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General Information
Symbol
Dmel\smo3
Species
D. melanogaster
Name
FlyBase ID
FBal0015766
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
smoQ14, smo3
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:
G279368A
Reported nucleotide change:
G1783A
Amino acid change:
W366term | smo-PA
Reported amino acid change:
W366term
Comment:
TGG to TGA
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference
Nucleotide substitution: G1783A.
Amino acid replacement: W366term.
The premature stop codon is just after the coding sequence for the third transmembrane domain.
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 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
lamina & neuron | precursor | somatic clone
morphogenetic furrow & nucleus | somatic clone
photoreceptor cell & neuron
photoreceptor cell R8 & eye disc | somatic clone
Detailed Description
Statement
Reference
The size of smo3 homozygous follicle cell clones in the germarium is significantly smaller than control clones; this phenotype is not associated with an increase in apoptosis (i.e. cDcp1-positive cells) in the germarium, as compared to controls.
smo3 homozygous somatic clones in third instar larval eye discs do not enter S transition during the second mitotic wave, except at the edges of the clones.
Homozygous mushroom body gamma neuron clones show normal axon pruning.
Homozygous clones in the eye induced using the ey-FLP/FRT system result in eyes that are smaller than normal with over-represented smo[+] tissue.
Somatic clones of homozygous smo3 mutant cells situated close to the anterior side of the anterior-posterior compartment boundary, but not on the posterior side, can be observed to round off. In addition, a tendency of the smo3 mutant clones that immediately straddle the boundary to migrate from anterior towards posterior territory (but not in the opposite direction) is observed.
The mutant wing vein phenotype produced by expression of smodsRNA.Scer\UAS.WIZ under the control of Scer\GAL4ptc-559.1 is enhanced by smo3; the extent of fusion of veins 3 and 4 is increased.
Cells in homozygous clones straddling the morphogenetic furrow in the eye disc can constrict apically and shorten along their apicobasal axis and can be part of a morphogenetic furrow, although the furrow in the mutant clone is often more posterior in comparison to neighbouring wild-type cells.
Homozygous clones generated using the eyFLP technique result in the occasional loss of one or both third antennal segments or maxillary palps. In animals containing homozygous smo3 clones induced by eyFLP and with two intact antennae, homozygous Or42a-expressing olfactory receptor neurons (ORNs) from the maxillary palp correctly target to their normal glomerulus. However, when both antenna fail to form in animals containing homozygous smo3 clones, Or42a-expressing maxillary palp ORNs mistarget (7 out of 9 cases), The axons often mistarget to areas normally occupied by antennal ORN axons. Or23a-expressing ORN axons from the antenna project to their normal glomeruli in animals containing homozygous smo3 clones induced by eyFLP and with no maxillary palp.
In smo3 somatic clones that span the morphogenetic furrow, nuclei remain apical, rather than moving to the basal side of the cell in the furrow as wild-type cells do.
At least some of the cells in smo3 homozygous somatic clones in the eye disc go on to express markers consistent with normal differentiation of photoreceptors. However, they fail to re-enter the cell cycle at the second mitotic wave. These clones also show evidence of increased cell-death, including dysmorphic nuclei and expression of cell-death markers.
smo3 homozygous clones in the dorsal air sac primordium grow normally and populate the tip of the air sac to the same degree as wild-type clones.
The reduction in distance between wing veins III and IV and partial fusions of these veins proximal to the anterior crossvein that is seen in flies expressing smo5A.Scer\UAS.T:Zzzz\FLAG under the control of Scer\GAL4C-765 are strongly enhanced by smo3/+.
G1 arrest is often delayed by 1-2 cell diameters in smo3 eye disc cells. S phases and mitoses of the second mitotic wave are delayed but not absent in smo3 mutant cells. However, if the cells immediately posterior are wild type, then smo3 mutant cells enter S phase at the normal time.
Unlike neutral somatic clones, smo3 homozygous somatic clones are rapidly lost from the somatic stem cell population of the germarium.
smo3 somatic clones in the scutellum differentiate microchaetes, indicative of transformation into scutum.
R8 photoreceptor differentiation is delayed in smo3 mutant somatic clones.
Somatic clones of smo3 in the ocellar triangle (ocellar cuticle) lead to reduced or absent ocelli. The medial ocellus is occasionally split in two.
Homozygous clones in the wing induced using Scer\FLP1hs.PS can result in the disruption or partial duplication of wing vein L4, and it may be shifted posteriorly. In addition, double-row wing margin bristles occasionally appear more posteriorly along the wing margin than normal. More severe phenotypes show an increasing anteriorisation of the wing. Homozygous clones in the wing induced using Scer\FLP1Scer\UAS.cCa expressed under the control of Scer\GAL4dpp.blk1, Scer\GAL4spalt or Scer\GAL4ptc-559.1 result in ectopic veins appearing between veins L3 and L4, but no displacement of L4 or defects of the bristle pattern are seen. Homozygous clones induced by using Scer\FLP1Scer\UAS.cCa expressed under the control of Scer\GAL4dpp.blk1 or Scer\GAL4ptc-559.1 result in defects in the thorax, head and legs that weaken the flies considerably. Homozygous clones induced by using Scer\FLP1Scer\UAS.cCa expressed under the control of Scer\GAL4vg.int2.1 result in a wide variety of adult wing defects, but despite the disruption in wing patter, these flies are fully viable and do not show defects in other tissues.
Ommatidial rotation is normal in smo3 mutant clones (n = 53).
Homozygous mutant clones of glial cells do not migrate prematurely at second instar and are found exclusively posterior to the morphogenetic furrow.
Large homozygous clones in the anterior tergite that abut the segment boundary and span the a1, a2 and a3 regions have completely normal polarity both within the clone and in surrounding wild-type cells. The a1 region shows transformation of the cuticle to a2 cuticle. Small homozygous clones in the anterior tergite entirely within the a1 region, and separated from the a2 region by a strip of untransformed a1 cuticle occasionally (2/13 cases) show altered polarity in 1 or 2 cells along the posterior edge of the clone.
Mosaic flies with eyes homozygous for smo3 (clones generated using the "eyFLP" system) have small eyes.
When somatic clones of smo3 are made in the developing eye, there is no significant reduction in the percentage of homozygous mutant cells, and the relative spatial distribution of the glia in the eye disc remains unaffected.
Photoreceptor development is blocked in the central regions of marginal homozygous clones in the eye. This effect is nonautonomous; photoreceptors develop along the outer edges of marginal clones and eventually, throughout internal clones in the eye.
Homozygotes embryos exhibit a lawn of denticles covering most of the ventral surface.
When analysed in clones in the developing eye the number of R8 cell precursors is reduced and their spacing is irregular. The timing of emergence of the mutant R8 cells is normal. Neuronal cells in clones autonomously suffer delay in differentiation. Packing in the ommatidial clusters is disrupted.
Early smo3 somatic clones (24-48hr after egg-laying (AEL)) in the female analia delete part of the dorsal anal plate but do not affect the ventral plate. Clones in the abdominal tergite 8 induce overgrowth. Clones in the perianal ring produce duplicated anal structures. The long bristle of the vaginal plates can also be duplicated. Small clones outside the A/P compartment border had no effect. Clones in male adult terminalia autonomously duplicate the structures close to the Antero-posterior border such as the genital arc, the claspers, and the hypandrium bristle. Large clones in the male analia delete most of the anal plate.
Cells in homozygous clones in the eye disc are capable of differentiating as photoreceptors. However, there is a significant delay - there is a clear posterior displacement in the onset of photoreceptor differentiation in mutant cells; differentiation is first seen at the posterior, and occasionally lateral, edges of the clone.
Denticle belts are made up of mostly type 5 denticles.
Clones induced in the embryo in the posterior domain of the A compartment make a3 cuticle. The most posterior clones move back, behind the twin clone. The mutant clone assumes a smooth elliptical shape. In the a3 territory the boundaries of the clone are wiggly.
smo3 clones induced before 72 hours development frequently produce regions of non-cuticular material, thought to be hindgut, in areas that are normally cuticular.
Homozygous clones that include the posterior margin of the lamina furrow lack S phase lamina neuron precursors (LPCs). The scattered S phase cells anterior to the lamina furrow, ad the distribution of S phase cells in other proliferation centres, such as the outer proliferation centre, are unaffected in homozygous clones.
Shows a weak dominant enhancing effect on B mutations.
Homozygous phenotype at 25oC is highly variable, ranging from almost wild type to the occasional partial fusion of denticle belts. At 18oC the denticle belts are completely eliminated and the ventral surface of the cuticle is covered in a continuous lawn of denticles of similar size and random polarity.
Clones of cells mutant for smo redirect the A/P affinity boundary in the developing wing disc. They form a straight boundary when juxtaposed with sister smo+ or smo+/smo- A cells, but a wiggly boundary with neighboring smo-/smo+ cells in the P compartment. Similar results are seen in the adult wing. smo- cells autonomously form anterior wing margin structures if they are derived from A cells, even when they are located in the domain normally occupied by P-compartment cells.
Clones in the anterior compartment of the adult abdomen develop normally when they arise in the middle of the anterior compartment. Clones that arise near or at the anterior/posterior compartment boundary are transformed, forming cuticle characteristic of a more anterior position within the anterior compartment. This transformation is autonomous. Hairs both within and surrounding the clone often have abnormal polarity, although mutant cells which lie very close to the boundary have hairs with normal polarity. Clones that arise in the a1 anterior region of the anterior compartment are transformed to make a2 cuticle.
Clones in the developing eye retard the progression of the morphogenetic furrow. Photoreceptor differentiation is retarded, but not prevented, concomitantly with furrow progression. Clones in the eye that lack both Pka-C1 and smo behave like loss of function Pka-C1 clones. Clones show ectopic photoreceptor differentiation and eventually merge with the endogenous field of differentiation, show no retardation of the furrow, pass through a furrow fate and induce non-autonomous ectopic photoreceptor differentiation outside the clone.
Mutant embryos show a cold sensitive segment polarity phenotype. At 25oC segmental defects are mild whereas at 18oC embryos variably show a classic segment polarity cuticle phenotype.
Homozygous clones in the developing wing that arise distant from the A/P boundary develop normally. Clones that arise immediately anterior to the A/P boundary are associated with reorganised wing patterns to form a mirror symmetric double-anterior winglet and conversely the posterior compartment is severely reduced.
Does not interact with RpII140wimp maternal effect.
cold-sensitive
External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Enhanced by
Statement
Reference
smo3 has photoreceptor cell R8 & eye disc | somatic clone phenotype, enhanceable | somatic clone by Mad1-2
smo3 has photoreceptor cell R8 & eye disc | somatic clone phenotype, enhanceable | somatic clone by tkv8
Suppressed by
Statement
Reference
NOT suppressed by
Statement
Reference
smo3 has phenotype, non-suppressible by eRF1[+]/eRF1F2
Enhancer of
Statement
Reference
smo[+]/smo3 is an enhancer of wing phenotype of MoeC858
NOT Enhancer of
Statement
Reference
smo[+]/smo3 is a non-enhancer of eye phenotype of Caf1-105NIG.12892R, Scer\GAL4ey.PH
Suppressor of
Statement
Reference
smo[+]/smo3 is a suppressor of follicle stem cell phenotype of boie01708
smo3 is a suppressor of denticle belt phenotype of ptcG12
NOT Suppressor of
Statement
Reference
smo3 is a non-suppressor | somatic clone of phenotype of enApa
Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference
The defects of smo3 homozygous somatic clones in third instar larval eye discs to enter S transition during the second mitotic wave, are suppressed by the expression of gigGD1454 (and Dicer-2 transgene, for efficient RNAi) under the control of Scer\GAL4mirr-DE.
24 hours after UV-induced nociceptive sensitization, early third instar smo3/+;TkΔ1C/+ larvae show a significant reduction of thermal allodynia (withdrawal responses to a sub-threshold 38[o]C probe) compared to heterozygotic smo3/+ or TkΔ1C/+ larvae.
One copy of smo3 does not enhance the small eye phenotype seen when Caf1-105NIG.12892R is expressed under the control of Scer\GAL4ey.PH.
The follicle stem cell hyper-proliferation and excess follicle cell accumulation phenotypes are suppressed in boie01708 mutants by smo3/+.
Cells in smo3 tkv4 double homozygous clones straddling the morphogenetic furrow fail to constrict apically and do not shorten along their apicobasal axis, failing to form a morphogenetic furrow. Expression of Cad86CScer\UAS.T:Ivir\HA1 under the control of Scer\GAL4Act5C.PP in smo3 tkv4 double homozygous clones in the region of the morphogenetic furrow can result in the formation of an epithelial invagination in some cases. Cells at the centre of this invagination are shorter along their apicobasal axis compared to smo3 tkv4 double homozygous clones or to wild-type cells within the morphogenetic furrow.
The more severe wing defects seen in Moec858 homozygotes (veination defects and the formation of vesicles between the dorsal and ventral wing surfaces) are enhanced by smo3/+.
Marker analysis shows that some photoreceptor differentiation begins in some fraction of the cells in smo3 tkv8 double homozygous cones in the late third instar eye disc.
In smo3, tkv8 double mutant eye disc clones, BrdU incorporation, a marker of S phase, is abolished in the second mitotic wave.
The rapid loss of smo3 homozygous somatic clone cells from the somatic stem cell population of the germarium is not significantly suppressed if the clone cells are also tkvQ199D.Scer\UAS; Scer\GAL4Act5C.PI (Scer\GAL80 method).
Independent ed1X5, smo3 double mutant clones that originate in different compartments (as evidenced by ci or en expression) can fuse together to form composite clones which have roundish, smooth shapes. Within such composite clones, the characteristic segregation of 'anterior' and 'posterior' cells is maintained - they do not intermix.
R8 differentiation fails in tkv8; smo3 or Mad1-2; smo3 double mutant clones, whereas it is only delayed in smo3 single mutant clones. The delay in R8 photoreceptor differentiation seen in smo3 mutant somatic clones is suppressed by ci94.
Expression of high levels of fz::smoSSF.Scer\UAS under the control of Scer\GAL4Bx-MS1096 in a smo3/+ background results in a reduction in the spacing between the 3rd and 4th wing vein. Co-expression of fuScer\UAS.cAb only weakly suppresses the reduction in spacing between the 3rd and 4th wing vein seen in flies expressing high levels of fz::smoSSF.Scer\UAS under the control of Scer\GAL4Bx-MS1096 in a smo3/+ background. The reduction in spacing between the 3rd and 4th wing vein seen in flies expressing high levels of fz::smoSSF.Scer\UAS under the control of Scer\GAL4Bx-MS1096 in a smo3/+ background is suppressed by co-expression of smoScer\UAS.cHa.T:Hsap\MYC. The ectopic venation and costal overgrowth caused by expression of smoC.Scer\UAS.T:Hsap\MYC,T:Uuuu\Myr4 under the control of hemizygous Scer\GAL4Bx-MS1096 in a smo3/+ background is enhanced by co-expression of fuScer\UAS.cAb, while the L3/4 narrowing is suppressed.
Ommatidial clusters situated posterior to smo3; tkv8 double mutant clones differentiate properly, but over-rotate at a much higher frequency than those situated in other regions of the same eye disc, with many of them reaching 110o-120o.
smo3 homozygous clones generated in an enApa/+ background have no effect on cell fate or polarity in the tergites; smo3 mutant cells located posterior to the line of symmetry retain posterior orientation, while smo3 mutant cells located anterior to the line retain anterior orientation. The smo3 clones interdigitate freely with the surrounding cells.
Pka-C1E95, sggM11 smo3 triple mutant clones in the wing disc exhibit some outgrowths from the notum but no significant wing pattern duplications. Wing discs with Pka-C1E95, smo3 clones have large expansions affecting the anterior compartment of the wing disc.
When Mad12, smo3 double mutant somatic clones are made in the developing eye, a small but significant reduction in the percentage of mutant cells is seen compared to Mad12 clones alone.
smo3 Mad1-2 double mutant clones in the eye never develop photoreceptors whether they lie at the margin or in the interior of the eye disc. Occasionally an ommatidium forms along the edge of the clone, such that some of the component photoreceptors lie within the clone.
Clones in the posterior compartment of the wing disc which are expressing hhαTub84B.PB in a smo3 background form wiggly borders with the surrounding cells. Clones in the anterior compartment of the wing disc which are expressing hhαTub84B.PB in a smo3 background form significantly smoother borders with neighbouring wild-type cells. Unlike Df(2R)enE single mutant clones, Df(2R)enE smo3 double mutant clones of posterior origin in the wing disc invariably occupy only posterior territory and define straight borders to anterior cells at the normal position of the anterior/posterior (A/P) boundary. Df(2R)enE smo3 double mutant clones of anterior origin also occupy posterior territory and define straight borders to anterior cells at the normal position of the A/P boundary.
Cells in tkv8 smo3 double mutant clones in the eye disc cannot differentiate as photoreceptors.
Cells in the A compartment of the adult abdominal tergite which are simultaneously mutant for Df(2R)enE and smo3 behave like smo3 clones: they transform a6, a5 and a4 into a3, and a1 into a2.
Clones mutant for smo3 and Df(2R)enE induced in the posterior compartment of the abdominal tergite make a3 or a2 cuticle. The small number of clones produced after clone formation in the embryo tend to be elliptical with smooth boundaries. Clone induction in the larva produces mutant clones with less pigment and small bristles. These cells survive better than Df(2R)enE clones, especially in the posterior part of the P compartment. The boundaries of these clones are smooth. Clones mutant for smo3 and Df(2R)enE induced in the posterior compartment of the pleura form a3 or a2 cuticle embedded in the A compartments, having been ejected from the posterior compartment.
smo3; slmb1/slmb2 clones generate a supernumerary 'double-anterior' wing.
ptcG12 homozygotes exhibit reduced number of denticle rows and each belt is rectangular shape. ptcG12 smo3 double homozygotes raised at 25oC show an essentially wild type phenotype. Scer\GAL4h-1J3-mediated expression of hhScer\UAS.cIa at 18oC does not modify the smo phenotype. Scer\GAL4h-1J3-mediated expression of wgScer\UAS.cLa at 18oC suppresses the smo denticle belt phenotype.
Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Images (0)
Mutant
Wild-type
Stocks (6)
Notes on Origin
Discoverer
Comments
Comments
The mutant phenotypes of smo2 and smo3 are indistinguishable.
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (5)
References (100)