FlyBase Allele Report: Dmel\Kr[mCD]

General Information

Symbol

Dmel\Kr^mCD

Species

D. melanogaster

Name

FlyBase ID

FBal0060613

Feature type

allele

Associated gene

Dmel\Kr

Associated Insertion(s)

Carried in Construct

P{Kr^CD+}

Also Known As

Kr^CD, Kr^CD+

Key Links

Transgenic product class

wild_type

(Romani et al., 1996)

Mutagen

in vitro construct

Nature of the Allele

Transgenic product class

wild_type

(Romani et al., 1996)

Mutagen

in vitro construct

(Hartmann et al., 1997, Romani et al., 1996)

Progenitor genotype

Carried in construct

P{Kr^CD+}

Cytology

Description

3.5kb upstream Kr fragment containing the cis-acting regulatory regions required for Kr in the central region of the blastoderm embryo, the anterior domain and larval photoreceptor organ and a 5.2kb fragment comprising the coding sequence and the Kr basal promoter.

(Romani et al., 1996)

Allele components

Component

Use(s)

Regulatory region(s)

Encoded product / tool

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

decreased occurrence of cell division | embryonic stage 13, with Kr¹

(Bahrampour et al., 2017)

decreased occurrence of cell division | embryonic stage 14, with Kr¹

(Bahrampour et al., 2017)

Phenotype Manifest In

embryonic ganglion mother cell | embryonic stage 14, with Kr¹

(Bahrampour et al., 2017)

embryonic neuroblast | embryonic stage 13, with Kr¹

(Bahrampour et al., 2017)

embryonic neuroblast | embryonic stage 14, with Kr¹

(Bahrampour et al., 2017)

EW1 neuron, with Kr¹

(Isshiki et al., 2001)

EW2 neuron, with Kr¹

(Isshiki et al., 2001)

EW3 neuron, with Kr¹

(Isshiki et al., 2001)

ganglion mother cell GMC1-1a, with Kr¹

(Isshiki et al., 2001)

mesoderm, with Kr¹

(Ruiz-Gomez et al., 1997)

muscle cell of A1-7 dorsal acute muscle 1, with Kr¹

(Ruiz-Gomez et al., 1997)

muscle cell of A1-7 lateral longitudinal muscle 1, with Kr¹

(Ruiz-Gomez et al., 1997)

muscle cell of A1-7 lateral transverse muscle 2, with Kr¹

(Ruiz-Gomez et al., 1997)

muscle cell of A1-7 lateral transverse muscle 4, with Kr¹

(Ruiz-Gomez et al., 1997)

muscle cell of A1-7 ventral oblique muscle 2, with Kr¹

(Ruiz-Gomez et al., 1997)

muscle cell of ventral acute muscle 2, with Kr¹

(Ruiz-Gomez et al., 1997)

muscle cell of ventral oblique muscle 5, with Kr¹

(Ruiz-Gomez et al., 1997)

neuroblast NB7-1, with Kr¹

(Isshiki et al., 2001)

Detailed Description

Statement

Reference

Kr^mCD/Kr¹ 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)

In Kr¹, Kr^mCD 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)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Phenotype Manifest In

Enhanced by

Statement

Reference

Kr¹, Kr^mCD has axon phenotype, enhanceable by caps⁰⁵¹²¹

(Abrell and Jackle, 2001)

Kr¹, Kr^mCD has axon phenotype, enhanceable by caps^65.2

(Abrell and Jackle, 2001)

Suppressed by

Statement

Reference

Kr¹, Kr^mCD, svp²/svp¹ has EW3 neuron phenotype, suppressible | partially by hb¹⁵/hb¹²

(Kanai et al., 2005)

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

(Kanai et al., 2005)

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

(Kanai et al., 2005)

Enhancer of

Statement

Reference

Kr^mCD, Kr¹/Kr¹ is an enhancer of EW2 neuron phenotype of svp²/svp¹

(Kanai et al., 2005)

Kr^mCD, Kr¹/Kr¹ is an enhancer of EW3 neuron phenotype of svp²/svp¹

(Kanai et al., 2005)

Kr^mCD, Kr¹/Kr¹ is an enhancer of larval DA3 motor neuron phenotype of svp²/svp¹

(Kanai et al., 2005)

Kr^mCD, Kr¹/Kr¹ is an enhancer of larval LL1 motor neuron phenotype of svp²/svp¹

(Kanai et al., 2005)

Kr¹/Kr^mCD is an enhancer of axon phenotype of caps⁰⁵¹²¹

(Abrell and Jackle, 2001)

Kr¹/Kr^mCD is an enhancer of axon phenotype of caps^65.2

(Abrell and Jackle, 2001)

Other

Statement

Reference

Fas2^EB112, Kr¹, Kr^mCD has larval abdominal segmental nerve phenotype

(Abrell and Jackle, 2001)

Fas2^EB112, Kr¹, Kr^mCD has RP neuron phenotype

(Abrell and Jackle, 2001)

Fas2^EB112, Kr¹/Kr^mCD has larval abdominal segmental nerve phenotype

(Abrell and Jackle, 2001)

Fas2^EB112, Kr¹/Kr^mCD has RP neuron phenotype

(Abrell and Jackle, 2001)

Kr¹, Kr^mCD, caps⁰⁵¹²¹ has larval abdominal segmental nerve phenotype

(Abrell and Jackle, 2001)

Kr¹, Kr^mCD, caps^65.2 has larval abdominal segmental nerve phenotype

(Abrell and Jackle, 2001)

Additional Comments

Genetic Interactions

Statement

Reference

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

(Dobi et al., 2014)

Kr^mCD; 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)

Kr^mCD, 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, caps^65.2 double homozygotes (that have been partially rescued by the addition of Kr^mCD) 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. Fas2^EB112/+, Kr¹/+, double heterozygotes (that have been partially rescued by Kr^mCD) 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)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Partially rescues

Kr^mCD partially rescues Kr[-]

(Ruiz-Gomez et al., 1997)

Kr^mCD partially rescues Kr¹

(Ruiz-Gomez et al., 1997)

Kr^mCD partially rescues Kr¹

(Romani et al., 1996)

Comments

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

(Abrell and Jackle, 2001)

Specifically rescues the segmentation defect of Kr^- mutants.

(Ruiz-Gomez et al., 1997)

Embryonic segmentation is normal but CNS is abnormal.

(Romani et al., 1996)

Images (0)

Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

Comments

Minigene lacks elements required for Kr expression in the posterior blastoderm domain, the Malpighian tubule anlagen, the muscle precursor cells and the nervous system.

(Romani et al., 1996)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (5)

Reported As

Symbol Synonym

Kr^CD+

(Ruiz-Gomez et al., 1997)

Kr^CD

(Rubio-Ferrera et al., 2023, Bahrampour et al., 2019, Bahrampour et al., 2017, Stratmann and Thor, 2017, Gabilondo et al., 2016, Stratmann et al., 2016, Kanai et al., 2005, Isshiki et al., 2001)

Kr^mCD

Kr^res

(Abrell and Jackle, 2001)

kr^CD

(Fox et al., 2022, Díaz-de-la-Peña et al., 2020, Herrero et al., 2014, Benito-Sipos et al., 2010, Losada-Pérez et al., 2010)

Name Synonyms

Secondary FlyBase IDs

References (20)

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