FlyBase Allele Report: Dmel\N[fa-g]

General Information

Symbol

Dmel\N^fa-g

Species

D. melanogaster

Name

facet-glossy

FlyBase ID

FBal0012868

Feature type

allele

Associated gene

Dmel\N

Associated Insertion(s)

flea{}N^fa-g

Carried in Construct

Also Known As

fa^g

Key Links

Allele class

loss of function allele

Mutagen

spontaneous

Nature of the Allele

Allele class

loss of function allele

(Larson et al., 2008)

Mutagen

spontaneous

(Grimwade et al., 1985)

Progenitor genotype

Associated Insertion(s)

flea{}N^fa-g

Cytology

Description

Insertion of flea into the second intron.

(Gorman and Girton, 1992)

Insertion of an unknown transposable element in an intronic region.

(Xu et al., 1990)

Insertion of a transposable element into an intronic region between exons B and C of N.

(Ramos et al., 1989)

Insertion of a copia-like element at coordinate -10kb (coordinates according to FBrf0045027 and FBrf0039003).

(Kelley et al., 1987)

Insert stated as cause: undefined Insertion of a 5kb copia-like element into an intron of the N locus.

(Welshons and Welshons, 1986)

Insert stated as cause: middle repetitive DNA (inserted between coordinates -8.4 and -10.9, zero coordinate is defined as the centre of the 2.2kb EcoRI fragment that encompasses the N^76b8 inversion breakpoint).

(Grimwade et al., 1985)

flea at -10.3 to -9.4

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 neuroanatomy

(Larson et al., 2008)

visible

(Larson et al., 2008, Rabinow and Birchler, 1990, Lefevre, 1974)

visible | recessive

(Duus et al., 1992, Gorman and Girton, 1992, Ramos et al., 1989, Welshons and Welshons, 1986, Shellenbarger and Mohler, 1975, Welshons, 1974)

Phenotype Manifest In

Detailed Description

Statement

Reference

Adult N^fa-g eyes have a glossy appearance, resulting from an excess of inter-ommatidial cells that is apparent in the pupal eye. Multiple cells enwrap the cone cells, although few will differentiate as primaries.

N^fa-g mutant ommatidia fail to limit the number of primary pigment cell precursors.

Inter-ommatidial precursor cells in the pupal retina are excessively motile. This abnormally dynamic behaviour persists after 22 hours a.p.f. and it can be observed as late as 30 hours a.p.f.

(Larson et al., 2008)

Primary pigment cells are not formed in hemizygous flies.

(Hayashi et al., 1998)

Rough eyes, irregular arrangements of facets and irregularities in internal retinal structures.

(Duus et al., 1992)

Glossy looking eyes. Additive interactions with dx alleles.

(Gorman and Girton, 1992)

Retina defects are not associated with optic lobe defects in 50% of homozygous N^fa-g retina clones generated by somatic recombination. The arrangement of ommatidia is severely disrupted, the number of ommatidia is reduced and they appear shorter than normal in homozygous clones in the retina. A disruption of the fenestrated zone, laminar cortex and neuropil can be seen in the underlying optic lobe if it is defective.

(Markopoulou and Artavanis-Tsakonas, 1991)

Mutations of mam, bib and neur in an heterozygous condition had no effect on the expression of N^Ax-59d or N^Ax-59b except when coupled in cis with N^fa-g. The neurogenic mutations suppress the wing venation phenotype of N.

(Portin and Rantanen, 1991)

Homozygotes exhibit rough eyes due to misrouting of primary pigment cells to the fate of secondary pigment cells (FBrf0049795). Phenotype can be altered by sca mutations, necrotic patches of tissue appears in both eyes.

(Rabinow and Birchler, 1990)

Pronounced eye phenotype. Does not interact with dx^ENU.

(Xu and Artavanis-Tsakonas, 1990)

The eye has a smooth, glossy appearance, because the corneal lenses are separated by a shallow trough rather than a sharp crevice as in the wild-type. The ommatidial array is less regular than in normal eyes. Few ommachrome containing primary pigment cells are present, and there are excess pteridine-containing secondary-like pigment cells. Eye bristles are not properly placed. Cell death in the eye is reduced.

(Cagan and Ready, 1989)

Expression was suppressed by Dl mutations and enhanced by E(spl) and H mutations.

(Siren and Portin, 1989)

Homozygous female and hemizygous male flies have rough, glossy eyes. N^fa-swb/N^fa-g flies have rough eyes that are not glossy.

(Welshons and Welshons, 1986)

Homozygotes have rough eyes with a glossy surface. This phenotype is the same at 18, 25 and 29^oC.

(Shellenbarger and Mohler, 1975)

N^fa-l2/N^fa-g flies have rough, irregular eyes.

(Lefevre, 1974)

Eyes have facets more irregular than fa, but surface is smoothed, giving a glossy effect. Equal mutant expression in both sexes. Pigment distribution may be uneven, contributing to an impression of altered eye color. No wing effect. Eyes of N^fa-g/N^fa-1 intermediate between the two homozygotes. Complementary with spl, N^nd-3, nd and N^nd-2 (Welshons, 1965). RK1. strong allele; temperature sensitive; dosage compensated

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressed by

Statement

Reference

N^fa-g has abnormal neuroanatomy phenotype, suppressible by α-Cat^UAS.sgGFP/Scer\GAL4^GMR.PF

(Larson et al., 2008)

Other

Statement

Reference

N^fa-g, sno¹ has lethal phenotype

(Lefevre and Peterson, 1972)

Phenotype Manifest In

Suppressed by

Statement

Reference

N^fa-g has primary pigment cell phenotype, suppressible by B-H1^sev.PH

(Hayashi et al., 1998)

Other

Statement

Reference

B-H1^sev.PH, N^fa-g has cone cell phenotype

(Hayashi et al., 1998)

Bpt¹, N^fa-g, w^a has eye phenotype

(Duus et al., 1992)

Bpt¹, N^fa-g, w^a has larval brain phenotype

(Duus et al., 1992)

Bpt¹, N^fa-g, w^a has adult optic lobe phenotype

(Duus et al., 1992)

Additional Comments

Genetic Interactions

Statement

Reference

Expression of Scer\GAL4^GMR.PF driven α-Cat^{Scer\UAS.T:Avic\GFP-sg} leads to a mild suppression of some of the N^fa-g pupal retina phenotypes.

(Larson et al., 2008)

Some of the primary pigment cells are restored if the N^fa-g flies are also carrying B-H1^sev.PH. The formation of these primary pigment cells is associated with cone cell loss.

(Hayashi et al., 1998)

Rough eye phenotype is not modified by mutations in any of the zygotic neurogenic loci: E(spl), mam, bib or neur.

(Xu et al., 1990)

Males carrying N^fa-g and sno¹ show an exaggerated phenotype: have difficulty in eclosion and survive only briefly.

(Lefevre and Peterson, 1972)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Complements

N^fa-1

(Shellenbarger and Mohler, 1975)