FB2026_02 , released June 18, 2026
Allele: Dmel\sfl03844
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General Information
Symbol
Dmel\sfl03844
Species
D. melanogaster
Name
FlyBase ID
FBal0009490
Feature type
allele
Associated gene
Dmel\sfl
Associated Insertion(s)
P{PZ}sfl03844
Carried in Construct
Also Known As
sfll(3)03844, l(3)0384403844
Key Links
Genomic Maps

Allele class
Mutagen
Nature of the Allele
Allele class
Mutagen
P-element activity
(Baeg et al., 2001, Lin and Perrimon, 1999, Lin et al., 1999, Hong and Hashimoto, 1995, BDGP Project Members, 1994-1999)
Progenitor genotype
Associated Insertion(s)
P{PZ}sfl03844
Caused by aberration
Df(3L)03844
Cytology
Description

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

(Lin and Perrimon, 1999)

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

(Hong and Hashimoto, 1995)
Allele components
Component
Use(s)
Inserted element
P{PZ}
Encoded product / tool
lacZ
Tagged with
Tag:NLS(P)
Mutations Mapped to the Genome
Associated Sequence Data
DDBJ / EMBL / GenBank
DNA sequence
Protein sequence
 
UniProtKB/Swiss-Prot
    UniProtKB/TrEMBL
      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.

      (Dejima et al., 2013)

      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.

      (Ren et al., 2009)

      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.

      (Zhu et al., 2007)

      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.

      (Zhu et al., 2005)

      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.

      (Baeg et al., 2001)

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

      (Lin and Perrimon, 1999)

      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).

      (Lin et al., 1999)

      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.

      (Perrimon et al., 1996)
      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      Enhanced by
      Statement
      Reference

      sfl03844 has increased mortality during development phenotype, enhanceable by Hsepid12

      (Dejima et al., 2013)
      Enhancer of
      Statement
      Reference

      sfl[+]/sfl03844 is an enhancer of abnormal neuroanatomy | embryonic stage phenotype of Scer\GAL4P52, Sema1aUAS.cYa, Sema1ak13702

      (Cho et al., 2012)
      Suppressor of
      Statement
      Reference

      sfl[+]/sfl03844 is a suppressor | partially of abnormal size phenotype of PsnRNAi.UAS.3, Scer\GAL4r4

      (Schultheis et al., 2024)

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

      (Reynolds-Peterson et al., 2020)
      Phenotype Manifest In
      Suppressed by
      Statement
      Reference

      sfl03844 has mesoderm phenotype, suppressible by Scer\GAL4twi.PG/htlλ.UAS

      (Lin et al., 1999)

      sfl03844 has larval tracheal system phenotype, suppressible by bnlUAS.cSa/Scer\GAL469B

      (Lin et al., 1999)
      Enhancer of
      Statement
      Reference

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

      (Dejima et al., 2013)

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

      (Dejima et al., 2013)

      sfl[+]/sfl03844 is an enhancer of larval posterior commissure | embryonic stage phenotype of Scer\GAL4P52, Sema1aUAS.cYa, Sema1ak13702

      (Cho et al., 2012)
      Suppressor of
      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.

      (Dejima et al., 2013)

      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.

      (Cho et al., 2012)

      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.

      (Lin et al., 1999)
      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).

      Complements: sgl08310. Complements: cpo08435.

      (BDGP Project Members, 1994-1999)
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (3)
      References (20)