FlyBase Allele Report: Dmel\shn[1]

General Information

Symbol

Dmel\shn¹

Species

D. melanogaster

Name

FlyBase ID

FBal0015635

Feature type

allele

Associated gene

Dmel\shn

Associated Insertion(s)

Carried in Construct

Also Known As

shn^IB, shn^IB09, shn^1B

Key Links

Genomic Maps

JBrowse

Allele class

amorphic allele - genetic evidence

hypomorphic allele - genetic evidence

Mutagen

ethyl methanesulfonate

Nature of the Allele

Allele class

amorphic allele - genetic evidence

(Arora et al., 1995)

hypomorphic allele - genetic evidence

(Horsfield et al., 1998, Burke and Basler, 1996)

Mutagen

ethyl methanesulfonate

(Arora et al., 1995, Tearle and Nusslein-Volhard, 1987)

Progenitor genotype

Cytology

Description

Nucleotide substitution C to T resulting in amino acid replacement at codon 1898 causing a premature stop codon. Protein is truncated downstream of the second pair of zinc finger DNA binding domains.

(Arora et al., 1995)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

point_mutation

2R:11,214,106..11,214,106 [+]

Nucleotide change:

C11214106T

Amino acid change:

(Arora et al., 1995)

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

(Rusten et al., 2002)

abnormal neuroanatomy (with shn^k04412)

(Rusten et al., 2002)

lethal

(Arora et al., 1995)

lethal - all die during embryonic stage | recessive

(Staehling-Hampton et al., 1995)

some die during embryonic stage | recessive

(Staehling-Hampton et al., 1995)

Phenotype Manifest In

double row of wing sensilla | cell autonomous | somatic clone

(Torres-Vazquez et al., 2000)

embryo | dorsal closure stage

(Rusten et al., 2002)

embryonic/first instar larval cuticle

(Arora et al., 1995)

embryonic/larval crystal cell

(Milchanowski et al., 2004)

embryonic/larval midgut | embryonic stage

(Staehling-Hampton et al., 1995)

embryonic abdominal dorsal sensory organ precursor cluster

(Rusten et al., 2002)

embryonic abdominal dorsal sensory organ precursor cluster (with shn^k04412)

(Rusten et al., 2002)

embryonic abdominal lateral sensory organ precursor cluster

(Rusten et al., 2002)

embryonic abdominal lateral sensory organ precursor cluster (with shn^k04412)

(Rusten et al., 2002)

embryonic dorsal epidermis

(Staehling-Hampton et al., 1995)

embryonic epidermis

(Ricos et al., 1999)

embryonic head

(Arora et al., 1995)

embryonic midgut constriction

(Staehling-Hampton et al., 1995)

Malpighian tubule

(Jack and Myette, 1999)

presumptive embryonic/larval peripheral nervous system

(Rusten et al., 2002)

triple row of wing sensilla | cell autonomous | somatic clone

(Torres-Vazquez et al., 2000)

ventral denticle belt

(Arora et al., 1995)

visceral trunk mesoderm

(Staehling-Hampton et al., 1995)

wing

(Burke and Basler, 1996)

wing | somatic clone

(Torres-Vazquez et al., 2000)

wing vein

(Burke and Basler, 1996)

Detailed Description

Statement

Reference

The average number of crystal cells per embryo is significantly reduced in homozygous stage 13-14 embryos compared to wild type.

(Milchanowski et al., 2004)

Homozygous embryos fail to undergo dorsal closure and show severe defects in the development of the peripheral nervous system (PNS); fewer neurons are present, especially in the dorsal and lateral PNS clusters (the ventral clusters are less affected). shn^k04412/shn¹ embryos show a reduction in the number of dorsal and lateral neurons of the peripheral nervous system.

(Rusten et al., 2002)

Homozygous somatic clones induced during mid to late third larval instar stage are recovered at a significantly higher frequency than those induced earlier. Although homozygous mutant somatic clones induced after 90h after egg laying can be recovered throughout the anterior wing margin, they are observed at a much higher frequency in the region containing the triple row bristles compared to the double row bristle domain. Clones recovered in the triple row bristle domain tend to be larger than clones in the double row domain.

(Torres-Vazquez et al., 2000)

The Malpighian tubules of homozygous embryos elongate properly to the two cell circumference, although they are located abnormally in the embryo, coiling around their point of origin from the hindgut.

(Jack and Myette, 1999)

Homozygous embryos show bunching of epidermal segments at the end of dorsal closure.

(Ricos et al., 1999)

Clones induced in the developing eye that span the morphogenetic furrow have condensed chromosomes indicative of early stages in mitosis at the interface between the CycB-expressing and non-expressing cells. Clones at the anterior edge of the furrow show mislocalized nuclei, they fail to reach the apical surface where mitosis normally takes place. Nuclei are also misplaced when the clone is within the furrow and posterior to it. Cell fate specification is not, however, affected.

(Penton et al., 1997)

Strong allele. Wing clones induced in mid-to-late third instar larvae are small due to their late induction time but cause visible mutant phenotypes: gaps, splits, vein indentations and additional vein material abutting normal veins. Wing veins are lost when the clone lies on the dominant, protruding, side of the vein. Cells at the edge on the clone are sometimes able to form vein material, reminiscent of the phenotypes of the "loss of vein" class of genes.

(Burke and Basler, 1996)

Dorsal closure fails, dorsal epidermis is significantly reduced. Denticles on the lateral region are abnormally oriented and disrupted.

(Arora et al., 1995)

Homozygous embryos show abnormal gut morphology and gut constrictions do not form. Cell fates are altered in the lateral position of the embryos, wing and haltere primordia do not express sna as they would in wild type.

(Staehling-Hampton et al., 1995)

Nondefective in gonad assembly.

(Warrior, 1994)

embryonic lethal. Embryos lack dorsal hypoderm. Internal organs appear normal and extruded through the open dorsal side of the embryo. Ventral hypoderm contracted.

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressed by

Statement

Reference

shn¹ has abnormal neuroanatomy phenotype, suppressible by brk^M68

(Rusten et al., 2002)

Enhancer of

Statement

Reference

shn¹/shn[+] is an enhancer of visible | dominant phenotype of Bx¹

(Bejarano et al., 2008)

Other

Statement

Reference

Mad^D15, shn¹ has visible | dominant phenotype

(Chen et al., 1998)

Mad^D24, shn¹ has visible | dominant phenotype

(Chen et al., 1998)

shn¹, tkv^D17 has visible | dominant phenotype

(Chen et al., 1998)

Mad^D3, shn¹ has visible | dominant phenotype

(Chen et al., 1998)

E(tkv)D1^D1, shn¹ has visible | dominant phenotype

(Chen et al., 1998)

gbb^D20, shn¹ has visible | dominant phenotype

(Chen et al., 1998)

gbb^D4, shn¹ has visible | dominant phenotype

(Chen et al., 1998)

gbb^D8, shn¹ has visible | dominant phenotype

(Chen et al., 1998)

shn¹, tkv⁶ has visible | dominant phenotype

(Chen et al., 1998)

Phenotype Manifest In

Suppressed by

Statement

Reference

shn¹ has phenotype, suppressible by eRF1[+]/eRF1^F2

(Chao et al., 2003)

shn¹ has embryonic abdominal dorsal sensory organ precursor cluster phenotype, suppressible by brk^M68

(Rusten et al., 2002)

shn¹ has embryonic abdominal lateral sensory organ precursor cluster phenotype, suppressible by brk^M68

(Rusten et al., 2002)

Enhancer of

Statement

Reference

shn¹/shn[+] is an enhancer of wing margin phenotype of Bx¹

(Bejarano et al., 2008)

shn¹ is an enhancer of phenotype of ea^161.13

(George and Terracol, 1997)

shn¹ is an enhancer of wing vein phenotype of tkv¹/Df(2L)tkv2

(Staehling-Hampton et al., 1995)

NOT Suppressor of

Statement

Reference

shn¹ is a non-suppressor of embryonic abdominal ventral sensory organ precursor cluster group phenotype of brk^M68

(Rusten et al., 2002)

Other

Statement

Reference

shn¹, tkv⁶ has unguis phenotype

(Chen et al., 1998)

shn¹, tkv⁶ has tarsal segment phenotype

(Chen et al., 1998)

shn¹, tkv⁶ has leg phenotype

(Chen et al., 1998)

shn¹, tkv⁶ has wing vein phenotype

(Chen et al., 1998)

dpp^s5, shn¹ has wing vein phenotype

(Staehling-Hampton et al., 1995)

tkv¹/Df(2L)tkv2, shn¹ has unguis phenotype

(Staehling-Hampton et al., 1995)

dpp^s5, shn¹ has wing vein L4 phenotype

(Staehling-Hampton et al., 1995)

Additional Comments

Genetic Interactions

Statement

Reference

shn¹ brk^M68 double mutant embryos show a clear rescue of the number of neurons in the dorsal and lateral clusters of the peripheral nervous system compared to shn¹ single mutants. The reduction in the number of neurons in the ventral clusters in shn¹ brk^M68 double mutant embryos is indistinguishable from that in brk^M68 single mutants.

(Rusten et al., 2002)

Dominantly enhances the wing vein defects of tkv⁶ flies, and also produces defects in proximal/distal patterning of the leg in these flies; distal elements such as claws and distal tarsal segments are deleted in tkv⁶ shn¹; tkv⁶ flies. No interaction with tkv⁶ is seen in double heterozygous flies. No interaction with tkv⁶, E(tkv)D2^D2, Mad^D14 or Mad^D16 is seen in double heterozygous flies. Double heterozygotes with tkv^D17, E(tkv)D1^D1, Mad^D3, Mad^D15, Mad^D24, gbb^D4, gbb^D8 or gbb^D20 may show imaginal disc development defects.

(Chen et al., 1998)

shn¹/dpp^s5 flies have a terminal gap at the end of the fourth longitudinal vein. This effect is rescued by addition of a dpp transgene. shn¹ also enhances the wing vein thickening of tkv¹/Df(2L)tkv2.

(Staehling-Hampton et al., 1995)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Complements

shn¹⁶⁶

(Horn et al., 2003)

Comments

Images (0)

Mutant

Wild-type