FlyBase Allele Report: Dmel\fz[hs.sev]

General Information

Symbol

Dmel\fz^hs.sev

Species

D. melanogaster

Name

FlyBase ID

FBal0082914

Feature type

allele

Associated gene

Dmel\fz

Associated Insertion(s)

Carried in Construct

P{sev-fz.T}

Also Known As

sev-Fz

Key Links

Transgenic product class

wild_type

(Tomlinson et al., 1997)

Mutagen

in vitro construct

Nature of the Allele

Transgenic product class

wild_type

(Tomlinson et al., 1997)

Mutagen

in vitro construct

(Tomlinson et al., 1997)

Progenitor genotype

Carried in construct

P{sev-fz.T}

Cytology

Description

Two copies of the sev enhancer are placed upstream of an Hsp70 promoter driving fz expression.

(Tomlinson and Struhl, 1999)

sev expression vector (sev enhancer and inducible Hsp70 promoter) drives expression of fz.

(Tomlinson et al., 1997)

Allele components

Component

Use(s)

Regulatory region(s)

Hsp70

sev

Encoded product / tool

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

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 cell polarity

(Klein et al., 2006)

abnormal planar polarity

(Chin and Mlodzik, 2013, Pichaud and Desplan, 2001, Pazman et al., 2000, Fanto and Mlodzik, 1999)

abnormal planar polarity | somatic clone

(Fanto and Mlodzik, 1999, Tomlinson and Struhl, 1999)

Phenotype Manifest In

Detailed Description

Statement

Reference

Expression of fz^hs.sev results in more than 70% of ommatidia being symmetrical.

(Chin and Mlodzik, 2013)

Expression of one copy of fz^hs.sev causes strong planar cell polarity defects in the eye.

(Klein et al., 2006)

Flies expressing fz^hs.sev show randomisation of chirality and rotation of the ommatidia. Many ommatidia are symmetrical, with both R4 and R3 cells developing as an R3 cell.

(Pichaud and Desplan, 2001)

The ommatidia appear disorganised in flies expressing fz^hs.sev, polarity is random and many ommatidial clusters remain symmetrical (showing R3/R3-type symmetry). In ommatidia that are mosaic in the R3/R4 photoreceptors, the fz^hs.sev cell always adopts the R3 fate. This can lead to polarity reversals and inverted chirality.

(Fanto and Mlodzik, 1999)

Expression of fz^hs.sev in a fz^- background (fz¹⁵ or fz³⁷) in either the presumptive R3 or R4 cell in mosaic ommatidia causes the cell expressing fz^hs.sev to become an R3 cell and the other to become an R4 cell. Ommatidia with inappropriate chirality arise at the mosaic interface in eyes that are mosaic for fz^hs.sev (in a wild-type background). In all these incorrectly patterned ommatidia, either one or both members of the R3/R4 pair carries fz^hs.sev. In these cases, whenever the R3/R4 pair are mosaic, the R3 cell always carries fz^hs.sev. The R3 cell also invariably carries fz^hs.sev in chirally correct ommatidia that are mosaic for the R3/R4 pair.

(Tomlinson and Struhl, 1999)

Ommatidial orientations are disturbed, chiral shape is choosen randomly. Heat induced expression in embryos causes nearly all the cells secrete smooth cuticle and narrow denticle belts are observed (deletion of the first 3-4 anterior rows of denticles). Weakly affected denticle belts only affect the first row of denticles.

(Tomlinson et al., 1997)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

fz^hs.sev has abnormal planar polarity phenotype, enhanceable by N[+]/N^264-39

(Fanto and Mlodzik, 1999)

fz^hs.sev has abnormal planar polarity phenotype, enhanceable by Delta^RevF10/Dl[+]

(Fanto and Mlodzik, 1999)

Suppressed by

Statement

Reference

fz^hs.sev has abnormal planar polarity phenotype, suppressible by fw[+]/fw⁴²

(Chin and Mlodzik, 2013)

fz^hs.sev has abnormal cell polarity phenotype, suppressible by dco^j3B9/dco[+]

(Klein et al., 2006)

Phenotype Manifest In

Enhanced by

Statement

Reference

fz^hs.sev has photoreceptor cell R4 phenotype, enhanceable by N[+]/N^264-39

(Fanto and Mlodzik, 1999)

fz^hs.sev has ommatidium phenotype, enhanceable by N[+]/N^264-39

(Fanto and Mlodzik, 1999)

fz^hs.sev has photoreceptor cell R4 phenotype, enhanceable by Delta^RevF10/Dl[+]

(Fanto and Mlodzik, 1999)

fz^hs.sev has ommatidium phenotype, enhanceable by Delta^RevF10/Dl[+]

(Fanto and Mlodzik, 1999)

NOT Enhanced by

Statement

Reference

fz^hs.sev has phenotype, non-enhanceable by ex^e1

(Blaumueller and Mlodzik, 2000)

fz^hs.sev has phenotype, non-enhanceable by rin^unspecified

(Pazman et al., 2000)

Suppressed by

Statement

Reference

fz^hs.sev has ommatidium phenotype, suppressible by fw⁴²

(Chin and Mlodzik, 2013)

fz^hs.sev has ommatidium phenotype, suppressible by dco^j3B9/dco[+]

(Klein et al., 2006)

NOT suppressed by

Statement

Reference

fz^hs.sev has phenotype, non-suppressible by ex^e1

(Blaumueller and Mlodzik, 2000)

fz^hs.sev has phenotype, non-suppressible by rin^unspecified

(Pazman et al., 2000)

NOT Enhancer of

Statement

Reference

fz^hs.sev is a non-enhancer of phenotype of ex^e1

(Blaumueller and Mlodzik, 2000)

NOT Suppressor of

Statement

Reference

fz^hs.sev is a non-suppressor of phenotype of ex^e1

(Blaumueller and Mlodzik, 2000)

fz^hs.sev is a non-suppressor of phenotype of dsh¹

(Boutros et al., 1998)

Additional Comments

Genetic Interactions

Statement

Reference

fw⁴²/+ partially suppresses the symmetrical ommatidia phenotype caused by fz^hs.sev. fw⁴²/Y also partially suppresses the symmetrical ommatidia phenotype caused by fz^hs.sev and in this case photoreceptor cell loss is also seen.

(Chin and Mlodzik, 2013)

The planar polarity defects seen in the eyes of fz^hs.sev/+ flies are significantly suppressed in fz^hs.sev/+, dco^j3B9/+ flies, although the eyes do not appear wild type.

(Klein et al., 2006)

The fz^hs.sev ommatidial phenotype is dominantly enhanced by N^264-39 or Dl^RevF10; most fz^hs.sev ommatidia show R3/R3-type symmetry in a N^264-39 or Dl^RevF10 heterozygous background.

(Fanto and Mlodzik, 1999)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Comments

Images (0)

Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

Comments

The dominant fz phenotype in the eye caused by expression (in an otherwise wild-type background) of the fz^hs.sev allele in the P{sev-fz.T} transgene (as reported in FBrf0099729) may be due to upregulation of fz transcription levels due to w enhancer sequences present in the P{sev-fz.T} transgene, since a construct (P{hs.2sev(-FRT)fz.1-1-1}) which also contains fz expressed under the control of sev enhancers and a heat shock promoter (fz^{1-1-1.hs.2sev}), but which does not contain w sequences does not show a dominant fz phenotype in the eye when expressed in an otherwise wild-type background.

(Strapps and Tomlinson, 2001)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (1)

Reported As

Symbol Synonym

fz^hs.sev

Name Synonyms

Secondary FlyBase IDs

References (15)

Report Sections

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