|Feature type||allele||Associated gene||Dmel\smo|
|Also Known As||smoQ14, smo3|
|Map ( GBrowse )|
|Allele class||cold sensitive amorphic allele - genetic evidence, cold sensitive loss of function allele|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
Amino acid replacement: W366@. Nucleotide substitution: G1783A.
Amino acid replacement: W366@. W366 falls just after the coding sequence for the third transmembrane domain.
|Phenotype Manifest In|
adult abdomen & cuticle | anterior compartment
adult abdomen & microchaeta | anterior compartment
lamina & neuron | precursor | somatic clone
morphogenetic furrow & nucleus | somatic clone
photoreceptor cell & neuron
photoreceptor cell R8 & eye disc | somatic clone
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 smo 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 smo 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 smo[dsRNA.Scer\UAS.WIZ] under the control of Scer\GAL4[ptc-559.1] is enhanced by smo; 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 smo 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 smo 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 smo 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 smo 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.
smo 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 smo eye disc cells. S phases and mitoses of the second mitotic wave are delayed but not absent in smo mutant cells. However, if the cells immediately posterior are wild type, then smo 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.
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.
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.
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.
|Phenotype Manifest In|
Scer\GAL4Bx-MS1096, smo3, smoC.Scer\UAS.T:Hsap\MYC,T:Uuuu\Myr4 has costal cell phenotype, enhanceable by fuScer\UAS.cAb/Scer\GAL4Bx-MS1096
Scer\GAL4Bx-MS1096, smo3, smoC.Scer\UAS.T:Hsap\MYC,T:Uuuu\Myr4 has wing vein | ectopic phenotype, enhanceable by fuScer\UAS.cAb/Scer\GAL4Bx-MS1096
smo3 has photoreceptor cell R8 & eye disc | somatic clone phenotype, enhanceable | somatic clone by Mad1-2
Scer\GAL4Bx-MS1096, fz::smoSSF.Scer\UAS, smo[+]/smo3 has 1st posterior cell phenotype, suppressible by Scer\GAL4Bx-MS1096, fz::smoSSF.Scer\UAS
Scer\GAL4Bx-MS1096, smo3, smoC.Scer\UAS.T:Hsap\MYC,T:Uuuu\Myr4 has 1st posterior cell phenotype, suppressible | partially by fuScer\UAS.cAb/Scer\GAL4Bx-MS1096
|NOT suppressed by|
smo3 has follicle stem cell | somatic clone phenotype, non-suppressible by Scer\GAL4Act5C.PI/Scer\GAL4Act5C.PI/tkvQ199D.Scer\UAS
|NOT Suppressor of|
The follicle stem cell hyper-proliferation and excess follicle cell accumulation phenotypes are suppressed in boi[e01708] mutants by smo/+.
Cells in smo tkv 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 Cad86C[Scer\UAS.T:Ivir\HA1] under the control of Scer\GAL4[Act5C.PP] in smo tkv 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 smo tkv 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 smo tkv double homozygous cones in the late third instar eye disc.
In smo, tkv 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 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.
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.
|Complementation & Rescue Data|
|Partially rescued by|
|Not rescued by|
|Stocks ( 2 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 4 )|
(Vrailas et al., 2006, Wei et al., 2005, Molnar and de Celis, 2006, Jia et al., 2005, Kirilly et al., 2005, Sweeney et al., 2007, Firth and Baker, 2005, Casso et al., 2008, Cabernard and Affolter, 2005, Shi et al., 2011, Vrailas and Moses, 2006, Schlichting and Dahmann, 2008, Khaliullina et al., 2009, Baonza and Freeman, 2005, Corrigall et al., 2007, Jia et al., 2009, Nicholson et al., 2011, Schilling et al., 2011, Christiansen et al., 2012, Melicharek et al., 2008, Hartman et al., 2010)
|Secondary FlyBase IDs|
|References ( 81 )|
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|Recent research papers ( 5 )|