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General Information
Symbol
Dmel\sfl03844
Species
D. melanogaster
Name
FlyBase ID
FBal0009490
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
sfll(3)03844, l(3)0384403844
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
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

The P{PZ} insertion is inserted at base 576 of the sfl cDNA, 686 bp upstream of a putative ATG start codon.

P{PZ}sfl03844 insertion is associated with a deletion.

Insertion components
P{PZ}sfl03844
Product class / Tool use(s)
Encoded product / tool
Caused by aberration
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 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

No abnormality is observed in longitudinal wing vein structures of sfl03844 homozygous mutant flies.

In response to nerve stimulation, sfl9B4/sfl03844 mutants exhibit a significantly increased EJP compared with wild-type or heterozygous control larvae (20-25% increase). Spontaneous release events (mEJPs) are substantially reduced compared with heterozygous or wild-type controls, suggesting that loss of Heparan Sulfate biosynthesis affects the spontaneous vesicle release probability in the motoneuron. Post-synaptic mEJP amplitudes are modestly increased in sfl9B4/sfl03844 mutants relative to heterozygous or wild-type controls.

sfl9B4/sfl03844 mutant synapses are reduced in size but do not exhibit a reduction in the number of boutons relative to muscle area. sfl9B4/sfl03844 motoneurons are bigger than normal, with a reduced number of 'buds'. sfl9B4/sfl03844 synapses consist primarily of large boutons without any buds.

sfl9B4/sfl03844 mutant synapses exhibit a gross reduction in the number of mitochondria beneath the postsynaptic membrane. The numbers of mitochondria in other parts of the muscle cell, such as between the contractile fibers, are unaffected and mitochondrial numbers in motoneurons are unchanged. sfl9B4/sfl03844 mutant synapses appear to be normal in many respects, with well aligned presynaptic and postsynaptic membranes. There are no changes in the number or morphology of motoneuron active zones. sfl9B4/sfl03844 mutant muscle exhibits gaps in the membranous structures around approximately 40% of boutons. Wild-type and sfl9B4/sfl03844 boutons have similar numbers and distributions of synaptic vesicles, but sfl9B4/sfl03844 mutants have reduced numbers of larger 70nm vesicles, or cisternae.

sfl9B4/sfl03844 mutants exhibit an increase in activity-dependent endocytosis at the neuromuscular junction.

When homozygous clones are induced in females using a technique that ensures that all eggs produced by these females are derived from homozygous germline clones and 76% of the follicles also carry homozygous somatic clones, then none of the cuticles of the resulting embryos have a dorsalised phenotype.

sfl03844 embryos that lack both maternal and zygotic sfl exhibit a segment polarity phenotype. Salivary glands are present in these mutants. Females carrying sfl03844 ventral follicle cell clones do not produce dorsalized embryos.

Clones of mutant cells are associated with wing margin nicks. However, some mutant margin cells that are located near wild-type margin cells have a wild-type morphology, indicating local cell non-autonomy of sfl.

neur expressing sensory organ mother cells are missing in sfl03844/sfl9B4 wing discs.

Migration of the mesoderm fails to occur properly in homozygous embryos derived from homozygous female germline clones (lacking both maternal and zygotic sfl function). The early steps in tracheal branching are significantly disturbed in stage 13 homozygous embryos (lacking zygotic sfl function). By late stage 15, tracheal branch formation is incomplete, as shown by the presence of large gaps in the dorsal and lateral trunks and stalled ganglionic branches. The penetrance of this phenotype is incomplete and the expressivity is variable; 16% of embryos show some degree of tracheal abnormality, ranging from one to all segments having breaks in the dorsal trunk. Virtually no tracheal branches are seen in homozygous embryos derived from homozygous female germline clones (lacking both maternal and zygotic sfl function).

Germline clones produce eggs with patterning defects: unrescued embryos exhibit mirror image duplication of denticle belts, rescued embryos are wild type. Lethality occurs during the larval and pupal stages.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference
Enhancer of
Statement
Reference
Suppressor of
Statement
Reference

sfl[+]/sfl03844 is a suppressor of abnormal flight phenotype of parkΔ21/park1

Phenotype Manifest In
Suppressed by
Enhancer of
Statement
Reference

sfl[+]/sfl03844 is an enhancer of wing vein phenotype of Hsepid12

sfl[+]/sfl03844 is an enhancer of wing vein L5 phenotype of Hsepid12

Suppressor of
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

Heterozygous sfl03844 mutants in a Hsepid12 mutant background exhibit truncation of the longitudinal vein L5.

Hs2std267 Hsepid12 double mutants do not exhibit ectopic wing vein material, indicating that Hs2std267 suppresses the ectopic posterior cross vein phenotype found in Hsepid12 mutants.

The commissural axon phenotype (failure to cross the midline) seen in embryos expressing Sema-1aScer\UAS.cYa under the control of Scer\GAL4P52 in a Sema-1ak13702 null background is significantly enhanced if the embryos are also heterozygous for sfl03844.

The mesoderm migration defects of sfl03844 embryos lacking both maternal and zygotic sfl function are partially rescued by htlScer\UAS.T:λ\cI-DD expressed under the control of Scer\GAL4twi.PG. Some tracheal branching is recovered if bnlScer\UAS.cSa is expressed under the control of Scer\GAL469B in sfl03844 embryos lacking both maternal and zygotic sfl function. The tracheal branching defects produced by expression of bnlScer\UAS.cSa under the control of Scer\GAL469B are weakly blocked if the embryos are homozygous for sfl03844.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer

A. Spradling.

Comments
Comments

This allele was listed in the BDGP database as a lethal or sterile line during the period 1994-1999, but was discarded from the gene disruption project prior to the summary publication (FBrf0111489). Reasons for excluding lines from the collection described in FBrf0111489 include presence of more than one P insertion on the mutant chromosome, separation of lethality (or sterility) from the location of the insertion, and loss of lethality (or sterility) from the stock. Further information is available from http://www.fruitfly.org/bfd/ and from Dr. Spradling (spradling@mail1.ciwemb.edu).

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
References (18)