FB2024_03 , released June 25, 2024
Allele: Dmel\rk1
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General Information
Symbol
Dmel\rk1
Species
D. melanogaster
Name
FlyBase ID
FBal0014574
Feature type
allele
Associated gene
Dmel\rk
Associated Insertion(s)
Carried in Construct
Also Known As
rk
Key Links
Genomic Maps

Allele class

hypomorphic allele - genetic evidence

Mutagen
Nature of the Allele
Allele class

hypomorphic allele - genetic evidence

(Loveall and Deitcher, 2010)
Mutagen
U.V.
(Ashburner et al., 1999.10.12)
Progenitor genotype
Cytology
Description

Nucleotide substitution: C?A.

(Baker and Truman, 2002)

Amino acid replacement: Y698term.

(Baker and Truman, 2002)
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
point_mutation
2L:13,985,468..13,985,468 [-]
Nucleotide change:

C13985468A

Reported nucleotide change:

C?A

Amino acid change:

Y698term | rk-PA

Reported amino acid change:

Y698term

(Baker and Truman, 2002)
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

      The midguts of 10-14 day old rk1/rk1 mutants display intestinal stem cell hyperproliferation, increased cellularity and abnormal epithelial multilayering, and an apparent increase in symmetric intestinal stem cell division; rk1/rk1 mutants also display wing inflation defects, as compared with wild type.

      Clones of rk1/rk1 cells within the intestinal epithelium show no significant difference in cell number when compared with control clones.

      (Scopelliti et al., 2014)

      Only 60.4% of rk1/Df(2L)BSC252 animals eclose.

      73.3% of legs are normal in homozygous flies, 21.3% have moderately kinked tarsi and only 5.3% have severely kinked legs.

      100% of rk1/Df(2L)BSC252 flies have several tarsal deformities.

      (Loveall and Deitcher, 2010)

      The programmed cell death which is seen in wild-type wings during wing maturation after eclosion still occurs in rk1/rk4 and rk1/Df(2L)BSC253 flies.

      The programmed cell death which is seen in wild-type wings during wing maturation after eclosion still occurs in homozygous rk1/rk1 flies.

      (Natzle et al., 2008)

      In rk1 homozygous adult wing blade cells persist for much longer after eclosion than in wild-type.

      (Kimura et al., 2004)

      rk1/rk2 is intermediate between rk1/rk1 and rk2/rk2, with the wings arched and papery, sometimes not unfolded.

      (Meyer et al., 1950)

      strong allele Legs, especially hind ones, flattened and bent. Femora and tibiae bowed in middle; first two tarsal joints shortened, bent, and flattened; last three tarsal joints almost a unit, shortened, and flattened; tarsal claws disarranged. Wings not expanded, sometimes partially extended, sometimes drooping. Postscutellar bristles crossed. Body small. Viability about 90% wild type. RK2.

      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      Suppressed by
      NOT suppressed by
      Statement
      Reference

      rk1 has visible phenotype, non-suppressible by vn[+]/vn10567

      (Scopelliti et al., 2014)
      Phenotype Manifest In
      Suppressed by
      Statement
      Reference

      rk1 has intestinal stem cell phenotype, suppressible by vn[+]/vn10567

      (Scopelliti et al., 2014)

      rk1 has adult midgut phenotype, suppressible by vn[+]/vn10567

      (Scopelliti et al., 2014)

      rk1 has intestinal stem cell phenotype, suppressible by vn[+]/vn1

      (Scopelliti et al., 2014)

      rk1 has adult midgut phenotype, suppressible by vn[+]/vn1

      (Scopelliti et al., 2014)

      rk1 has intestinal stem cell phenotype, suppressible by vn10567/vn1

      (Scopelliti et al., 2014)

      rk1 has adult midgut phenotype, suppressible by vn10567/vn1

      (Scopelliti et al., 2014)
      NOT suppressed by
      Statement
      Reference

      rk1 has wing phenotype, non-suppressible by vn[+]/vn10567

      (Scopelliti et al., 2014)
      Additional Comments
      Genetic Interactions
      Statement
      Reference

      vn10567/+ partially suppresses the intestinal stem cell hyperproliferation seen in the midgut, but fails to rescue the wing inflation defect of rk1/rk1 mutants.

      vn1/+ or vn10567/vn1 suppresses the intestinal stem cell hyperproliferation seen in rk1/rk1 mutant midguts.

      (Scopelliti et al., 2014)
      Xenogenetic Interactions
      Statement
      Reference
      Complementation and Rescue Data
      Rescued by

      rk1 is rescued by rkUAS.cSa/Scer\GAL4rk.pan

      (Scopelliti et al., 2014)
      Partially rescued by

      rk1 is partially rescued by rkUAS.cSa/Scer\GAL4how-24B

      (Scopelliti et al., 2014)
      Comments

      Expression of rkScer\UAS.cSa under the control of Scer\GAL4rk.pan rescues the wing inflation defect and adult midgut phenotypes of rk1/rk1 mutants.

      Expression of rkScer\UAS.cSa under the control of Scer\GAL4how-24B restores intestinal stem cell quiescence but fails to rescue the developmental defects of rk1/rk1 mutants.

      (Scopelliti et al., 2014)

      rkcrm/rk1 phenotype is like homozygous rkcrm.

      (Grell, 1969)
      Images (0)
      Mutant
      Wild-type
      Stocks (2)
      Notes on Origin
      Discoverer

      Edmondson, Aug. 1948.

      There was probably a second mutation, floating in the original "rk[1]" stock, that affects apoptosis; experiments carried out with rk[1] homozygotes obtained in 2008 from the Bloomington Stock Center indicate that apoptosis during wing maturation is not affected in the homozygotes, whereas experiments carried out in 2004 with rk[1] homozygotes (which used a rk[1] stock obtained in 2004 from the Bloomington Stock Center) occasionally resulted in wings with a uniform epithelial later with non-apoptotic nuclei 25 hours post eclosion.

      (Natzle et al., 2008)
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (2)
      References (13)