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General Information
Symbol
Dmel\sax4
Species
D. melanogaster
Name
FlyBase ID
FBal0050458
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Nucleotide change:

C7807780T

Reported nucleotide change:

C?T

Amino acid change:

Q114term | sax-PA; Q79term | sax-PB; Q126term | sax-PC

Reported amino acid change:

Q114term

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

A premature stop codon in the extracellular domain.

Amino acid replacement: Q114term.

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

The neuromuscular junctions of sax4/sax5 homozygous transheterozygous third instar larvae present significantly less boutons than controls.

sax4/sax5 third instar larval C4da neurons do not show any obvious defects in the dendritic arborization, as compared to controls.

sax4/+ adults do not have any obvious wing phenotypes.

Large posterior clones of sax4 show no wing patterning abnormalities.

Less than 5% of sax4/Df(2R)H23 hemizygous mutant larvae exhibit developmental delay, lethargy, a reduction in the size of imaginal discs, brain | larval stage, and midgut structures, as well as trachea | larval stagel truncations.

When the anterior border of a sax4 clone falls between L2 and L3 in the wing, an ectopic L2 may form at the anterior boundary of the clone. sax4 clones near but anterior to L2 result in the formation of an ectopic wing vein adjacent to their anterior border. These clones often exhibit non-autonomous effects such as ectopic veins forming in wild-type tissue outside the boundaries of the clone.

Heterozygotes show a direct effect on the shape of the wing.

When neutral marked clones are induced in the ovary, the proportion of germaria carrying marked somatic stem cells 3 weeks after clone induction is around 70% of that seen one week after clone induction. For sax4 homozygous clones, the equivalent figure is around 60%.

Clones of male sax4 homozygous germline stem cells are still present in 32% of testes one week after clone induction and 6.3% two weeks after clone induction. This is in contrast to wild-type control clones, which are present in 82% of testes one week after clone induction and 64% two weeks after clone induction.

sax4/Df(2R)sax-H9 larvae show a reduction in size of the neuromuscular junction (NMJ) compared to wild type; the number of synaptic boutons/muscle surface area at muscle 6/7 is 44.1 +/- 1.0% of wild type. The evoked excitatory junctional potential (EJP) (measured at muscle 6 of segment A3) shows a decrease in amplitude in sax4/sax5 animals compared to wild type. Quantal content is reduced compared to wild type.

Mutant stage 13-14 embryos contain the normal number of crystal cells per embryo.

sax4/Df(2R)cn7969 larvae show a significant decrease in bouton number at the neuromuscular junction.

Mutant embryos lacking both maternal and zygotic sax function have a reduced number of amnioserosa cells.

Homozygous clones that occupy the entire posterior compartment of the wing have no effect on venation. Homozygous clones that occupy the entire anterior compartment of the wing have no effect on venation, but the wing is reduced in size. Homozygous wing clones where the clone boundary subdivides a compartment result in an ectopic wing vein at the clone boundary.

Clones induced in the developing eye that span the morphogenetic furrow have condensed chromosomes indicative of early stages in mitosis at the interface between the CycB-expressing and non-expressing cells. Clones at the anterior edge of the furrow show mislocalized nuclei, they fail to reach the apical surface where mitosis normally takes place. Nuclei are also misplaced when the clone is within the furrow and posterior to it. Cell fate specification is not, however, affected.

A large anterior clone in the wing (induced early in larval development) reduces the size of the wing, blunts the wing tip and causes ectopic venation. At the anterior clone boundary cells shift to a more anterior cell fate. At the anterior edge of clones that intersect the margin several margin cells posterior to wing vein L3 produce double row bristles (and not the posterior row of hairs), at other points of the wing margin double row cells fates are transformed to triple row. At the anterior edge of clones adjacent to the naked stretch of margin, ectopic distal costa are produced in the naked region. A large posterior clone in the wing (induced early in larval development) variably disrupts wing venation. Dorsal or ventral clones located anterior to wing vein L2 or dorsal clones posterior to wing vein L5 do not cause ectopic venation. Clones posterior to L2 or anterior of L5 do allow ectopic venation. Where the clone diverges from the line of the normal vein the ectopic vein is produced as a ridge on the dorsal surface.

In germline clones, only 10-25% of normal number of eggs is produced, over a much briefer time period than for wild type. Most are normal though 20% show aberrant dorsal appendages and short length.

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

sax4/sax[+] is an enhancer of visible phenotype of Scer\GAL4A9, gbbUAS.cKa

NOT Enhancer of
Statement
Reference
Suppressor of
Statement
Reference

sax4/sax[+] is a suppressor | partially of visible | adult stage phenotype of Scer\GAL4A9, anchorGD3613

sax4/sax[+] is a suppressor | partially of decreased fecundity | female phenotype of mir-184Δ

sax4/sax[+] is a suppressor | partially of abnormal neuroanatomy phenotype of spictmut

sax4/sax[+] is a suppressor | partially of visible phenotype of Scer\GAL4A9, dppUAS.cHa

sax4 is a suppressor of visible phenotype of upd1GMR.PB

NOT Suppressor of
Statement
Reference
Other
Phenotype Manifest In
Suppressed by
Statement
Reference
Enhancer of
Statement
Reference

sax4/sax[+] is an enhancer of wing vein phenotype of Scer\GAL4A9, gbbUAS.cKa

NOT Enhancer of
Statement
Reference
Suppressor of
Statement
Reference

sax4/sax[+] is a suppressor | partially of wing vein phenotype of Scer\GAL4A9, anchorGD3613

sax4/sax[+] is a suppressor | partially of wing phenotype of Scer\GAL4A9, anchorGD3613

sax4/sax[+] is a suppressor | partially of wing vein phenotype of DdG0269

sax4 is a suppressor | partially of wing phenotype of dppd5/dpphr56

sax4/sax[+] is a suppressor | partially of wing phenotype of Scer\GAL4A9, dppUAS.cHa

sax4 is a suppressor of eye phenotype of upd1GMR.PB

sax4/sax[+] is a suppressor of bouton | increased number phenotype of spink09905/spin10403

NOT Suppressor of
Statement
Reference
Other
Additional Comments
Genetic Interactions
Statement
Reference

Addition of sax4/+ to animals expressing anchorGD3613 under the control of Scer\GAL4A9 partially suppresses the thickened wing vein phenotype, but does not suppress the increased wing size phenotype.

The aberrant wing vein phenotype seen in DdG0269/Y animals is suppressed by sax4/+.

One copy of sax4 substantially rescues the infertility of mir-184Δ females; they produce many more eggs and do not become sterile over time.

When dpp[hr4]/+ males are crossed to sax4/+ females, the resulting dpphr4/+ progeny do not show any significant drop in viability compared to the dpphr4/+ progeny of wild-type mothers in control crosses.

sax4 slightly suppresses the dppd5/dpphr56 wing phenotype.

spictmut neuromuscular junction overgrowth phenotypes are fully suppressed in sax4/Df(2R)cn7969 mutants. The synaptic undergrowth phenotypes in larvae homozygous for spictmut in a sax4/Df(2R)cn7969 background are indistinguishable from that of sax4/Df(2R)cn7969 mutants alone. In addition, a heterozygous sax4 background partially suppresses the neuromuscular junction expansion of spictmut larvae.

Expression of gbbScer\UAS.cKa, under the control of Scer\GAL4A9, in a sax4/+ background partially suppresses the extra wing vein phenotype; over 90% of flies expressing both UAS transgenes show the most severe form of the Scer\GAL4A9>gbbScer\UAS.cKa phenotype, compared to about 20% of Scer\GAL4A9>gbbScer\UAS.cKa flies.

A sax4/+ background causes a mild suppression of the Scer\GAL4A9>dppScer\UAS.cHa wing phenotype; with fewer wings showing the more severe forms of the phenotype.

sax4 clones induced in a gbb4 background that are posterior to L5 or anterior to L2 never lead to ectopic wing vein formation.

The number of synaptic boutons/muscle surface area at muscle 6/7 in sax4/witHA3 double heterozygotes is 85.2 +/- 3.6 % of wild type.

One copy of sax4 suppresses the increased bouton number seen at the neuromuscular junction in spin10403/spink09905 animals. spin10403/spink09905 animals which are also mutant for sax4/Df(2R)cn7969 show a further decrease in bouton number.

Dominantly reduces the viability of gbb1/gbb4 flies.

Xenogenetic Interactions
Statement
Reference

sax::Agam\saxAgamEX.DmelIN.sax completely rescues the lethality of sax4/Df(2R)BSC265 animals.

Complementation and Rescue Data
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
Comments
Comments
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
References (32)