FlyBase Allele Report: Dmel\key[1]

General Information

Symbol

Dmel\key¹

Species

D. melanogaster

Name

FlyBase ID

FBal0123807

Feature type

allele

Associated gene

Dmel\key

Associated Insertion(s)

Carried in Construct

Also Known As

kenny¹, IKK^key1, DmIkkγ^key1

Key Links

Genomic Maps

JBrowse

Allele class

Mutagen

Nature of the Allele

Allele class

Mutagen

Progenitor genotype

Cytology

Description

5bp deletion starting at position 699, resulting in a frame shift which introduces a stop codon halfway through the coding region.

(Rutschmann et al., 2000)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

deletion

2R:24,786,339..24,786,343 [-]

Comment:

A 5 bp deletion after CDS position 698, causing a frameshift and early translation termination halfway through the coding sequence.

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 ( 1 )

Disease

Interaction

References

ameliorates retinal disease

modeled by norpA^EE5

(Chinchore et al., 2012)

Comments on Models/Modifiers Based on Experimental Evidence ( 0 )

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

Phenotype Manifest In

intestinal stem cell

(Wang et al., 2013)

Detailed Description

Statement

Reference

key¹/Df(2R)BSC856 transheterozygotes infected with DCV do not show significant differences in survival or viral load, as compared to infected controls.

(Goto et al., 2018)

As measured by H[[2]]O[[2]] ingestion, key¹ mutants are more resistant to oxidative stress than wild-type.

In the absence of infection, key¹ mutants have rates of intestinal stem cell (ISC) division that is at least three time as high as those of control flies. Vibrio cholerae infection results in decreased ISC proliferation, however, compared with wild-type, ISC division rates remain elevated in the mutant.

There is no significant difference in bacterial load after infection with Vibrio cholerae between control and mutant flies.

(Wang et al., 2013)

Mutant flies are sensitive to injection with E. coli and all flies die within 40 hours of infection.

(Aymeric et al., 2010)

Homozygous flies are resistant to V. cholerae infection compared to controls.

Compared to controls, homozygous flies are more resistant to infection with a V. cholerae ΔctxB mutant.

The susceptibility of homozygous mutants to infection by V. cholerae by septic injury is not significantly different to controls.

(Berkey et al., 2009)

key¹ mutant flies show a very high bacterial load and a strong susceptibility to E. cloacae or E. coli infection.

(Bischoff et al., 2006)

key¹ flies exhibit a dramatically decreased viability when pricked with a needle dipped in a concentrated solution of gram-negative Esherichia coli or Erwinia carotovora.

(Kim et al., 2006)

High mortality levels are observed when key¹ flies are fed on the ROS-resistant KNU53775 yeast strain but are not observed when they are fed on a standard yeast strain (W303). Wild-type flies do not show the same sensitivity to the KNU53775 strain.

(Ryu et al., 2006)

Mutant flies show reduced survival compared to wild-type controls after infection with E. coli.

(Bischoff et al., 2004)

key¹ flies are susceptible to infection by Gram-negative bacteria.

(Ligoxygakis et al., 2002)

key¹ homozygous flies show a severe susceptibility to E.coli infection (all flies die within 3 days of infection) and close to wild type resistance to Gram-positive Streptococcus faecalis.

(Naitza et al., 2002)

Mutant flies show significantly lower resistance to E.coli infections than wild-type flies. Mutant flies show the same level of resistance to B.bassiana (when their cuticles are coated with spores) as wild-type flies.

(Rutschmann et al., 2000)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhancer of

Statement

Reference

key¹ is an enhancer of visible | adult stage phenotype of PGRP-LF^RNAi.1.UAS, Scer\GAL4^en.PU

(Maillet et al., 2008)

NOT Enhancer of

Statement

Reference

key¹ is a non-enhancer of abnormal immune response phenotype of Dif¹

(Rutschmann et al., 2002)

Suppressor of

Statement

Reference

key¹ is a suppressor of abnormal neuroanatomy | adult stage | progressive | conditional phenotype of norpA^EE5

(Chinchore et al., 2012)

key⁴/key¹ is a suppressor of abnormal neuroanatomy | adult stage | progressive | conditional phenotype of norpA^EE5

(Chinchore et al., 2012)

key¹ is a suppressor of partially lethal - majority die phenotype of PGRP-LF²⁰⁰

(Maillet et al., 2008)

NOT Suppressor of

Statement

Reference

key¹ is a non-suppressor of visible | adult stage phenotype of PGRP-LF²⁰⁰

(Maillet et al., 2008)

key¹ is a non-suppressor of abnormal immune response phenotype of Dif¹

(Rutschmann et al., 2002)

Other

Statement

Reference

Dif¹, key¹ has abnormal immune response | recessive | adult stage phenotype

(Brown et al., 2009)

Phenotype Manifest In

Enhancer of

Statement

Reference

key¹ is an enhancer of wing phenotype of PGRP-LF^RNAi.1.UAS, Scer\GAL4^en.PU

(Maillet et al., 2008)

NOT Suppressor of

Statement

Reference

key¹ is a non-suppressor of wing phenotype of PGRP-LF²⁰⁰

(Maillet et al., 2008)

Additional Comments

Genetic Interactions

Statement

Reference

Short term starvation does not improve the survival of Dif¹-key¹ double mutants following infection with Gram-negative bacteria.

(Brown et al., 2009)

key¹ does not suppress the notching phenotypes and low adult viability seen in homozygous PGRP-LF²⁰⁰ mutants.

A key¹ background suppresses the wing notches seen when PGRP-LF^{dsRNA.1.Scer\UAS} is expressed under the control of Scer\GAL4^en.PU.

(Maillet et al., 2008)

Dif¹ key¹ double mutants die at the same rate as Dif¹ single mutants when infected with either P.acidolactici, E.faecalis, or S.saprophyticus.

(Rutschmann et al., 2002)

Dif¹ key¹ double mutants die at the same rate as Dif¹ mutants when their cuticles are coated with spores of B.bassiana.

(Rutschmann et al., 2000)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Comments

Images (0)

Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

Arose as: possible cluster with key², key³, key⁵, key⁶, key⁷, key⁸, key⁹ and key¹⁰ - the identical mutation found in these alleles may have been present in the starting stock used in the mutagenesis screen.

(Rutschmann et al., 2000)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (8)

Reported As

Symbol Synonym

DmIKKγ^key1

(Vidal et al., 2001)

DmIkkγ^key1

(Khush et al., 2002)

IKK^key1

(Maillet et al., 2008, Bischoff et al., 2006, Bischoff et al., 2004)

IKKγ

(Maillet et al., 2008)

Key¹

(Acheampong et al., 2026, Nandy et al., 2018, Aymeric et al., 2010, Bergeret et al., 2008)

kenny¹

(Tavignot et al., 2017, Pili-Floury et al., 2004, Georgel et al., 2001)

key1

(Ligoxygakis et al., 2002)

key¹

(Goto et al., 2018, Tusco et al., 2017, Wang et al., 2013, Chinchore et al., 2012, Wang et al., 2012, Glittenberg et al., 2011, Radyuk et al., 2010, Berkey et al., 2009, Delaney et al., 2006, Gottar et al., 2006, Kim et al., 2006, Leclerc et al., 2006, Mulinari et al., 2006, Ryu et al., 2006, Castillejo-Lopez and Häcker, 2005, Naitza et al., 2002, Rutschmann et al., 2002)

Name Synonyms

Secondary FlyBase IDs

References (37)

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