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General Information
Symbol
Dmel\PakUAS.Tag:Myr(Src64B)
Species
D. melanogaster
Name
FlyBase ID
FBal0147693
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
UAS-Pakmyr, Pakmyr
Key Links
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Carried in construct
Cytology
Nature of the lesion
Statement
Reference

Expression of fusion protein produced by PakGMR.Tag:Myr(Src64B) is under the control of UAS sequences.

Allele components
Product class / Tool use(s)
Encoded product / tool
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 ( 1 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Expressing of PakScer\UAS.T:Myr-Src64B (which is tethered to the plasma membrane) under the control of Scer\GAL4eve.RN2 resulted in the expansion of the region containing primary dendritic processes in the embryonic aCC motoneurons but does not affect the initiation time of the dendrite development.

The mushroom body axons of flies expressing PakScer\UAS.T:Myr-Src64B under the control of Scer\GAL4ey-OK107 fail to extend to form peduncles and lobe structures (the 'posterior arrest' phenotype). Scer\GAL4ey-OK107>PakScer\UAS.T:Myr-Src64B expressing clones that exhibit the posterior arrest phenotype display ectopic regions of F-actin in the posteriorly arrested axons.

Expression of PakScer\UAS.T:Myr-Src64B under the control of Scer\GAL4ato.3.6 results in clustering of dorsal cluster neuron axons. There is an increase in the number of medulla axons compared to wild type.

Expression of PakScer\UAS.T:Myr1 under the control of Scer\GAL4GMR.PFa results in high levels of lethality.

Expression of PakScer\UAS.T:Myr1 under the control of Scer\GAL4AB1 causes the expansion of the posterior lumen in third instar salivary glands.

Expression of PakScer\UAS.T:Myr1, under the control of Scer\GAL4SG18.1, results in disruption of the antennal lobe anatomy. The neuropil is partitioned as in wild type but the compartments are hard to identify as known glomeruli.

Expression of PakScer\UAS.T:Myr1 driven by Scer\GAL4elav.PLu does not lead to a significant reduction in commissural axon thickness.

Motor neurons in PakScer\UAS.T:Myr1; Scer\GAL4elav.PLu embryos do not exhibit failure of axonal outgrowth. However, some exhibit axon guidance errors: Segmental nerve b (SNb) motorneuron axons exhibit guidance errors in 32% of the cases, either failing to innervate their target muscles or stalling in the ventral musculature before reaching them. (SNb axons form part of the abdominal posterior fascicle). In PakScer\UAS.T:Myr1; Scer\GAL4elav.PLu embryo segmental nerve (SN)b motor growth cones, the average filopodia length is 7% greater than wild-type, while both the rates of extension and retraction are 6% greater than wild-type (significance: P < 0.01 with two-tailed t test). These animals also exhibit a significant increase in filopodial activity in LBD sensory neuron (innervating the Kolbchen) growth cones: the average filopodia length increases by 40%, while the rates of extension and retraction increase by 52 and 43%, respectively. Despite increasing the filopodial parameters of the growth cone, hyperactivation of Pak did not affect the outgrowth of the axon of the LBD sensory neurons or any other motor neurons examined.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Enhancer of
Suppressor of
NOT Suppressor of
Other
Phenotype Manifest In
Enhanced by
Suppressed by
Enhancer of
Suppressor of
NOT Suppressor of
Other
Additional Comments
Genetic Interactions
Statement
Reference

Expression of PakScer\UAS.T:Myr-Src64B under the control of Scer\GAL4332.3 in embryos expressing crb+tfos in a crbGX24w-/crb11A22 background leads to complete embryonic lethality with most embryos exhibiting dorsal closure defects ranging in severity from open cuticle and dorsal holes, to closed cuticles but failure to hatch.

The dendritogenesis defects in the embryonic aCC motoneurons characteristic for embryos expressing either Dscam1HMS01859 or dockJF02810 RNAi under the control of Scer\GAL4eve.RN2 are partially suppressed by co-expression of PakScer\UAS.T:Myr-Src64B : the reduced dendritic number is fully restored but the region containing primary dendritic processes is expanded compared to controls. This rescue effect is however blocked in the presence of either Cdc426 or Cdc424 (in hemizygous state).

The number of medulla axons in animals co-expressing both bskDN.Scer\UAS and PakScer\UAS.T:Myr-Src64B under the control of Scer\GAL4ato.3.6 is similar to that seen in animals expressing bskDN.Scer\UAS alone under the control of Scer\GAL4ato.3.6.

Co-expression of PakScer\UAS.T:Myr1 and kstGD1472 under the control of Scer\GAL4AB1 results in the enhancement of the irregular surface of apical membrane and does not rescue the expansion of the salivary gland lumen resulting from the overexpression of PakScer\UAS.T:Myr1.

Co-expression of PakScer\UAS.T:Myr1 and kstMinikarst.Scer\UAS under the control of Scer\GAL4AB1 results in the expansion of the whole salivary gland including the lumen and even the appearance of multiple lumens.

Expression of kstβH33.Scer\UAS in combination with PakScer\UAS.T:Myr1 under the control of Scer\GAL4AB1 strongly suppresses the salivary gland lumen size defect caused by PakScer\UAS.T:Myr1 expression.

Co-expression of shgScer\UAS.T:Avic\GFP-rs with PakScer\UAS.T:Myr1 under the control of Scer\GAL4AB1 completely suppresses the bulging phenotype, and partially suppresses the PakScer\UAS.T:Myr1 salivary gland lumen expansion phenotype.

Expression of PakScer\UAS.T:Myr1 under the control of Scer\GAL4SG18.1 in a Df(1)LIMK1-5 background suppresses the antennal lobe anatomy phenotype seen when this transgene is expressed in a wild type background.

Overexpression of PakScer\UAS.T:Myr1 under the control of Scer\GAL4elav.PLu enhances the longitudinal axon defects seen in transheterozygous sli1, robo5 mutants. An average of 14.3 defects are seen per animal. 130% of segments (calculated as number of defects/segments) show defects. The combination of heterozygous sli2 and pan-neural overexpression of PakScer\UAS.T:Myr1 under the control of Scer\GAL4elav.PLu leads to longitudinal axon ectopic midline crossing defects. An average of 5.6 defects are seen per animal, and an average of 51% of segments have defects. Co-expression of PakScer\UAS.T:Myr1 and fra::roboScer\UAS.FR.T:Hsap\MYC under the control of Scer\GAL4elav.PLu leads to a striking reduction in commissural axon thickness. Co-expression of PakScer\UAS.T:Myr1 partially suppresses longitudinal axon ectopic midline crossing defects seen in sli2/+, Rac1N17.Scer\UAS ; Scer\GAL4elav.PLu animals. An average of 5 defects are seen per animal, and an average of 45% of segments have defects.

Overexpression of PakScer\UAS.T:Myr1 under the control of Scer\GAL4elav.PLu enhances the longitudinal axon defects seen in transheterozygous sli1, robo5 mutants. An average of 14.3 defects are seen per animal.

The combination of heterozygous sli2 and pan-neural overexpression of PakScer\UAS.T:Myr1 under the control of Scer\GAL4elav.PLu leads to longitudinal axon ectopic midline crossing defects. An average of 5.6 defects are seen per animal.

Co-expression of PakScer\UAS.T:Myr1 and fra::roboScer\UAS.FR.T:Hsap\MYC under the control of Scer\GAL4elav.PLu leads to a striking reduction in commissural axon thickness.

Co-expression of PakScer\UAS.T:Myr1 partially suppresses longitudinal axon ectopic midline crossing defects seen in sli2/+, Rac1N17.Scer\UAS ; Scer\GAL4elav.PLu animals. An average of 5 defects are seen per animal, and an average of 45% of segments have defects.

Xenogenetic Interactions
Statement
Reference

Expression of PakScer\UAS.T:Myr-Src64B partially suppresses the dendrite defects seen in class IV da neurons expressing Hsap\ATXN3tr.Q78.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4ppk.PG. The reduction in F-actin structures in the distal dendrites of dorsal cluster neurons when Hsap\ATXN3tr.Q78.Scer\UAS.T:Ivir\HA1 is expressed under the control of Scer\GAL4109(2)80 is also partially rescued.

Complementation and Rescue Data
Comments
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Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
Reported As
Symbol Synonym
PakScer\UAS.T:Myr-Src64B
PakScer\UAS.T:Myr1
PakUAS.Tag:Myr(Src64B)
Name Synonyms
Secondary FlyBase IDs
    References (14)