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General Information
Symbol
Dmel\Stat92E06346
Species
D. melanogaster
Name
FlyBase ID
FBal0009559
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
stat92E6346, stat1681, Stat92EP1681, mrl6346, stat92E-lacZ, mrl06346, D-stat6346, Stat92E1681, stat06346
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{PZ} is inserted in opposite orientation into an intron that separates the promoter and first exon from the main body of the coding sequence.

Insertion components
P{PZ}Stat92E06346
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 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In

hindgut & nucleus

Detailed Description
Statement
Reference

Stat92E06346 heterozygosity does not significantly affect the mitotic index in the adult midgut epithelium, as compared to controls.

22% of Stat92E06346/Df(3R)H-B79 animals die during embryogenesis and the remainder die during the first larval instar.

Wild type eyes containing Stat92E06346 mutant clones are normal in size. Eyes containing Stat92E06346 mutant clones in a Minute background are small compared with Minute controls. Elimination of cells adjacent to Stat92E06346 mutant clones (using hid) also results in reduced eye size.

40% of embryos from Stat92E06346 germ line clones show germ-band extension defects.

Stat92E06346 homozygous embryos have mild patterning defects, in which somatic muscles generally appear thinner than normal.

Embryos derived from Stat92E06346 germ-line clones, and which also express Stat92EScer\UAS.cSa via Scer\GAL4en.PU (to rescue segmentation defects), have extensive defects in somatic muscle development, especially in lateral and dorsal regions of the embryo where many muscles are missing and myoblasts remain unfused. These phenotypes are even more severe where embryos are additionally zygotically mutant for Stat92E06346 - a large percentage of somatic muscles are absent and the remaining muscles have no clear identity or shape. These somatic muscle defects show complete penetrance and affect all segments of the embryo. Visceral muscle develops relatively normally.

Very few Stat92E06346 mutant cyst progenitor cell clones are recovered compared to controls.

Adults with Stat92E06346 clones in a Minute background have aberrantly small eyes.

When Stat92E06346/Stat92EF females are shifted to the non-permissive temperature (30oC), the number of gemline stem cells per ovariole falls from 2, to an average of 1.3 per per ovariole at day 2 and to just 0.6 per ovariole at day 6. By this time only 9% of ovarioles contain 2, and in these cases they are no longer associated with cap cells, and 48% contain none. Within a few days of shifting to 30oC, escort stem cells and escort cells lose their wild-type, extended shape and form an epithlial monolayer around the remaining aggregated germ cells. Shifting these animals to the permissive temperature also has dramatic effects on ovariole shape: the space between the basement membrane and the sheath muscle swells dramatically, filling with amorphous material and making the ovariole shrink in diameter. Some sheath associated cells undergo extra endocycles to form giant polyploid nuclei.

Border cell migration is inhibited in Stat92E06346/Stat92EF following maintenance of egg chambers at the restrictive temperature. The severity of the phenotype increases with time spent at the restrictive temperature, with over 90% of egg chambers affected following 4 hours at 29oC. However, border cell number is not reduced.

The proliferation of germ cells in male Stat92E06346 embryos is reduced compared to controls.

At 18oc, Stat92EF/Stat92E06346 male adults have wild-type testes. After a 1 day shift to 29oC, one to three clusters of germ cells with branching fusomes contact the hub in 95% of Stat92EF/Stat92E06346 testes (in wild-type males, only germline stem cells (GSCs) with round fusomes contact the hub). In addition there is an increased number of two- and four-cell cysts in the mutant testes, indicating that multiple GSCs have differentiated. As the length of time at 29oC is increased, GSCs, then spermatogonia and finally spermatocytes are lost in the mutant testes. Dying GSCs are not detected in Stat92EF/Stat92E06346 testes at 29oC and a similar number of dying spermatogonial cysts are detected in both mutant and control testes at 29oC, indicating that differentiation and not cell death accounts for the progressive loss of GSCs and their progeny within the mutant testes at 29oC. The number of somatic cells (excluding hub cells) in the Stat92EF/Stat92E06346 testes declines progressively at 29oC. When Stat92EF/Stat92E06346 male adults shifted to 29oC for 1 day are returned to 18oC for 4 days, the number of germline stem cells (GSCs) increases significantly. After 2 days at 29oC, only 22.5% of Stat92EF/Stat92E06346 testes still contain GSCs, but after a brief recovery at 18oC (2 days), the number of mutant testes containing GSCs increases to 75,8%, indicating that testes which had completely lacked GSCs have regained them. These testes are different from wild type; although GSCs surround the hub, they contact spermatocytes, because the intermediate spermatogonial cells are missing. After a longer recovery period at 18oC, a normal zone of spermatogonial cysts is regained in the mutant testes, indicating that the regenerated GSCs are functional. Somatic stem cells also return in testes undergoing repopulation with GSCs. Stat92EF/Stat92E06346 males that have been shifted to 29oC for 6 days (which lack spermatogonia but contain spermatocytes) never regain lost GSCs when returned to 18oC, suggesting that the regained GSCs are derived from spermatogonia that have reverted to stem cell fate. This is confirmed by labelling of spermatogonial cysts in Stat92EF/Stat92E06346 males which have been shifted to 29oC for 4 days (the testes of these males lack GSCs but contain spermatogonia); labelled spermatogonial cysts are detected near the hub in 6% of testes before recovery, and after a recovery of 2 days at 18oC, 6% of testes regain labelled GSCs (which are only detected near the hub). In addition, the level of labeling in each GSC indicates that each spermatogonial cyst breaks apart and regenerates multiple single GSCs during recovery at 18oC.

The proventriculus development is normal in early stages of proventriculus development in mutants. However in the keyhole stage, the anterior boundary cells fail to move inward into the endodermal keyhole domain and arrest anterior to the proventricular endoderm until late stages of embryonic development. Furthermore, the endodermal cell layer of the keyhole is disorganised and the proventriculus is collapsed.

Paternally rescued Stat92E06346 germ-line clone embryos are missing denticle belt A5 and part of A4. In the absence of paternal rescue, more severe segmentation defects are seen.

Homozygous embryos derived from homozygous female germline clones (lacking both maternal and zygotic Stat92E function) have incompletely elongated hindguts which are wider than normal. There are a greater number of cells in the circumference of the mutant hindgut than in wild type. The total number of hindgut epithelial cells is 85% of wild type.

Embryos derived from homozygous Stat92E06346 female germ line clones have 20-30% fewer pole cells by the cellularization stage, due to mitotic defects, when compared with wild-type cells. At stage 11, the pole cells in these mutants are still associated with the gut, while those in wild-type embryos of the same stage have already become associated with the dorsal mesoderm. Embryos derived from homozygous Stat92E06346 female germ line clones that have also inherited Stat92E06346 from their father are unable to form gonads, and contain randomly scattered pole cells in the cavity of the embryo. Mutant embryos that have inherited wild-type Stat92E from their father have a less severe phenotype; the majority lack one gonad and have more pole cells in the remaining gonad when compared to wild-type embryos. Mosaic flies can be recovered following the transplantation of pole cells from Stat92E06346 female germ line clones and wild-type fathers into wild-type embryos. Such mosaic flies are never recovered when the transplanted pole cells are derived from a Stat92E06346 father as well as a Stat92E06346 germ line clone mother. These transplanted pole cells migrate to ectopic locations instead of migrating toward the somatic gonad of the transplanted embryo.

In zygotic null embryos, the tracheal pits form later and remain smaller than in wild-type siblings. IN late stages they exhibit severe defects in the tracheal branches. In embryos lacking both zygotic and maternal contributions all the tracheal pits are missing and little or no tracheae are found in later stage embryos. The hindgut of maternally and zygotically null (Stat92E06346) embryos are shorter and have fewer cells than those of wild-type. The hindgut nuclei are staggered into double layers in the gut epithelium, making it thicker than wild-type. The central nervous system (CNS) of maternally and zygotically null (Stat92E06346) embryos is grossly disrupted and in some segments of the CNS are completely missing. Similar but milder defects are seen in animals lacking only the maternal contribution, these defects include gaps in the longitudinal tracts and missing commissures. Often neurons that remained (e.g pCC and aCC) failed to grow axons. Similar defects in the peripheral nervous system are seen. Many PNS neurons fail to extend their axons in maternal mutants, and maternal and zygotic mutants many neurons are absent.

Follicle cell clones of Stat92E06346 cause a cell-autonomous loss-of-stalk fate.

Stat92EF/Stat92E06346 mutants show a temperature sensistive reduction in female fecundity. At 20oC females lay on average 50-60 eggs, most of them unfertilized. Approximately 10% develop into adults. At 25oC young females lay only a few eggs which are small and have abnormal dorsal appendages. When cultured at 25oC then shifted to 29oC as early pupae Stat92EF/Stat92E06346 mutant females produce no eggs. Dissected ovaries of the mutants grown at these temperatures show abnormalities in the ovaries including fused egg chambers and the lack of interfollicle cells. The severity of the phenotype increases with age of the females and increasing temperature. A considerable amount of cell death is seen in the ovarioles of older females. More severe defects are seen in females shifted to 29oC during the pupal stage; oogenesis is arrested at or before stage 4 and no egg chambers are pinched off from the germarium. Stat92EF/Stat92E06346 adults have a number of defects including tissue protruding from the adult humeral cuticle, abnormal anterior spiracles, ectopic wing veins, additional spermatheca and adult leg defects. Mosaic ovarioles in which the follicle cells are homozygous for Stat92E06346 are often fused and degenerating. Mosaic ovarioles which have primarily mutant follicle cells, but wild type follicle cells at the termini are phenotypically wild type.

When homozygous mutant clones are made in the ovary, mutant border cells are found at the anterior tip, or displaced along the side of the egg chamber. Displacement of the border cell cluster is only observed when flanking stretch cells are mutant as well. Clones of mutant stretch cells are sometimes thicker than normal. Mutant centripetal cells appear normal in morphology and movement.

Paternally rescued embryos derived from females containing homozygous germ-line clones lack abdominal segment 5 and part of abdominal segment 4. These embryos form a defective tracheal system with several disruptions in the main trunk and many branches.

Embryos derived from homozygous female germline clones show deletion of segment A5.

Homozygous embryos have a mild spiracle phenotype with slightly thinner filzkorper than normal. Homozygous embryos have segmentation defects. The trachea are mostly absent in homozygous embryos derived from homozygous female germline clones. The trachea form in paternally rescued embryos derived from homozygous female germline clones (which still have segmentation defects).

Homozygous clones are generated in the germ line of the testis at the same frequency as in wild-type controls, but homozygous germ line stem cells do not establish persistent clones; although clusters of differentiating mutant spermatocytes are seen, no early-stage homozygous germ cells are evident in testes containing clones 7 days after clone induction.

When homozygous somatic clones are made in the egg chamber, defects in border cell migration are seen. Border cell clusters in which the polar cells are wild-type, but the outer border cells are mutant, exhibit migration failure. Large mutant clones in the remaining follicle epithelium do not produce border cell migration failure. In mutant egg chambers outer border cell clusters consist of an average of 2.2 cells, as compared to 6 in wild-type.

Homozygous germ line stem cells are frequently detected in the testis two days after clone induction. However, the percentage of testes containing germ line stem cell clones decreases over time and they are absent by 9 days after clone induction.

Somatic clones in the eye show no detectable defects.

Stat92E06346 embryos derived from homozygous female germ line clones show loss of the fifth abdominal denticle band and the posterior mid-ventral portion of the fourth band. Variable reduction of the second thoracic and eighth abdominal denticle bands and variable fusion of the sixth and seventh denticle bands is seen.

Embryos exhibit segmentation defects. Homozygotes die at the end of embryogenesis or as young larvae.

Maternal effect segmentation phenotype is similar to that caused by loss of hop activity during embryogenesis. Both paternally rescued and unrescued embryos show a consistent deletion of the fifth abdominal segment and the posterior midventral portion of the fourth abdominal segment. Additional defects are seen in the head and tail of the unrescued embryos. Homozygous dead larvae have a normal cuticle pattern, but larval diploid imaginal tissues are reduced in size.

Germline clones produce eggs with patterning defects: defects in T2, A5 and A8 mainly.

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

Stat92E[+]/Stat92E06346 is a suppressor | partially of melanotic mass phenotype | dominant phenotype of hopTum

Stat92E[+]/Stat92E06346 is a suppressor of size defective | adult stage phenotype of upd1GMR.PB

Stat92E06346 is a suppressor of visible phenotype of Su(var)2-1003697, upd11

Stat92E06346 is a suppressor | partially of melanotic mass phenotype | dominant | heat sensitive phenotype of hopT42

Stat92E06346 is a suppressor of increased mortality phenotype of hopT42

Stat92E06346 is a suppressor of partially lethal phenotype of hopTum

NOT Suppressor of
Statement
Reference
Other
Phenotype Manifest In
Enhanced by
Statement
Reference
NOT suppressed by
Enhancer of
NOT Enhancer of
Suppressor of
Statement
Reference

Stat92E[+]/Stat92E06346 is a suppressor of germarium phenotype of Scer\GAL4C587, smoJF02363

Stat92E[+]/Stat92E06346 is a suppressor of spectrosome phenotype of Scer\GAL4C587, smoJF02363

Stat92E[+]/Stat92E06346 is a suppressor of germarium phenotype of Scer\GAL4C587, ciGD1403

Stat92E[+]/Stat92E06346 is a suppressor of spectrosome phenotype of Scer\GAL4C587, ciGD1403

Stat92EF/Stat92E06346 is a suppressor of eye phenotype of Lfee

Stat92E[+]/Stat92E06346 is a suppressor of eye | somatic clone phenotype of TSG1012

Stat92E[+]/Stat92E06346 is a suppressor | partially of melanotic mass phenotype of hopTum

Stat92E[+]/Stat92E06346 is a suppressor of eye phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, upd1UAS.cZa

Stat92E06346/Stat92E06346 is a suppressor of phenotype of tor11D

Stat92E[+]/Stat92E06346 is a suppressor | partially of lamellocyte phenotype of hopTum

Stat92E[+]/Stat92E06346 is a suppressor | partially of plasmatocyte phenotype of hopTum

Stat92E[+]/Stat92E06346 is a suppressor | partially of podocyte phenotype of hopTum

Stat92E[+]/Stat92E06346 is a suppressor of lamellocyte phenotype of Tl10b

Stat92E[+]/Stat92E06346 is a suppressor of podocyte phenotype of Tl10b

Stat92E06346 is a suppressor of eye phenotype of Su(var)2-1003697, upd11

Stat92E06346 is a suppressor of eye phenotype of Df(1)os1, Su(var)2-1003697

Stat92E06346 is a suppressor of phenotype of hopTum

Stat92E06346 is a suppressor of phenotype of hopT42

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

Stat92E06346 heterozygosity suppresses the increased mitotic index in the adult midgut epithelium induced by the adulthood-only expression of UvragHMS01357 under the control of Scer\GAL4esg-NP5130 (and Gal80[ts], for the temporal control of expression).

Stat92E06346/+ suppresses the increased number of spectrosomes in the germaria of flies expressing smoJF02363 under the control of Scer\GAL4C587.

Stat92E06346/+ suppresses the increased number of spectrosomes in the germaria of flies expressing smoJF02363 under the control of Scer\GAL4C587.

Stat92E06346/+ enhances germline stem cell premature differentiation in lid10424/Df(2L)BSC184 third instar larval testes, with spermatocytes found in direct association with hub cells.

Src42A26-1/+ ; Stat92E06346/+ double heterozygous embryos show defects in head formation and have segmentation and spiracle defects. This phenotype is enhanced if the embryos are also heterozygous for Src64BPI.

Stat92E06346 in eye-antennal disc clones that express Ras85DV12.Scer\UAS under the control of Scer\GAL4Act.PU, and in which adjacent cells are mutant for scrib1, partially suppresses the overgrowth and completely abrogates the invasion of the nerve cord.

Stat92E06346 partially suppresses the overgrowth and invasion of the nerve cord seen in scrib1 mutant eye-antennal disc clones that simultaneously express Ras85DV12.Scer\UAS under the control of Scer\GAL4Act.PU.

The eye is reduced in size when scrib1 mutant clones are generated in eye-antennal discs in which adjacent cells are mutant for Stat92E06346.

Eye size is almost restored to normal in Lfee; Stat92E06346/Stat92EF animals.

One copy of Stat92E06346 partially suppresses the invasive border cell phenotype seen in aptKG05830/apt167 mutant stage 10 egg chambers. A reduction is seen in both the frequency of affected egg chambers and the number of cells. On average 26% of egg chambers contain "stretched border cells" compared to ~80% in aptKG05830/apt167 alone. The border cell cluster also detaches much more easily from the anterior end of the egg chamber.

Stat92E06346/+ strongly suppresses the nonautonomous eye overgrowth phenotype due to mosaicism for TSG1012.

The upd1GMR.PB eye overgrowth phenotype is significantly suppressed by one copy of Stat92E06346. One copy of Stat92E06346 reduces the size and the frequency of the melanotic tumours induced by hopTum/+.

Stat92E06346/+ partially suppresses the overgrowth of wild-type adult eye tissue caused by Vps25A3 homozygous somatic clones.

Stat92E06346. Cskj1D8 mutant larval eye-antennal discs frequently show reduced sizes relative to the single mutants. Mutants also frequently show a reduction or absence of developing antennal tissues. Mutant larval eye tissue also contains many apoptotic cells.

The large eye-phenotype observed in flies expressing upd1Scer\UAS.cZa under the control of Scer\GAL4GMR.PF is suppressed in a Stat92E06346/+ background.

The enlarged eye phenotype seen in flies carrying one copy of upd1GMR.PB is strongly suppressed by one copy of Stat92E06346.

The denticle belt defects seen in the cuticles of Stat92E06346 germ-line clone embryos are not suppressed by Cdk4hs.PC.

Embryos derived from double mutant Stat92E06346; Ras85DΔC40B female germ line clones have 54% fewer pole cells by the cellularization stage than wild-type embryos, which is a greater reduction than is seen in embryos derived from either single mutant female germline clone. Pole cells of these double mutant embryos appear slightly larger than wild-type cells, consistent with their slower mitotic division rate.

Expression of Socs36EScer\UAS.P\T.cCa, under the control of Scer\GAL4en-e16E, in a Stat92E06346/+ background results in an exacerbation of the outstretched wing phenotype seen in Socs36EScer\UAS.P\T.cCa expressing flies. The outgrowth appears to be made of wing material. The missing anterior crossvein phenotype is not affected. However, 60% of these flies show ectopic venation in the wing.

The segmentation phenotype seen in embryos derived from tor12D/+ females is suppressed if the females also carry Stat92E06346 homozygous germline clones. These embryos have phenotypes similar to embryos derived from Stat92E homozygous germline clones.

The increased concentration of circulating hemocytes seen in mxcG43 larvae is not suppressed by Stat92E06346/+. The increased concentration of circulating hemocytes seen in Tl8/+ larvae is not suppressed by Stat92E06346/+, but the increased numbers of podocytes and lamellocytes seen in Tl8/+ larvae are strongly suppressed by Stat92E06346/+.

The addition of Stat92E06346 significantly enhances the eye size and roughness seen in Su(var)2-10537.Scer\UAS, Scer\GAL4ey.PH flies. The enhancement frequently goes further, progeny grow antenna in place of eyes.

The addition of Su(var)2-1003697 to Df(1)os1 mutants leads to a slight suppression of the small eye phenotype seen in Df(1)os1 flies. The further addition of Stat92E06346 increases the suppression.

The weak posterior spiracle phenotype of domeG0367 embryos is enhanced in domeG0367; Stat92E06346 double mutants.

Can suppress the premature differentiation and aggregation but not the overproliferation of hopT42 or hopTum larval haemocytes.

Suppresses the dominant lethality and melanotic tumor phenotype of hopTum.

Xenogenetic Interactions
Statement
Reference

Heterozygosity for Stat92E06346 does not modify the fully penetrant rough eye phenotype resulting from the co-expression of HPV18\E6Scer\UAS.T:Hsap\MYC and Hsap\UBE3AScer\UAS.cRa under the control of Scer\GAL4GMR.PU, leading to severe eye necrosis.

Complementation and Rescue Data
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer

A. Spradling.

Comments
Comments

Precise excision of the P{PZ} is accompanied by reversion of the mutant phenotype.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (26)
Reported As
Symbol Synonym
D-Stat1681
STAT92EP1681
Stat92E1681
Stat92E6346(P:lacZ)
Stat92e06346
l(3)0634606346
stat92E1681
stat92EP1681
stat92Emrl6346
Name Synonyms
Secondary FlyBase IDs
    References (87)