FB2025_01 , released February 20, 2025
Allele: Dmel\Kr1
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General Information
Symbol
Dmel\Kr1
Species
D. melanogaster
Name
FlyBase ID
FBal0005790
Feature type
allele
Associated gene
Dmel\Kr
Associated Insertion(s)
Carried in Construct
Key Links
Allele class

amorphic allele - genetic evidence

loss of function allele

Mutagen
Nature of the Allele
Allele class

amorphic allele - genetic evidence

(Hoch and Jackle, 1998, Irish et al., 1989, Harding and Levine, 1988)

loss of function allele

(Eldon and Pirrotta, 1991)
Mutagen
spontaneous
Progenitor genotype
Cytology
Description
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
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

      abdomen

      (Carroll and Scott, 1986)

      embryonic/first instar larval cuticle

      (Bullock et al., 2004)

      embryonic/larval hindgut | embryonic stage

      (Harbecke and Janning, 1989)

      embryonic/larval Malpighian tubule

      (Harbecke and Janning, 1989)

      embryonic ganglion mother cell | embryonic stage 14, with KrmCD

      (Bahrampour et al., 2017)

      embryonic neuroblast | embryonic stage 13, with KrmCD

      (Bahrampour et al., 2017)

      embryonic neuroblast | embryonic stage 14, with KrmCD

      (Bahrampour et al., 2017)

      EW1 neuron, with KrmCD

      (Isshiki et al., 2001)

      EW2 neuron, with KrmCD

      (Isshiki et al., 2001)

      EW3 neuron, with KrmCD

      (Isshiki et al., 2001)

      ganglion mother cell GMC1-1a, with KrmCD

      (Isshiki et al., 2001)

      glial cell

      (Romani et al., 1996)

      larval abdomen | anterior | embryonic stage

      (Lehmann, 1988)

      larval abdominal segment

      (Matyash et al., 2004)

      larval longitudinal connective

      (Romani et al., 1996)

      larval thorax

      (Matyash et al., 2004)

      larval thorax | embryonic stage

      (Lehmann, 1988)

      Malpighian tubule

      (Hoch and Jackle, 1998)

      mesoderm, with KrmCD

      (Ruiz-Gomez et al., 1997)

      mitotic domain 1 | extended germ band stage

      (Irvine and Wieschaus, 1994)

      muscle cell of A1-7 dorsal acute muscle 1, with KrmCD

      (Ruiz-Gomez et al., 1997)

      muscle cell of A1-7 lateral longitudinal muscle 1, with KrmCD

      (Ruiz-Gomez et al., 1997)

      muscle cell of A1-7 lateral transverse muscle 2, with KrmCD

      (Ruiz-Gomez et al., 1997)

      muscle cell of A1-7 lateral transverse muscle 4, with KrmCD

      (Ruiz-Gomez et al., 1997)

      muscle cell of A1-7 ventral oblique muscle 2, with KrmCD

      (Ruiz-Gomez et al., 1997)

      muscle cell of ventral acute muscle 2, with KrmCD

      (Ruiz-Gomez et al., 1997)

      muscle cell of ventral oblique muscle 5, with KrmCD

      (Ruiz-Gomez et al., 1997)

      neuroblast NB7-1, with KrmCD

      (Isshiki et al., 2001)

      serotonergic neuron

      (Romani et al., 1996)

      symmetrical commissure

      (Romani et al., 1996)

      thorax

      (Carroll and Scott, 1986)
      Detailed Description
      Statement
      Reference

      Kr1/KrmCD transheterozygotes present a significant decrease in the number of dividing neuroblasts during stages 13 and 14 of embryogenesis and a significant decrease in the number of dividing neuroblast daughters during stage 14, but not stage 13, of embryogenesis, as compared to controls; these embryos, however, show no significant differences in the number of neuroblasts, as compared to controls.

      (Bahrampour et al., 2017)

      Targeting of dendrites to antennal lobe glomeruli occurs normally in antennal lobe projection neurons that are part of Kr1 homozygous somatic clones.

      (Komiyama and Luo, 2007)

      Around 80% of Kr1/+ first instar larvae have cuticular segmentation defects, particaularly in segments T3, A1 and A2.

      (Bullock et al., 2004)

      Homozygous larvae lack thorax and the anterior abdominal segments.

      (Matyash et al., 2004)

      Kr1/+, KrmCD embryos have normal axon guidance.

      (Abrell and Jackle, 2001)

      In Kr1, KrmCD mutants, the first born 1/1G sibling neurons are variably affected; both can be missing (about 17% of the time) 1G can be missing (73%) or both can be normal (10%); however the second-born interneuron 2 is always missing. The third born interneuron is almost always normal. In the 7-1 lineage in these animals, one of the U3/U4 motorneurons is frequently missing (about 73%) although all earlier and later born neurons develop normally.

      (Isshiki et al., 2001)

      Kr1 mutants carrying two copies of KrmCD show severe and consistent disruptions of the muscle pattern, confined to the Kr expressing subset. Muscles DO1 and VL3 are apparently unaffected. DA1, LL1, VO2 and VA2 are present but have abnormal morphology or orientation. LT2, LT4 and VO5 are occasionally absent or transformed. The muscle that forms in the position of VA2 is transformed and has the characteristics of VA1, so that two muscles with the orientation and insertion sites of VA1 form. DA1 is routinely transformed to either an oblique or a transverse muscle at the DA1 position. An ectopic ventral longitudinal muscle can also occur, always associated with the loss of the adjacent ventral oblique muscle.

      (Ruiz-Gomez et al., 1997)

      Embryos exhibit multiple CNS and PNS defects. Segmentation in Kr1 KrmCD embryos is normal but the overall pattern of commissures and connectives in the CNS of late embryos is abnormal due to apparent stalling and misrouting of axons. Embryos lack medial-lateral cluster of serotoninergic neurons and have a reduced number of glial cells.

      (Romani et al., 1996)

      Enhances the embryonic stomodeal nervous system phenotype of Df(1)B57.

      (Gonzalez-Gaitan and Jäckle, 1995)

      Mutant embryos show reduction in rate of germ band extension. Where eve expression falls in broad stripes, cell intercalation is greatly reduced.

      (Irvine and Wieschaus, 1994)

      Expression of ctLS enhancer trap lines in a Kr1 or Kr9 mutant background demonstrate that the Malpighian tubule cells are transformed into a structure consistent in appearance and cell number with a change in cell fate to a hindgut. ct expression in the Malpighian tubules is greatly reduced.

      (Liu and Jack, 1992)

      gt stripe 4 is greatly expanded anteriorly invading the Kr and kni domains of expression. The posterior expression of kni does not reach wild type levels.

      (Eldon and Pirrotta, 1991)

      Interacts with RpII140wimp maternal effect.

      (Parkhurst and Ish-Horowicz, 1991)

      Strong segmentation phenotype. Homozygous embryos do not differentiate Malpighian tubules. The hindgut is larger than wild-type. Kr28/Kr1 transheterozygotes have a similar Malpighian tubule phenotype to Kr28 homozygotes. Kr29/Kr1 transheterozygotes have a similar Malpighian tubule phenotype to Kr29 homozygotes.

      (Harbecke and Janning, 1989)

      Extend the anterior limit of the posterior gt expression domain.

      (Mohler et al., 1989)

      The development of the thorax and anterior abdomen is abnormal in homozygous embryos.

      (Lehmann, 1988)

      Larval phenotype: Thoracic and anterior abdominal segments missing, mirror-image duplication of posterior abdomen, dominant defects in T3 and A2.

      (Carroll and Scott, 1986)

      Kr1/+ adult sometimes has thoracic malformation; a leg or wing may be absent. Penetrance low. RK2.

      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      Enhancer of
      Statement
      Reference

      Kr[+]/Kr1 is an enhancer of embryonic/larval segmentation phenotype | maternal effect | recessive phenotype of Acsl1

      (Zhang et al., 2011)
      NOT Enhancer of
      Statement
      Reference

      Kr1 is a non-enhancer of lethal | embryonic stage | maternal effect phenotype of Gugunspecified

      (Zhang et al., 2002)
      Phenotype Manifest In
      Enhanced by
      Statement
      Reference

      Kr1, KrmCD has axon phenotype, enhanceable by caps05121

      (Abrell and Jackle, 2001)

      Kr1, KrmCD has axon phenotype, enhanceable by caps65.2

      (Abrell and Jackle, 2001)
      NOT Enhanced by
      Statement
      Reference

      Kr1 has embryonic/first instar larval cuticle phenotype, non-enhanceable by egl3e/egl1

      (Bullock et al., 2004)
      Suppressed by
      Statement
      Reference

      Kr1, KrmCD, svp2/svp1 has EW3 neuron phenotype, suppressible | partially by hb15/hb12

      (Kanai et al., 2005)

      Kr1, KrmCD, svp2/svp1 has larval DA3 motor neuron phenotype, suppressible | partially by hb15/hb12

      (Kanai et al., 2005)

      Kr1, KrmCD, svp2/svp1 has larval LL1 motor neuron phenotype, suppressible | partially by hb15/hb12

      (Kanai et al., 2005)
      NOT suppressed by
      Statement
      Reference

      Kr1 has embryonic/first instar larval cuticle phenotype, non-suppressible by egl3e/egl1

      (Bullock et al., 2004)
      Enhancer of
      Statement
      Reference

      Kr[+]/Kr1 is an enhancer of wing margin phenotype of Bx2

      (Bronstein et al., 2010)

      KrmCD, Kr1/Kr1 is an enhancer of EW2 neuron phenotype of svp2/svp1

      (Kanai et al., 2005)

      KrmCD, Kr1/Kr1 is an enhancer of EW3 neuron phenotype of svp2/svp1

      (Kanai et al., 2005)

      KrmCD, Kr1/Kr1 is an enhancer of larval DA3 motor neuron phenotype of svp2/svp1

      (Kanai et al., 2005)

      KrmCD, Kr1/Kr1 is an enhancer of larval LL1 motor neuron phenotype of svp2/svp1

      (Kanai et al., 2005)

      Kr1/KrmCD is an enhancer of axon phenotype of caps05121

      (Abrell and Jackle, 2001)

      Kr1/KrmCD is an enhancer of axon phenotype of caps65.2

      (Abrell and Jackle, 2001)
      Other
      Additional Comments
      Genetic Interactions
      Statement
      Reference

      Embryos trans-heterozygous for Sin3A08269 and Kr1 KrmCD (a Kr loss-of-function allele) do not show mesodermal defects.

      (Dobi et al., 2014)

      Kr1/+ significantly enhances the percentage of segmentation-impaired embryos caused by maternal mutant homozygous Acsl1, although the severity is not obviously changed.

      (Zhang et al., 2011)

      The epidermis of crb1 Kr1 double mutant embryos exhibit relatively normal distributions of cell polarity and junctional proteins. There is some suppression of the crb1 phenotype; a continuous, through reduced, cuticle sheet is formed.

      (Campbell et al., 2009)

      KrmCD; Kr1/Kr1 enhances the reduction in later born neurons of the NB7-1 an NB2-3 lineages see in svp1/svp2 embryos so that U4 and U5 are almost completely eliminated, as are EW2 and EW3. This enhanced phenotype is partially suppressed if the embryos are also hb12/hb15.

      (Kanai et al., 2005)

      The frequency of cuticular segmentation phenotypes in Kr1/+ first instar larvae is not significantly changed in animals with a egl3e/egl1 mutant mothers, however the identity of segments affected differs slightly: there are less defects in A1 and A2, and more defects in A3.

      (Bullock et al., 2004)

      KrmCD, Kr1/+, caps05121/+ embryos show a SNb nerve phenotype, without affecting the ISN and SNa. In about 1/3 of cases the SNb stops along the ventral longitudinal muscles, ending with a large growth cone structure. In addition properly defasciculated RP axons fail to continue along their normal paths, a portion of them elongate and stall along their normal paths; a portion of them elongate and stall either in a position close to the transversal nerve or are directly connected to it. Kr1, caps05121 or Kr1, caps65.2 double homozygotes (that have been partially rescued by the addition of KrmCD) develop an even stronger phenotype; the SNb is absent in most of the double mutants analysed or do not extend beyond its second choice point close to muscle 28. In only a few cases the SNb stalls in the ventral muscle field. Fas2EB112/+, Kr1/+, double heterozygotes (that have been partially rescued by KrmCD) exhibit an axon guidance phenotype. The SNb enters the ventral muscle field normally in most cases but the nerve stops at the second choice point by forming a growth cone-like structure. No individual RP axons are observed.

      (Abrell and Jackle, 2001)

      Reduced maternal RpL36 activity increases the penetrance and severity of the segmental defects observed in larvae heterozygous for Kr or kni mutations. Heterozygous Kr or eve embryos derived from heterozygous l(2)41Ae34-4, Nipped-A1/+ females show increase in embryonic cuticular phenotypes.

      (Duffy et al., 1996)
      Xenogenetic Interactions
      Statement
      Reference
      Complementation and Rescue Data
      Partially rescued by

      Kr1 is partially rescued by Kr10.7.Tag:FLAG

      (Matyash et al., 2004)

      Kr1 is partially rescued by Krm650

      (Hoch and Jackle, 1998)

      Kr1 is partially rescued by KrmCD

      (Ruiz-Gomez et al., 1997)

      Kr1 is partially rescued by KrmCD

      (Romani et al., 1996)
      Comments

      Pan-muscular expression of Kr can partially rescue the SNb phenotype of the Kr1, KrmCD, caps05121 double homozygotes.

      (Abrell and Jackle, 2001)

      The Malpighian tubule phenotype of Kr1 embryos can be completely rescued by Krm650.

      (Hoch and Jackle, 1998)
      Images (0)
      Mutant
      Wild-type
      Stocks (3)
      Notes on Origin
      Discoverer

      Graber.

      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (4)
      References (84)