FlyBase Allele Report: Dmel\smo[2]

General Information

Symbol

Dmel\smo²

Species

D. melanogaster

Name

FlyBase ID

FBal0015765

Feature type

allele

Associated gene

Dmel\smo

Associated Insertion(s)

Carried in Construct

Also Known As

smo^IIX43, smo^11X43

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: C115Y. Nucleotide substitution: G1089A. Also carries nucleotide substitutions: T226G, C593G (A96G), G815T, T1240C, 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:278,674..278,674 [+]

Nucleotide change:

G278674A

Reported nucleotide change:

G1089A

Amino acid change:

C155Y | smo-PA

Reported amino acid change:

C155Y

(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 ( 0 )

Disease

Interaction

References

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

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

abnormal size | somatic clone

(Molnar et al., 2007)

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

Follicle stem cell clones homozygous for smo² are present at a much lower frequency than control clones at 7 days (34% vs 73%) and 14 days (8% vs 57%) after clone induction.

(Vied and Kalderon, 2009)

Wings developing from smo² mutant cells are extremely reduced in size and have lost most pattern elements.

(Molnar et al., 2007)

Embryos lacking maternal smo function (derived from females carrying smo² germline clones and fertilised with a wild-type sperm) develop normally into fertile adults. Somatic gonadal precursor cells form normally in these embryos. Germ cells show no apparent cell cycle defects in these embryos. Defects are seen at stages 12-13, when many of the germ cells fail to associate with the somatic gonadal precursor cells and instead scatter randomly in the mesoderm. At stage 15, these migration defects seem to be largely rectified and the number of germ cells in the primitive gonad approaches that of wild type. Embryos lacking both maternal and zygotic smo function (derived from females carrying smo² germline clones and fertilised with a smo² sperm) show severe segmentation defects, having a lawn of denticles phenotype.

(Deshpande et al., 2001)

Homozygous clones in the female germ cells do not show significant developmental defects during oogenesis.

(Vied and Horabin, 2001)

Mutant embryos derived from homozygous germline clones lack Bolwig's organs without loss of the optic lobe.

(Suzuki and Saigo, 2000)

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)

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.

(Strutt and Mlodzik, 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)

At 25^oC naked cuticle is deleted sporadically between adjacent denticle belts. At 18^oC naked cuticle is replaced by denticle belts with reversed polarity.

(van den Heuvel and Ingham, 1996)

cold-sensitive

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Phenotype Manifest In

NOT suppressed by

Statement

Reference

smo² has Bolwig organ | germline clone phenotype, non-suppressible by hh^UAS.cKa/Scer\GAL4^da.G32

(Suzuki and Saigo, 2000)

Other

Statement

Reference

Mad^B1, smo² has eye disc & neuron | somatic clone phenotype

(Brennan et al., 2001)

Mad^B1, smo² has eye disc & nucleus | somatic clone phenotype

(Brennan et al., 2001)

Additional Comments

Genetic Interactions

Statement

Reference

Neural differentiation is blocked in smo² ; Mad^B1 double mutant clones in the eye disc. Aberrant nuclear migration is seen in double mutant clones spanning the furrow.

(Brennan et al., 2001)

The phenotype of smo² embryos derived from homozygous germline clones is not rescued by expression of hh^Scer\UAS.cKa under the control of Scer\GAL4^da.G32.

(Suzuki and Saigo, 2000)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Comments

Images (0)

Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

Comments

The mutant phenotypes of smo² and smo³ are indistinguishable.

(Strutt and Mlodzik, 1997)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (10)

Reported As

Symbol Synonym

Smo²

(Molnar et al., 2007)

Smo^X43

(Rallis et al., 2020)

Smo^smo2

(Deshpande et al., 2001)

smo^11X43

(Ohlmeyer and Kalderon, 1998)

smo^11x43

(Ohlmeyer and Kalderon, 1997)

smo²

(Little et al., 2020, Garcia-Garcia et al., 2017, Kupinski et al., 2013, Marks and Kalderon, 2011, Molnar et al., 2011, Su et al., 2011, Zhou and Kalderon, 2011, Zhou and Kalderon, 2010, Vied and Kalderon, 2009, Smelkinson and Kalderon, 2006, Zhou et al., 2006)

smo^IIX43

(Rallis et al., 2020, Gallet et al., 2008, Ruel et al., 2003, van den Heuvel and Ingham, 1996, Sampedro et al., 1993, van den Heuvel et al., 1993)

smo^IIX

(Tearle and Nusslein-Volhard, 1987)

smo^IIx43

(van den Heuvel and Ingham, 1996)

smoIIX43

(Therond et al., 1999)

Name Synonyms

Secondary FlyBase IDs

References (36)

Report Sections

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