of Eph^x652 third instar larvae, the dorsal lobe projections of the γ neurons are either reduced compared to wild type or missing. Reduced dorsal lobe projections are accompanied by increased medial axonal projections. In 60% of adults, the α' and α lobes are reduced or absent and the β' and β lobes show an increase in thickness. In 10% of cases the β lobes appear to be fused at the midline. Analysis of individual Eph^x652 α/β neuron clones within the mushroom body shows that these neurons bifurcate normally, but sometimes extend both branches into the β lobe, instead of extending one branch dorsally along the α lobe. When this defect occurs, supernumerary branches can be seen along the length of the β lobe. The extent to which the neuron projections are defective reflects the overall severity of the mushroom body phenotype; in Eph^x652 mushroom bodies where the α lobe is missing, all neurons in a clone show projection defects, while in mushroom bodies with a normal overall morphology, α/β neuron clones show normal bifurcation and branching. (Boyle et al., 2006)
External Data
Linkouts
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
NOT suppressed by
Statement Reference Eph^x652 has neuroanatomy defective phenotype, non-suppressible by Scer\GAL4^elav.PLu/Ephrin^{Scer\UAS.T:Hsap\MYC} (Boyle et al., 2006) Eph^x652 has neuroanatomy defective phenotype, non-suppressible by Scer\GAL4^ey-OK107/Ephrin^{Scer\UAS.T:Hsap\MYC} (Boyle et al., 2006)
NOT Enhancer of
Statement Reference Eph[+]/Eph^x652 is a non-enhancer of neurophysiology defective \| recessive \| third instar larval stage phenotype of GluRIIA^SP16 (Frank et al., 2009)
Suppressor of
Statement Reference Eph^x652 is a suppressor \| partially of neurophysiology defective \| recessive \| third instar larval stage phenotype of GluRIIA^SP16 (Frank et al., 2009) Exn^EY01953, Exn[+], Eph[+], Eph^x652 is a suppressor \| partially of neurophysiology defective \| recessive \| third instar larval stage phenotype of GluRIIA^SP16 (Frank et al., 2009)
NOT Suppressor of
Statement Reference Eph[+]/Eph^x652 is a non-suppressor of neurophysiology defective \| recessive \| third instar larval stage phenotype of GluRIIA^SP16 (Frank et al., 2009)
Other
Statement Reference Eph^x652, GluRIIA^SP16 has neurophysiology defective \| recessive \| third instar larval stage phenotype (Frank et al., 2009)
Phenotype Manifest In
NOT suppressed by
Statement Reference Eph^x652 has mushroom body vertical lobe phenotype, non-suppressible by Scer\GAL4^elav.PLu/Ephrin^{Scer\UAS.T:Hsap\MYC} (Boyle et al., 2006) Eph^x652 has mushroom body vertical lobe phenotype, non-suppressible by Scer\GAL4^ey-OK107/Ephrin^{Scer\UAS.T:Hsap\MYC} (Boyle et al., 2006)
NOT Enhancer of
Statement Reference Eph[+]/Eph^x652 is a non-enhancer of embryonic/larval neuromuscular junction phenotype of GluRIIA^SP16 (Frank et al., 2009)
Suppressor of
Statement Reference Eph^x652 is a suppressor \| partially of embryonic/larval neuromuscular junction phenotype of GluRIIA^SP16 (Frank et al., 2009) Eph^x652 is a suppressor of commissure phenotype of Ephrin^{Scer\UAS.T:Hsap\MYC}, Scer\GAL4^sim.PS (Boyle et al., 2006) Exn^EY01953, Exn[+], Eph[+], Eph^x652 is a suppressor \| partially of embryonic/larval neuromuscular junction phenotype of GluRIIA^SP16 (Frank et al., 2009)
NOT Suppressor of
Statement Reference Eph[+]/Eph^x652 is a non-suppressor of embryonic/larval neuromuscular junction phenotype of GluRIIA^SP16 (Frank et al., 2009) Eph^x652 is a non-suppressor of mushroom body vertical lobe phenotype of Ephrin^{Scer\UAS.T:Hsap\MYC}, Scer\GAL4^elav.PLu (Boyle et al., 2006) Eph^x652 is a non-suppressor of mushroom body vertical lobe phenotype of Ephrin^{Scer\UAS.T:Hsap\MYC}, Scer\GAL4^ey-OK107 (Boyle et al., 2006)
Additional Comments
Genetic Interactions
Statement Reference The neuromuscular junction (NMJ) bouton numbers in GluRIIA[SP16]; ;Eph[x652] double mutants are not significantly different from that of the GluRIIA[SP16] single mutant. The spontaneous miniature release event (mepsp) amplitudes are significantly decreased in GluRIIA[SP16]; ;Eph[x652] double mutants compared to Eph[x652] single mutants or wild-type. This double mutant phenotype is similar to the one observed in GluRIIA[SP16] single mutants. The average homeostatic increase in presynaptic release observed in GluRIIA[SP16] single mutants is significantly suppressed in GluRIIA[SP16]; ;Eph[x652] double mutants. The heterozygous Eph[x652]/+ mutation alone does not significantly change the recessive GluRIIA[SP16] phenotype involving the synaptic homeostatic compensation at the neuromuscular junction (NMJ). The combination of Exn[EY01953]/+ and Eph[x652]/+ heterozygous mutations does not significantly change the GluRIIA[SP16] phenotype involving spontaneous miniature release event (mepsp) amplitudes, while it does partially suppress the GluRIIA[SP16] quantal content phenotype at the neuromuscular junction (NMJ). (Frank et al., 2009) Expression of Ephrin^{Scer\UAS.T:Hsap\MYC} in the midline glia of embryos, driven by Scer\GAL4^sim.PS, in an Eph^x652 background does not cause the disruption of commissural axons seen when the transgene is expressed in wild-type embryos. Eph^x652/onecut^x122 and Eph^x652/onecut^x49 mutants show no defects in dorsal lobe formation, indicating that the dorsal lobe phenotype of Eph^x652 mutants is due to the disruption of Eph. Flies that express Ephrin^{Scer\UAS.T:Hsap\MYC} under the control of either Scer\GAL4^OK107 or Scer\GAL4^elav.PLu, in an Eph^x652 background, show the same α'/α lobe defects as flies expressing the transgene in a wild-type background and as Eph^x652 flies with no transgene. (Boyle et al., 2006)
Xenogenetic Interactions
Statement Reference
Complementation & Rescue Data
Comments
Stocks ( 0 )

Notes on Origin
Discoverer

External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 1 )
Reported As
Symbol Synonym	Eph^x652 (Frank et al., 2009, Howell et al., 2012)
Name Synonym
Secondary FlyBase IDs

References ( 3 )
Research paper	Howell et al., 2012, Immunogenetics 64(2): 155--161 A directed miniscreen for genes involved in the Drosophila anti-parasitoid immune response. [FBrf0217123] Frank et al., 2009, Neuron 61(4): 556--569 A presynaptic homeostatic signaling system composed of the Eph receptor, ephexin, Cdc42, and CaV2.1 calcium channels. [FBrf0207531] Boyle et al., 2006, Development 133(9): 1845--1854 Drosophila Eph receptor guides specific axon branches of mushroom body neurons. [FBrf0190278]

Allele Dmel\Ephx652

Allele Dmel\Eph^x652