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General Information
Symbol
Dmel\slsj1D7
Species
D. melanogaster
Name
FlyBase ID
FBal0043793
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
l(3)j1D7
Key Links
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

P{lacW} insertion in an exon encoding part of the PEVK-2 domain.

P{lacW} insertion in the coding region, disrupting the coding region at amino acid 471.

Insertion components
P{lacW}slsj1D7
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

slsj1D7 heterozygous adults have an apparently normal morphology and are able to fly, as are able to sustain high frequency wing beat, as compared to controls.

23.7% of nuclei in slse4/slsj1D7 larval brain neuroblasts show chromosome undercondensation (under condensation of heterochromatin as well as euchromatin is seen). Additional mitotic defects such as premature sister chromatid separation, polyploidy, aneuploidy and chromosome breakage are also seen.

Mutant embryos show grossly normal morphology, normal segmentation, normal epidermal denticle belts and normal patterning of the neuromusculature. They show greatly reduced movement compared to wild-type. Mature embryos show striking defects in individual muscle fibre morphology. The parallel myofilament array seen in wild-type muscles is disrupted and myofilaments are arranged irregularly, both longitudinally and transversely. The unit of a thick myosin filament surrounded by an array of thin actin filaments can form correctly, whereas the overall arrangement of myofilaments is largely disrupted.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
NOT Enhanced by
Statement
Reference

slsg65/slsj1D7 has visible | pupal stage phenotype, non-enhanceable by tn[+]/tnΔA

Enhancer of
Statement
Reference
NOT Enhancer of
Statement
Reference

sls[+]/slsj1D7 is a non-enhancer of visible | pupal stage phenotype of tnΔA/tn1

Suppressor of
Statement
Reference

sls[+]/slsj1D7 is a suppressor of decreased body size phenotype of tnMJO-348

Other
Phenotype Manifest In
Enhancer of
Statement
Reference
Suppressor of
Statement
Reference

sls[+]/slsj1D7 is a suppressor of visceral muscle fiber phenotype of tnMJO-348

sls[+]/slsj1D7 is a suppressor of filamentous actin phenotype of tnMJO-348

Additional Comments
Genetic Interactions
Statement
Reference

slsj1D7 heterozygotes also heterozygous for either cherEPSΔ5 or chersko, but not cherQ1042X, exhibit flight defects, since high frequency wing beat is only sustained for a few seconds, as compared to wild-type and single heterozygous controls; in both genetic background, however, there are no obvious sarcomere defects.

Heterozygosity for slsj1D7 enhances the semi-lethality and the myofibril shredding defects (even leading to the loss of the sarcomere structure) resulting from the expression of cherJF02077 under the control of Scer\GAL4Mef2.PU.

Pupae trans-heterozygous for tnMJO-348 and slsj1D7 undergo proper pupal morphogenesis and eclosion. Notably, mutant pupae homozygous for tnMJO-348 and heterozygous for slsj1D7 are slim and show a statistically significant increase in length when compared to homozygous tnMJO-348 pupae. This result indicates a suppression of the muscle contraction and morphogenetic defects that are associated with the tnMJO-348 mutant phenotype.

slsj1D7/+ does not enhance the tn1/tnΔA thin pupae phenotype.

slsj1D7/+ enhances the Df(3R)Mlp84BP8/Df(3R)dsx2M thin pupae phenotype.

tnΔA/+ does not enhance the slsj1D7/slsg65 thin pupae phenotype.

slsj1D7 heterozygosity greatly increases the adult lethality of Df(3R)Mlp84BP8/Df(3R)dsx2M mutants. slsj1D7 heterozygosity also exacerbates the pupal case elongation phenotype associated with Df(3R)Mlp84BP8/Df(3R)dsx2M or Mlp84BP20/Df(3R)dsx2M.

slsj1D7 heterozygosity reduces the viability of Mlp84BP20/Df(3R)dsx2M mutants to zero.

slsj1D7 heterozygosity in a Df(3R)Mlp84BP8/Df(3R)dsx2M mutant background leads to striking muscle abnormalities. Most muscle fibers are wavy and/or spindly in appearance. A significant number of fibers are torn or show some degree of fraying. Closer examination of the double mutants reveals a profound loss of sarcomeric structure of single muscle fibers from third instar fillet preparations. Neither Df(3R)Mlp84BP8/Df(3R)dsx2M hemizygotes, nor slsj1D7 heterozygotes on their own display any obvious structural abnormalities at the light microscopic level.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer

L. and Y. Jan.

Comments
Comments

Excision of the P{lacW} element can give viable revertants. Based on the lethal stage and antibody staining, sls alleles form the series: slsS000201 (weakest), slsB173, slsC995, slsj1D7, slsB68, slsC872 (strongest).

Excision of the P{lacW} reverts the lethal phenotype.

External Crossreferences and Linkouts ( 1 )
Crossreferences
GenBank Nucleotide - A collection of sequences from several sources, including GenBank, RefSeq, TPA, and PDB.
Synonyms and Secondary IDs (6)
References (12)