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General Information
Symbol
Dmel\captE636
Species
D. melanogaster
Name
FlyBase ID
FBal0117577
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
acuE636
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:

G1153004A

Amino acid change:

W145term | capt-PA; W504term | capt-PB; W145term | capt-PC

Reported amino acid change:

W145term

Comment:

G to A nucleotide change at the second or third position of the Trp codon leads to a nonsense mutation. (exact site of mutation unspecified). Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Amino acid replacement: W145term.

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 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Homozygous and captK304/captE636 larvae have punctate-like accumulations expressing Act5CScer\UAS.T:Avic\GFP in the dendrites of the sensory neuron dorsal cluster (these actin accumulations are absent in the dendrites of wild-type larvae).

Two days after their induction in the wing disc, captE636 clones cause strong disturbances of the dorsoventral boundary. The disruptions are bidirectional and non-autonomous in nature; ventral cells can appear in the dorsal part of the disc and dorsal cells can appear in the ventral part of the disc, and wild-type cells adjacent to clones are also affected. The anterior-posterior compartment boundary is not affected and there is no cell death or cell loss from the disc epithelium.

Homozygotes show lethality with a variable onset, from the embryonic to the second larval instar stage. Homozygous clones overlapping the morphogenetic furrow show premature photoreceptor differentiation. Many cells in posterior homozygous clones in the eye disc fail to differentiate as neurons and later appear to die, leaving scars in the adult eye. Eye discs in which all capt function has been removed (by inducing clones in a Minute background) show a severe disorganisation of the pattern of differentiation. Clones at the wing margin have wing margin bristles of abnormal shapes and sizes and the bristles are sometimes missing. Females containing homozygous germ line clones do not lay eggs. Homozygous clones in the eye disc show excessive actin polymerisation; actin filaments appear to fill the cell bodies of the photoreceptor cells, rather than being restricted to a small region of each ommatidium (as occurs in wild type). Mutant cells in the region of the morphogenetic furrow do not undergo the normal shape changes and instead retain large apical profiles. Apical constriction of cells at the lateral edges of mutant clones in the eye disc is seen.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference

A captE636 heterozygous mutant background modifies the actin remodelling and subsequent basolateral invasion of epithelial cells seen in flies expressing CskGD9345 in a stripe of cells at the anterior/posterior boundary of the larval wing disc under the control of Scer\GAL4ptc-559.1.

capt Dys double heterozygous flies (captE636/Df(3R)Exel6184) exhibit indirect flight muscle degeneration.

captE636 DgO86 double heterozygous flies do not exhibit indirect flight muscle degeneration.

One copy of captE636 enhances the indirect flight muscle degeneration seen when DysdsRNA.NH2.Scer\UAS is expressed under the control of Scer\GAL4Act.PU.

One copy of captE636 does not enhance the indirect flight muscle degeneration seen when DgdsRNA.Scer\UAS is expressed under the control of Scer\GAL4tub.PU.

captE636 Dg323 double heterozygous flies do not exhibit indirect flight muscle degeneration.

captE636/+ mutant flies do not exhibit temperature-induced mobility defects.

Combination of Df(3R)Exel6184 in heterozygous state with a single copy of captE636 results in a significantly increased frequency of lamina plexus defects in the third instar larval brain and reduced rhabdomere length in the adult eye in the double heterozygotes.

Combination of DgO86 in heterozygous state with a single copy of captE636 does not significantly affect the frequency of lamina plexus defects in the third instar larvae but results in a significantly reduced rhabdomere length in the adults.

Central nervous system axons are seen to cross the midline in Abl2 captE636 double heterozygous embryos. Expression of captScer\UAS.cBa under the control of Scer\GAL4elav.PLu completely rescues the midline crossing defects seen in captE636 Abl2 double heterozygotes. Expression of captC.Scer\UAS under the control of Scer\GAL4elav.PLu partially rescues the midline crossing defects seen in captE636 Abl2 double heterozygotes.

Clones in the eye disc which are doubly mutant for captE636 and chic221 show predominantly the chic221 mutant phenotype.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Fails to complement
Comments

Expression of captScer\UAS.cBa under the control of Scer\GAL4da.G32 rescues captE593/captE636 animals to viability, although the rescued adults sometimes show wing or eye defects. Expression of captC.Scer\UAS under the control of Scer\GAL4da.G32 rescues captE593/captE636 animals to viability and restores normal photoreceptor differentiation.

Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
References (9)