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General Information
Symbol
Dmel\DAAMEx68
Species
D. melanogaster
Name
FlyBase ID
FBal0194072
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
dDAAMEx68
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

Imprecise excision of the P{EP}EP1542 element, resulting in deletion of the C-terminal 457 amino acids, including sequences corresponding to the 'DAD' domain and most of the 'FH2' domain.

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 ( 0 )
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

DAAMEx68 mutant larvae develop small muscles, as compared to controls.

The ISNb nerve terminals in DAAMEx68 mutant embryos often show guidance defects and premature terminations, as compared to controls.

The larval neuromuscular junctions at muscles 4 and 6/7 in DAAMEx68 hemizygous males are significantly smaller, display significantly fewer synaptic boutons and significantly fewer synaptic vesicles, but do not show actin organization defects nor obvious active zone or T-bar defects, as compared to controls; the enervated muscles, however, do not show significant size defects, as compared to controls. DAAMEx68 heterozygous females, however, do not show defects in synaptic bouton number compared to controls.

The larval muscle 4 neuromuscular junctions in DAAMEx68 hemizygous males expressing DAAMUAS.cMb under the control of Scer\GAL4btl.PS larvae show fragmented/absent presynaptic microtubules bundles and 'bouton fusion', as compared to controls. Synaptic transmission across this junction show a significant decrease in evoked excitatory junction current amplitude, but do not show significant changes in evoked excitatory junction current frequency or in miniature excitatory junction current amplitude, as compared to controls.

The tracheal dorsal trunk of DAAMEx68 homozygous stage 17 embryos exhibit heterogeneous patterns of hardly detected taenidial folds and thin F-actin bundles with stretches of perpendicular structures followed by stretches of parallel structures when compared to controls.

Single cell DAAMEx68 mutant mushroom body clones in a DAAMEx68/+ mutant background display a wild type morphology with a single bifurcated axon.

DAAMEx68 mutant neuroblast clones in a DAAMEx68/+ mutant background display abnormal axonal morphology in the mushroom bodies.

The body size and somatic musculature of early DAAMEx68 third instar larvae appear normal, but late third instar larvae (100 hours after egg laying) are shorter than normal and have slight muscle defects (muscles are smaller than normal, some myofibres are split and their general organisation is looser than in wild type). Muscle VL3 is reduced in both length and width, due to both sarcomere shortening and a reduction in sarcomere numbers.

Motility of mutant early third instar larvae is normal, but mutant late third instar larvae have significantly reduced motility compared to wild type.

Cultured primary neurons derived from DAAMEx1/DAAMEx68 embryos show a significant reduction in the number of filopodia compared to control neurons.

DAAMEx68 homozygous mutant embryos display subtle defects in the neuropile, such as thinning of or gaps in the connectives (in 1.5% of embryos), or partial lack of the lateral most Fas2 positive tract. DAAMEx68 maternal and zygotic mutant embryos fail to cellularise properly.

DAAMEx68/DAAMEx1 mutant embryos (in which both maternal and zygotic functions are impaired) show severe CNS phenotypes. Thirty-four percent of these embryos exhibit severe morphological aberrations, some with completely disorganized nerve cords. Another 35% display frequent breaks in connectives and commissures, misrouted axons, or failures in commissure separation and, in extreme cases, an almost complete lack of axon bundles. There do not appear to be differences in neuron numbers between DAAMEx68/DAAMEx1 and wild-type embryos, suggesting that the CNS phenotypes are caused by defects in neurite growth rather than aberrant lineage formation. Axonal growth defects are seen before stages 12 and 13, indicating cell death/degeneration is not involved.

Primary neuronal cultures developed from DAAMEx68/DAAMEx1 or DAAMEx68 homozygous mutant embryos are able to develop axons of similar length as their wild-type counterparts. However, filopodia of mutant neurons are reduced in number by 62% and in length by 26%.

DAAMEx68 mutant larvae display severe trachea defects, including the collapse and flattening of the tracheal tubes in both the main airways and the side branches. Tracheal tubes of DAAMEx68 mutant larvae fail to secrete such a highly ordered cuticle as that observed in wild-type larvae. Although some local order is visible, short and curvy apical ridges that rarely run perpendicular to the tube axis can be observed throughout the tracheal system.

DAAMEx68/Df(1)AD11 transheterozygotes show the same strong larval tracheal phenotype as DAAMEx68 homozygotes.

In contrast to the actin organization found in wild-type tracheal cells, in DAAMEx68 mutants this organization is completely abolished. The overall level of apical F-actin is not reduced in the DAAMEx68 mutant tracheal cells but the actin bundles display abnormal morphology and fail to be organized into parallel running actin rings under the apical surface of the cells. Although the global actin organization is severely impaired , local order can often be detected in small patches within a cell. The cuticle pattern of DAAMEx68 mutants displays a similar phenotype.

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

DAAMEx68 has neuropil phenotype, enhanceable by Rho172F

DAAMEx68 has fascicle phenotype, enhanceable by Rho172F

DAAMEx68 has embryo phenotype, enhanceable by Rac1J11

DAAMEx68 has neuropil phenotype, enhanceable by Rac1J11/Rac2Δ

DAAMEx68 has fascicle phenotype, enhanceable by Rac1J11/Rac2Δ

DAAMEx68 has connective phenotype, enhanceable by Rac1J11/Rac2Δ

DAAMEx68 has embryo phenotype, enhanceable by Rac1J11/Rac2Δ

DAAMEx68, Rac1J11 has neuropil phenotype, enhanceable by Rac2Δ

DAAMEx68, Rac1J11 has fascicle phenotype, enhanceable by Rac2Δ

DAAMEx68, Rac1J11 has connective phenotype, enhanceable by Rac2Δ

DAAMEx68 has connective phenotype, enhanceable by Rho172F

DAAMEx68, Rac1J11 has embryo phenotype, enhanceable by Rac2Δ

DAAMEx68 has neuropil phenotype, enhanceable by Rac1J11/Rac2Δ/MtlΔ

DAAMEx68 has fascicle phenotype, enhanceable by Rac1J11/Rac2Δ/MtlΔ

DAAMEx68 has embryo phenotype, enhanceable by Rac1J11/Rac2Δ/MtlΔ

DAAMEx68, Rac1J11, Rac2Δ has neuropil phenotype, enhanceable by MtlΔ

DAAMEx68, Rac1J11, Rac2Δ has fascicle phenotype, enhanceable by MtlΔ

DAAMEx68, Rac1J11, Rac2Δ has connective phenotype, enhanceable by MtlΔ

DAAMEx68, Rac1J11, Rac2Δ has embryo phenotype, enhanceable by MtlΔ

DAAMEx68 has neuropil phenotype, enhanceable by chic[+]/chic221

DAAMEx68 has fascicle phenotype, enhanceable by chic[+]/chic221

DAAMEx68 has connective phenotype, enhanceable by chic[+]/chic221

DAAMEx68 has embryo phenotype, enhanceable by Rho172F

DAAMEx68 has embryo phenotype, enhanceable by chic[+]/chic221

DAAMEx68 has neuropil phenotype, enhanceable by ena[+]/enaGC5

DAAMEx68 has fascicle phenotype, enhanceable by ena[+]/enaGC5

DAAMEx68 has connective phenotype, enhanceable by ena[+]/enaGC5

DAAMEx68 has embryo phenotype, enhanceable by ena[+]/enaGC5

DAAMEx68 has neuropil phenotype, enhanceable by ena02029/ena[+]

DAAMEx68 has fascicle phenotype, enhanceable by ena02029/ena[+]

DAAMEx68 has connective phenotype, enhanceable by ena02029/ena[+]

DAAMEx68 has embryo phenotype, enhanceable by ena02029/ena[+]

DAAMEx68 has neuropil phenotype, enhanceable by Rac1J11

DAAMEx68 has fascicle phenotype, enhanceable by Rac1J11

DAAMEx68 has connective phenotype, enhanceable by Rac1J11

NOT Enhanced by
Statement
Reference

DAAMEx68 has NMJ bouton | larval stage phenotype, non-enhanceable by Ank2XLΔ/Ank2XLΔ

DAAMEx68 has NMJ bouton | larval stage phenotype, non-enhanceable by futschCR13

Suppressed by
NOT suppressed by
Statement
Reference

DAAMEx68 has LL1 motor neuron | larval stage phenotype, non-suppressible by Lar[+]/Lar13.2

DAAMEx68 has NMJ bouton | larval stage phenotype, non-suppressible by Ank2[+]/Ank2f00518

DAAMEx68 has LL1 motor neuron | larval stage phenotype, non-suppressible by Ank2[+]/Ank2f00518

DAAMEx68 has NMJ bouton | larval stage phenotype, non-suppressible by wg[+]/wgl-8

DAAMEx68 has LL1 motor neuron | larval stage phenotype, non-suppressible by wg[+]/wgl-8

DAAMEx68 has NMJ bouton | larval stage phenotype, non-suppressible by tkv7/tkv[+]

DAAMEx68 has LL1 motor neuron | larval stage phenotype, non-suppressible by tkv7/tkv[+]

DAAMEx68 has NMJ bouton | larval stage phenotype, non-suppressible by dia[+]/dia5

DAAMEx68 has LL1 motor neuron | larval stage phenotype, non-suppressible by dia[+]/dia5

DAAMEx68 has NMJ bouton | larval stage phenotype, non-suppressible by Lar[+]/Lar13.2

Enhancer of
Suppressor of
Other
Additional Comments
Genetic Interactions
Statement
Reference

The larval muscle 4 neuromuscular junctions in either trio1, DAAMEx68 double heterozygotes or dia5, DAAMEx68 double heterozygotes do not show significant changes in synaptic bouton number, as compared to controls.

The larval muscle 4 neuromuscular junctions in DAAMEx68, futschCR13 double mutants show fragmented presynaptic microtubules bundles, as compared to controls.

DAAMEx68/DAAMEx68; FrlEx83/FrlEx83 double mutant eye R-cell clones lack rhabdomere-associated pigment granules and double mutant R-cells show a partially penetrant cell autonomous small rhabdomere phenotype (compared to DAAMEx68/DAAMEx68 mutants).

Cultured primary neurons derived from DAAMEx1/DAAMEx68 Sop21 embryos show a very strong reduction in the number of filopodia (to 5% of the wild type average) compared to control neurons. In live analyses, the mutant neurons show modestly increased protrusion rates and strongly increased retraction rates of filopodia.

Only 20% of cultured primary neurons derived from DAAMEx1/DAAMEx68 Sop21/Sop2Q25sd embryos have neurites.

Cultured primary neurons derived from DAAMEx68/+ Sop21/+ and DAAMEx68/+ ena23/+ double heterozygous embryos show a significant reduction in the number of filopodia compared to control neurons.

Cultured primary neurons derived from DAAMEx68/+ chic221/+ double heterozygous embryos have a normal number of filopodia.

A Rho172F heterozygous background weakly enhances the zygotic DAAMEx68 CNS phenotype.

A Rac1J11 background enhances the zygotic DAAMEx68 CNS phenotype, with the severity of the phenotype correlating with the number of Rac1 copies removed. A DAAMEx68 heterozygous background strongly enhances the axonal growth defects exhibited by Rac1J11 mutants.

A Rac1J11/+; Rac2Δ/+ background enhances both the zygotic DAAMEx68 and DAAMEx68; Rac1J11/+ CNS phenotypes.

A Rac1J11; Rac2Δ, Mtl[Δ] heterozygous background enhances the zygotic DAAMEx68, DAAMEx68; Rac1J11/+ and DAAMEx68; Rac1J11/+; Rac2Δ/+CNS phenotypes.

A chic221 heterozygous background increases the proportion of DAAMEx68 mutant embryos that exhibit CNS defects.

A enaGC5 heterozygous background increases the proportion of DAAMEx68 mutant embryos that exhibit CNS defects.

A ena02029 heterozygous background increases the proportion of DAAMEx68 mutant embryos that exhibit CNS defects.

Xenogenetic Interactions
Statement
Reference

Expression of Mmus\Daam1Scer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4elav-C155 rescues central nervous system axon defects in 70% of DAAMEx68/DAAMEx1 embryos derived from homozygous DAAMEx1 females.

Complementation and Rescue Data
Comments

Expression of DAAMScer\UAS.P\T.cMa under the control of Scer\GAL4Mef2.PU partially rescues the reduced motility and almost fully rescues the body and muscle size of late third instar DAAMEx68 larvae.

Expression of DAAMScer\UAS.PD under the control of Scer\GAL4Mef2.PU almost fully rescues the reduced motility and the body and muscle size of late third instar DAAMEx68 larvae.

Expression of DAAMI1042A.Scer\UAS.PD under the control of Scer\GAL4Mef2.PU fails to rescue the reduced motility and the body and muscle size of late third instar DAAMEx68 larvae.

The CNS defects revealed in DAAMEx68/DAAMEx1 mutants are fully rescued when DAAMScer\UAS.P\T.cMa is expressed under the control of the pan-neuronal Scer\GAL4elav-C155 or the ubiquitous Scer\GAL4Act5C.PI driver.

Expression of DAAMScer\UAS.P\T.cMa under the control of Scer\GAL4btl.PS rescues the tracheal phenotype of DAAMEx68 mutants.

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External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (6)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (11)