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General Information
Symbol
Dmel\shn1
Species
D. melanogaster
Name
FlyBase ID
FBal0015635
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
shnIB, shnIB09, shn1B
Key Links
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Nucleotide change:

C11214106T

Amino acid change:

Q1852term | shn-PA; Q1852term | shn-PB; Q1852term | shn-PC; Q1897term | shn-PD; Q1852term | shn-PE; Q1897term | shn-PF

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

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.

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
Phenotype Manifest In
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.

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). shnk04412/shn1 embryos show a reduction in the number of dorsal and lateral neurons of the peripheral nervous system.

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.

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.

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

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.

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.

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

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.

Nondefective in gonad assembly.

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
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Statement
Reference
Enhancer of
Statement
Reference

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

Other
Phenotype Manifest In
Suppressed by
Statement
Reference

shn1 has phenotype, suppressible | maternal effect by eRF1[+]/eRF1F2

Enhancer of
Statement
Reference

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

shn1 is an enhancer of phenotype of ea161.13

NOT Suppressor of
Statement
Reference

shn1 is a non-suppressor of ventral abdominal cluster phenotype of brkM68

Other
Additional Comments
Genetic Interactions
Statement
Reference

shn1 brkM68 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 brkM68 double mutant embryos is indistinguishable from that in brkM68 single mutants.

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)D2D2, MadD14 or MadD16 is seen in double heterozygous flies. Double heterozygotes with tkvD17, E(tkv)D1D1, MadD3, MadD15, MadD24, gbbD4, gbbD8 or gbbD20 may show imaginal disc development defects.

shn1/dpps5 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.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (3)
Notes on Origin
Discoverer
Comments
Comments

Strong hypomorph.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
References (31)