|Feature type||allele||Associated gene||Dmel\smo|
|Also Known As||smoIIG26, smoIIG25|
|Map ( GBrowse )|
|Allele class||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: C298Y. Nucleotide substitution: G1518A. Also carries nucleotide substitutions: T226G, C593G (A96G), G815T, T1240C (N205N), C2197T (A504A), G3022A (S735N), C3686T (T956T), T4161A; all thought to be conservative changes or polymorphisms.
|Phenotype Manifest In|
Homozygous clones of anterior origin in the wing disc, if located along the anterior-posterior boundary, extend into the anatomically posterior territory.
Posterior clones of posterior origin in the wing show no defects in venation or wing morphology. Clones in the anterior compartment of the wing between veins L3 and L4 give rise to defects such as loss of veins or ectopic venation. Clones of anterior origin located near the A/P compartment boundary usually either cross the A/P boundary or displace it posteriorly. Anterior clone cells that are located in the posterior compartment retain anterior-like features and do not associate normally with posterior cells.
Shows a weak dominant enhancing effect on B mutations. smo1 ptc9 double homozygous embryos have a fused denticle belt phenotype, indicating that smo is epistatic to ptc.
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.
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.
cold-sensitive embryonic lethal. All denticles in abdominal segments point posteriorly. At 18oC naked cuticle deleted and denticle belts of adjacent segments fused and locally arranged as mirror-image duplications.
|Phenotype Manifest In|
|NOT Suppressor of|
The small size of E2f[rM729] clones in the eye disc is partially rescued if they are also mutant for smo.
The addition of smo1 to ptcH84/ptc559.1 animals produces an enhancement of the head capsule defect phenotype. 35% of animals exhibit the phenotype, compared to 4%. The addition of smo1 to ptcH84/ptchdl animals has no effect on the head capsule defect phenotype. All animals continue to show the phenotype. 2% of ptcH84, smo1/+ animals show a head capsule defect. 10% of ptcH84, smo1/+, babok07737 animals exhibit head capsule defects. The addition of smo1 to babok07737/Df(2R)Np3 animals has no effect on head capsule defects.
|Complementation & Rescue Data|
|Not rescued by|
|Stocks ( 1 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 5 )|
|Secondary FlyBase IDs|
|References ( 19 )|