FB2024_03 , released June 25, 2024
Allele: Dmel\snk1
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General Information
Symbol
Dmel\snk1
Species
D. melanogaster
Name
FlyBase ID
FBal0015909
Feature type
allele
Associated gene
Dmel\snk
Associated Insertion(s)
Carried in Construct
Also Known As
snk073, mel(3)4
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
(Lindsley and Zimm, 1992, Tearle and Nusslein-Volhard, 1987)
Progenitor genotype
Cytology
Description

Point mutation in the catalytic site.

(Lemaitre et al., 1996)

Amino acid replacement: Q109term.

(Smith et al., 1994)

Nucleotide substitution: C325T.

(Smith et al., 1994)

Mutation is within the middle of the proenzyme region.

(Smith et al., 1994)
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
point_mutation
3R:13,041,293..13,041,293 [-]
Nucleotide change:

C13041293T

Reported nucleotide change:

C325T

Amino acid change:

Q109term | snk-PA; Q109term | snk-PB; Q109term | snk-PC

Reported amino acid change:

Q109term

(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 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)

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

      (Großhans et al., 1994)

      Strongly dorsalized.

      (Smith et al., 1994)

      Embryos produced by homozygous mothers show extreme dorsalized phenotype; only dorsally derived cuticle remains, resulting in a hollow tube of dorsal ectoderm. No paternal rescue, even by two doses of snk+; dorsalizes the expression of ftz such that entire ftz stripes in the blastoderm exhibit the wide dorsal conformation and do not narrow ventrally as is normal.

      (Lindsley and Zimm, 1992)

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

      (Stein and Nusslein-Volhard, 1992)

      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

      snk1 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)

      The zygotic semi-lethality of cact7 homozygotes is not suppressed by snk1.

      (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
      Comments
      Images (0)
      Mutant
      Wild-type
      Stocks (0)
      Notes on Origin
      Discoverer

      Rice.

      (Lindsley and Zimm, 1992)
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (5)
      References (36)