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General Information
D. melanogaster
FlyBase ID
Feature type
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Nature of the Allele
Mutations Mapped to the Genome
Additional Notes
Associated Sequence Data
DNA sequence
Protein sequence
Progenitor genotype
Nature of the lesion
Expression Data
Reporter Expression
Additional Information
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Modifiers Based on Experimental Evidence ( 0 )
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
Disease-implicated variant(s)
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description

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.

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

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

Homozygous larvae lack thorax and the anterior abdominal segments.

Kr1/+, KrmCD embryos have normal axon guidance.

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.

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.

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.

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

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

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.

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.

Interacts with RpII140wimp maternal effect.

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.

Extend the anterior limit of the posterior gt expression domain.

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

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

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

External Data
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhancer of
NOT Enhancer of
Phenotype Manifest In
Enhanced by

Kr1, KrmCD has axon phenotype, enhanceable by caps05121

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

NOT Enhanced by
Suppressed by

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

Kr1, KrmCD, svp2/svp1 has U4 neuron phenotype, suppressible | partially by hb15/hb12

Kr1, KrmCD, svp2/svp1 has U5 neuron phenotype, suppressible | partially by hb15/hb12

NOT suppressed by
Enhancer of

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

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

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

KrmCD, Kr1/Kr1 is an enhancer of U4 neuron phenotype of svp2/svp1

KrmCD, Kr1/Kr1 is an enhancer of U5 neuron phenotype of svp2/svp1

Kr1/KrmCD is an enhancer of axon phenotype of caps05121

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

Additional Comments
Genetic Interactions

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

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

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.

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.

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.

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.

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.

Xenogenetic Interactions
Complementation and Rescue Data
Partially rescued by

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

Kr1 is partially rescued by Krm650

Kr1 is partially rescued by KrmCD

Kr1 is partially rescued by KrmCD


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

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

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Notes on Origin


External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
References (79)