FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\snk2
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General Information
Symbol
Dmel\snk2
Species
D. melanogaster
Name
FlyBase ID
FBal0015910
Feature type
allele
Associated gene
Dmel\snk
Associated Insertion(s)
Carried in Construct
Also Known As
snk229, snk233
Key Links
Genomic Maps

Allele class

amorphic allele - genetic evidence

Mutagen
Nature of the Allele
Allele class

amorphic allele - genetic evidence

(Ray et al., 1991)
Mutagen
ethyl methanesulfonate
(Tearle and Nusslein-Volhard, 1987)
Progenitor genotype
Cytology
Description

Point mutation in the catalytic site.

(Lemaitre et al., 1996)

Point mutation that alters the last nucleotide of intron 1 from a G to an A. A cryptic splice site is revealed downstream of the normal site resulting in a 32 nucleotide deletion which causes a shift in the reading frame of the mRNA, introducing a stop codon 24 amino acids downstream of the cryptic splice site. Protein produced is predicted to include only the signal peptide plus 30 amino acids.

(Smith et al., 1994)
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
point_mutation
3R:13,041,539..13,041,539 [-]
Nucleotide change:

G13041539A

Reported nucleotide change:

G?A

Comment:

A point mutation that alters the last nucleotide of intron 1 from a G to an A. A cryptic splice site is revealed downstream of the normal site resulting in a 32 nucleotide deletion in the mRNA, which causes a shift in the reading frame, introducing a stop codon 24 amino acids downstream of the cryptic splice site.

(Smith et al., 1994)
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
      Phenotype Manifest In
      Detailed Description
      Statement
      Reference

      Embryos produced by snk1/snk2 mothers are completely dorsallzed, lacking both ventral denticles and Filzkorper.

      (Stein et al., 2010)

      The mean ln (natural logarithm) circulating hemocyte concentration (CHC) value of snk2/snk1 larvae is statistically indistinguishable from that of control siblings. The ability of snk2/snk1 larvae to encapsulate L.boulardi eggs is not significantly different from the encapsulation activity of control larvae.

      (Sorrentino et al., 2004)

      Embryos from snk1/snk2 mothers lack all ventral structures.

      (Großhans et al., 1999)

      Bacterially challenged snk2/snk4 mutants exhibit a wild type Drs response. Pattern of response of CecA1 and CecA2 parallels that of Drs. Dpt and Dro remain fully inducible and pattern of expression of AttA and Def in intermediate.

      (Lemaitre et al., 1996)

      Embryos are strongly dorsalised and exhibit no dorsoventral (d-v) asymmetry in their gastrulation pattern. snkcSa protein injected into the perivitelline space on the ventral side at the cleavage stage allows 46% to gastrulate with normal d-v asymmetry. Injection at syncitial blastoderm stage allows 63% to show a normal pattern of gastrulation with respect to egg shape.

      (Smith et al., 1995)

      Injection of tor::tubt4021t construct and the pll::tort4021p construct into snk1/snk2 embryos induces dorsoventral pattern elements.

      (Großhans et al., 1994)

      Cell intercalation in lateralized snk mutant embryos proceeds normally during germ band extension.

      (Irvine and Wieschaus, 1994)

      Homozygous embryos are completely dorsalised. Injection of snkΔne.T:ea into the central region causes development of ventrolateral cuticular pattern elements in rings, typical of lateralised phenotypes, extreme dorsal or ventral cuticular features are missing and intermediate cuticular features are expanded. Injection posteriorly causes lateralisation at the site of injection, injection of snkΔne.S381A fails to lateralise.

      (Smith and DeLotto, 1994)

      Strongly dorsalized.

      (Smith et al., 1994)

      Perivitelline fluid from Tl and dl donors was capable of restoring polarized gastrulation movements and cuticular elements.

      (Stein and Nusslein-Volhard, 1992)

      Does not interact with RpII140wimp maternal effect.

      (Parkhurst and Ish-Horowicz, 1991)

      Dorsalized embryos: all cuticle cells along the dorsoventral axis behave like dorsal cells of the wild type embryo. zen expression pattern refines at stage 5, dpp pattern does not refine at all, twi and sna are expressed during late stages of embryogenesis.

      (Ray et al., 1991)

      Embryos derived from homozygous females are dorsalised.

      (Carroll et al., 1987)

      Strong allele.

      (Tearle and Nusslein-Volhard, 1987)
      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      NOT Suppressor of
      Statement
      Reference

      snk2 is a non-suppressor of partially lethal - majority die | recessive phenotype of cact7

      (Qiu et al., 1998)
      Phenotype Manifest In
      Additional Comments
      Genetic Interactions
      Statement
      Reference

      Embryos derived from Spn27Aex32/Df(2L)BSC7 ; snk1/snk2 females are completely dorsalised.

      (Ligoxygakis et al., 2003)

      Embryos derived from snk4 Tl3/snk2 + females differentiate cuticles encircled by ventral denticles. Injection of these embryos with tkvQ253D.SP6 RNA restores dorsal structures in a dose-dependent manner. Injection of these embryos with saxQ263D.SP6 RNA has little or no effect; none of these embryos develop amnioserosa and only 2% differentiate dorsal hairs. Injection of these embryos with saxQ263D.SP6 and tkvwt.SP6 RNA does not promote the formation of any dorsal structures. Injection of these embryos with both tkvQ253D.SP6 and saxQ263D.SP6 RNA results in a striking increase in the percentage of embryos that differentiate dorsal tissue types compared to embryos injected with the same concentration of tkvQ253D.SP6 RNA alone. Injection of these embryos with both tkvQ253D.SP6 and saxwt.SP6 RNA does not increase the formation of dorsal structures compared to embryos injected with tkvQ253D.SP6 RNA alone. Injection of these embryos with both tkvQ253D.SP6 and tkvDN.SP6 RNA does not increase the formation of dorsal structures compared to embryos injected with tkvQ253D.SP6 RNA alone.

      (Neul and Ferguson, 1998)

      The zygotic semi-lethality of cact7 homozygotes is not suppressed by snk2.

      (Qiu et al., 1998)

      Double mutant combinations with eaD1 and eaD3 are strongly dorsalized.

      (Chasan et al., 1992)
      Xenogenetic Interactions
      Statement
      Reference
      Complementation and Rescue Data
      Rescued by

      snk2 is rescued by snk+t13.5

      (DeLotto and Spierer, 1986)
      Comments
      Images (0)
      Mutant
      Wild-type
      Stocks (0)
      Notes on Origin
      Discoverer
      Comments
      Comments

      snk2 and "snk3" were isolated in the same screen and sequence analysis reveals the same molecular lesion, indicating that they are different isolates of the same mutational event. The GA at the 3' end of intron 1 is a highly conserved splice acceptor site, possible consequences of the change include cryptic splicing to a nearby site, skipping exons through the next intron, failure to splice the intron, and possibly, normal splicing.

      (Smith et al., 1994)
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (5)
      References (33)