A premature stop codon in the extracellular domain.
Amino acid replacement: Q114term.
C7807780T
C?T
Q114term | sax-PA; Q79term | sax-PB; Q126term | sax-PC
Q114term
lethal (with Df(2R)sax1rv2)
lethal (with Df(2R)saxPE7)
lethal (with Df(2R)sax-H9)
lethal | larval stage (with Df(2R)H23)
lethal | larval stage (with sax1rv1)
lethal | larval stage (with sax3)
lethal | larval stage (with sax5)
lethal | larval stage (with sax6)
sax4/+ adults do not have any obvious wing phenotypes.
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.
sax4/Df(2R)BSC265 has lethal phenotype, suppressible by sax::Agam\saxAgamEX.DmelIN.sax
sax4/sax[+] is an enhancer of visible phenotype of Scer\GAL4A9, gbbUAS.cKa
sax4/sax[+] is a non-enhancer of visible phenotype of I-2UAS.Tag:polyHis,Tag:MYC, Scer\GAL4vg.PM, putUAS.cMa
sax4/sax[+] is a suppressor | partially of abnormal size | adult stage phenotype of Scer\GAL4A9, anchorGD3613
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/Df(2R)cn7969 is a suppressor of abnormal neuroanatomy phenotype of spictmut
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.cUa
sax4 is a suppressor of visible phenotype of upd1GMR.PB
sax4/sax[+] is a suppressor of abnormal neuroanatomy phenotype of spink09905/spin10403
sax4/Df(2R)cn7969 is a suppressor of abnormal neuroanatomy phenotype of spink09905/spin10403
sax4/sax[+] is a non-suppressor of visible phenotype of I-2UAS.Tag:polyHis,Tag:MYC, Scer\GAL4vg.PM, putUAS.cMa
Cln784D, sax4/sax5 has lethal - all die before end of second instar larval stage phenotype
sax4, witHA3/wit[+] has abnormal neuroanatomy | dominant phenotype
sax4/sax[+], witHA3 has abnormal neuroanatomy phenotype
gbb4, sax4 has partially lethal phenotype
gbb4/gbb1, sax4 has partially lethal phenotype
sax4 has wing vein | ectopic | somatic clone | cell non-autonomous phenotype, suppressible by gbb4/gbb4
sax4/sax[+] is an enhancer of wing vein phenotype of Scer\GAL4A9, gbbUAS.cKa
sax4/sax[+] is a non-enhancer of wing phenotype of I-2UAS.Tag:polyHis,Tag:MYC, Scer\GAL4vg.PM, putUAS.cMa
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 of wing vein phenotype of Ctdnep1G0269
sax4/Df(2R)cn7969 is a suppressor of embryonic/larval neuromuscular junction phenotype of spictmut
sax4/sax[+] is a suppressor | partially of embryonic/larval neuromuscular junction phenotype of spictmut
sax4/sax[+] is a suppressor | partially of wing phenotype of Scer\GAL4A9, dppUAS.cUa
sax4 is a suppressor of eye phenotype of upd1GMR.PB
sax4/sax[+] is a suppressor of bouton | increased number phenotype of spink09905/spin10403
sax4/Df(2R)cn7969 is a suppressor of bouton | increased number phenotype of spink09905/spin10403
sax4/sax[+] is a suppressor of neuromuscular junction phenotype of spink09905/spin10403
sax4/Df(2R)cn7969 is a suppressor of neuromuscular junction phenotype of spink09905/spin10403
sax4/sax[+] is a non-suppressor of wing phenotype of I-2UAS.Tag:polyHis,Tag:MYC, Scer\GAL4vg.PM, putUAS.cMa
sax4, witHA3/wit[+] has neuromuscular junction phenotype
sax4, witHA3 has neuromuscular junction phenotype
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.
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.
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.
sax::Agam\saxAgamEX.DmelIN.sax completely rescues the lethality of sax4/Df(2R)BSC265 animals.
sax4/Df(2R)BSC265 is rescued by sax+t8.7
sax4/Df(2R)sax-H9 is rescued by saxhs.PB
sax4/Df(2R)sax-H9 is rescued by saxUAS.Tag:HA/Scer\GAL4elav.PLu
Null allele.