FlyBase Allele Report: Dmel\smo[1]

General Information

Symbol

Dmel\smo¹

Species

D. melanogaster

Name

FlyBase ID

FBal0015764

Feature type

allele

Associated gene

Dmel\smo

Associated Insertion(s)

Carried in Construct

Also Known As

smo^IIG26, smo^IIG25

Key Links

Genomic Maps

JBrowse

Allele class

cold sensitive loss of function allele

Mutagen

ethyl methanesulfonate

Nature of the Allele

Allele class

cold sensitive loss of function allele

(Alcedo et al., 1996)

Mutagen

ethyl methanesulfonate

(Tearle and Nusslein-Volhard, 1987)

Progenitor genotype

Cytology

Description

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.

(Alcedo et al., 2000)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

point_mutation

2L:279,103..279,103 [+]

Nucleotide change:

G279103A

Reported nucleotide change:

G1518A

Amino acid change:

C298Y | smo-PA

Reported amino acid change:

C298Y

Comment:

Also carries eight other nucleotide substitutions, all thought to be conservative changes or polymorphisms.

(Alcedo et al., 2000)

Variant Molecular Consequences

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

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

ameliorates neurodegenerative disease

modeled by ptc^559.1

(Gazi et al., 2009)

Comments on Models/Modifiers Based on Experimental Evidence ( 0 )

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

lethal | recessive | cold sensitive

(Alcedo et al., 1996)

segment polarity phenotype | cold sensitive

(Alcedo et al., 1996)

segment polarity phenotype | recessive | cold sensitive

(Alcedo et al., 1996)

Phenotype Manifest In

Detailed Description

Statement

Reference

Homozygous clones of anterior origin in the wing disc, if located along the anterior-posterior boundary, extend into the anatomically posterior territory.

(Wang and Holmgren, 2000)

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.

(Blair and Ralston, 1997)

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.

(Epps et al., 1997)

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.

(Rodriguez and Basler, 1997)

Mutant embryos show a cold sensitive segment polarity phenotype. At 25^oC segmental defects are mild whereas at 18^oC embryos variably show a classic segment polarity cuticle phenotype.

(Alcedo et al., 1996)

cold-sensitive embryonic lethal. All denticles in abdominal segments point posteriorly. At 18^oC naked cuticle deleted and denticle belts of adjacent segments fused and locally arranged as mirror-image duplications.

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressor of

Statement

Reference

smo¹/smo[+] is a suppressor | partially of partially lethal - majority live | progressive phenotype of Df(2R)Np3/ptc^559.1

(Gazi et al., 2009)

smo¹/smo[+] is a suppressor | partially of abnormal locomotor behavior | adult stage | progressive phenotype of Df(2R)Np3/ptc^559.1

(Gazi et al., 2009)

Phenotype Manifest In

Enhancer of

Statement

Reference

smo¹ is an enhancer of adult head capsule phenotype of ptc^559.1/ptc^H84

(Shyamala and Bhat, 2002)

Suppressor of

Statement

Reference

smo¹/smo[+] is a suppressor | partially of synapse | adult stage phenotype of Df(2R)Np3/ptc^559.1

(Gazi et al., 2009)

smo¹ is a suppressor of eye disc | somatic clone phenotype of E2f1^rM729

(Ambrus et al., 2007)

NOT Suppressor of

Statement

Reference

smo¹ is a non-suppressor of adult head capsule phenotype of ptc^hdl/ptc^H84

(Shyamala and Bhat, 2002)

smo¹ is a non-suppressor of adult head capsule phenotype of Df(2R)Np3/babo^k07737

(Shyamala and Bhat, 2002)

Other

Statement

Reference

babo^k07737, ptc^H84, smo¹ has adult head capsule phenotype

(Shyamala and Bhat, 2002)

babo^k07737, ptc^H84, smo¹/smo[+] has adult head capsule phenotype

(Shyamala and Bhat, 2002)

ptc^H84, smo¹ has adult head capsule phenotype

(Shyamala and Bhat, 2002)

Additional Comments

Genetic Interactions

Statement

Reference

The locomotor defects and increased lethality as well as the decrease in density of synaptic terminals in adult brain calyx characteristic for aged ptc^559.1/Df(2R)Np3 mutants can be partially suppressed by combination with smo¹ in heterozygous state.

(Gazi et al., 2009)

The small size of E2f^rM729 clones in the eye disc is partially rescued if they are also mutant for smo¹.

(Ambrus et al., 2007)

The addition of smo¹ to ptc^H84/ptc^559.1 animals produces an enhancement of the head capsule defect phenotype. 35% of animals exhibit the phenotype, compared to 4%. The addition of smo¹ to ptc^H84/ptc^hdl animals has no effect on the head capsule defect phenotype. All animals continue to show the phenotype. 2% of ptc^H84, smo¹/+ animals show a head capsule defect. 10% of ptc^H84, smo¹/+, babo^k07737 animals exhibit head capsule defects. The addition of smo¹ to babo^k07737/Df(2R)Np3 animals has no effect on head capsule defects.

(Shyamala and Bhat, 2002)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Rescued by

smo¹/smo³ is rescued by Scer\GAL4^prd.RG1/smo^{UAS.cHa.Tag:MYC}

(Hooper, 2003)

Not rescued by

smo¹/smo³ is not rescued by Scer\GAL4^prd.RG1/smo^{N.UAS.Tag:MYC}

(Hooper, 2003)

smo¹/smo³ is not rescued by Scer\GAL4^prd.RG1/smo^{C.UAS.Tag:MYC,Tag:Myr(v-Src)}

(Hooper, 2003)

Comments

Images (0)

Mutant

Wild-type

Stocks (1)

Kyoto

101417

CyO / smo¹ cn¹ bw¹ speck¹

Notes on Origin

Discoverer

Comments

ci^D is epistatic to smo¹.

(Von Ohlen et al., 1997)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (5)

Reported As

Symbol Synonym

smo¹

(Gazi et al., 2009, Umetsu et al., 2006)

smo^IIG16

(Shyamala and Bhat, 2002)

smo^IIG25

(Hepker et al., 1999, Blair and Ralston, 1997)

smo^IIG26

(Ambrus et al., 2007, Kwon et al., 2004, Nussbaumer et al., 2000, Wang and Holmgren, 2000, Hays et al., 1999, van den Heuvel and Ingham, 1996)

smo^IIG

(Tearle and Nusslein-Volhard, 1987)

Name Synonyms

Secondary FlyBase IDs

References (20)

Report Sections

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