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General Information
Symbol
Dmel\kis1
Species
D. melanogaster
Name
FlyBase ID
FBal0005693
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:
C240078T
Reported nucleotide change:
C2113T
Amino acid change:
Q704term | kis-PA; Q704term | kis-PC; Q704term | kis-PD; Q704term | kis-PE; Q704term | kis-PF
Reported amino acid change:
Q704term
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference
Point mutation (C2113T) in the transcript that encodes the long kis isoform; this is predicted to result in a premature stop codon (E704term).
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 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference
kis1/kis1 somatic clones in a heterozygous background contain a greater overall number of cells and significantly more intestinal stem cells in adult flies compared to controls.
81.5% of heterozygous females have ectopic wing veins.
Clones of kis1 mutant cells induced between wing veins L2 and L5 engender ectopic vein formation close to the position of longitudinal veins in both the anterior and posterior compartments and broadening of the L3-L4 intervein region. When mutant kis1 clones occupy the entire wing, this results in a reduction in wing size, loss of the L2 vein and increase in the distance between the L3 and L4 veins. Somatic clones of kis1 mutant cells in the posterior compartment engender the formation of ectopic wing veins of normal thickness and dorso-ventral characteristics. kis1 mutant clones located adjacent or in longitudinal wing vein 3 (L3) cause the duplication of this vein. kis1 mutant cells contribute to L3 when the size of the clone is very small, but in most cases kis1 mutant cells differentiate as intervein, and the ectopic L3 vein is composed of wild-type cells surrounding the mutant clone. kis1 mutant clones located between longitudinal wing veins L3 and L4 cause a variable increase in the L3-L4 intervein. This increase is proportional to the fraction of kis1 mutant cells occupying the L3-L4 intervein.
One copy of kis1 is unable to suppress position effect variegation (PEV) at the w locus caused by In(1)wm4. One copy of kis1 weakly suppresses the telomeric position effect (TPE) in stocks carrying a variegating P{hsp26-pt-T}39C-5 insertion at the telomere of the left arm of chromosome two.
Homozygous clones in the fifth adult abdominal segment show transformation to a more anterior identity, as shown by the loss of the black pigmentation characteristic of this segment. The effect is cell autonomous. The average size and frequency of homozygous clones induced at the cellular blastoderm stage are not significantly reduced in any body segments relative to control clones. Clones in the second leg have no phenotypic abnormalities. Clones in the third leg show abnormalities, particularly in the distal leg structures; the femur and tibia are slightly abnormal, while the tarsal segments are severely distorted. All five tarsal segments are present but are truncated and have a hooked shape. Homozygous embryos derived from homozygous female germline clones (lacking both maternal and zygotic kis function) show a deletion of pattern elements approximating alternate segments. The most common defect is a reduction in size of one or more alternate segments (T3, A2, A4, A6 and sometimes A8). In more extreme cases only one or two patches of denticle belt are seen. The second thoracic segment is often missing or severely distorted and the head region is grossly abnormal. The cephalopharyngeal skeleton is internalised and malformed (possibly as a consequence of the major pattern alterations). The loss of the T2 and T3 denticle belts is accompanied by loss of their associated sensory organs (both the Keilin's organ and campaniform sensilla). The first thoracic segment does not appear to be deleted or transformed.
brm2 shows little if any interaction in double heterozygous combination with kis1; less than 3% of flies have held-out wings.
Mutation does not affect the level of w expression in ph-plac+3 flies.
External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Statement
Reference
kis1 has visible | dominant phenotype, suppressible | partially by EloA[+]/EloAG4930
kis1 has visible | dominant phenotype, suppressible | partially by EloCSH1520/l(2)SH1520[+]
kis1 has visible | dominant phenotype, suppressible | partially by Elongin-C[+]/EloCSH1299
Enhancer of
Statement
Reference
kis1 is an enhancer of visible | dominant phenotype of tna1
NOT Enhancer of
Statement
Reference
Suppressor of
Statement
Reference
kis1 is a suppressor of lethal phenotype of Ras85DV12.sev, sevS11.Tag:MYC
NOT Suppressor of
Statement
Reference
Other
Statement
Reference
Phenotype Manifest In
Suppressed by
Statement
Reference
kis1 has wing vein | ectopic phenotype, suppressible | partially by EloCSH1520/l(2)SH1520[+]
kis1 has wing vein | ectopic phenotype, suppressible | partially by Elongin-C[+]/EloCSH1299
kis1 has wing vein | ectopic phenotype, suppressible | partially by EloA[+]/EloAG4930
Enhancer of
Statement
Reference
kis[+]/kis1 is an enhancer of eye | heat sensitive phenotype of Df(3R)p13/ato1090
kis[+]/kis1 is an enhancer of photoreceptor cell | heat sensitive phenotype of Df(3R)p13/ato1090
kis[+]/kis1 is an enhancer of wing vein | ectopic phenotype of Snr1E1
kis1 is an enhancer of wing phenotype of tna1
NOT Enhancer of
Statement
Reference
kis1 is a non-enhancer of eye phenotype of CycEJP
kis1 is a non-enhancer of eye phenotype of BEAF-32UAS.cYa, Scer\GAL4GMR.PS
Suppressor of
Statement
Reference
kis1 is a suppressor of phenotype of Pc4
NOT Suppressor of
Statement
Reference
kis1 is a non-suppressor of eye phenotype of Scer\GAL4ey.PH, brmK804R.UAS.Tag:HA
kis1 is a non-suppressor of eye phenotype of CycEJP
kis1 is a non-suppressor of eye phenotype of BEAF-32UAS.cYa, Scer\GAL4GMR.PS
Additional Comments
Genetic Interactions
Statement
Reference
The formation of ectopic wing veins observed in adult flies expressing Marcal1Scer\UAS.cBa under the control of Scer\GAL4tub.PU is exacerbated by combination with a single copy of kis1.
The penetrance of the ectopic wing vein phenotype seen in kis1/+ females (81.5% penetrance) is reduced if they are also heterozygous for one of EloAG4930 (48.8% penetrance), EloCSH1520 (17.5%) or EloCSH1299 (9.2%).
A kis1 heterozygous background gives a dominant mild enhancement to the ato1090/Df(3R)p13 eye phenotype at 25[o]C.
Has little or no effect on the phenotype of E2fGMR.PD DpGMR.PD BacA\p35GMR.PH flies.
The lethality caused by sevS11.T:Hsap\MYC in combination with Ras85DV12.sev is suppressed by kis1.
Suppresses the extra sex comb phenotype of Pc4, Ts(YLt;2Lt)L124. Causes between 50% and 100% suppression of the Pc4/+ extra sex combs phenotype.
Xenogenetic Interactions
Statement
Reference
The formation of ectopic wing veins observed in adult flies expressing Hsap\SMARCAL1Scer\UAS.cBa under the control of Scer\GAL4Bx-MS1096 is exacerbated by combination with a single copy of kis1.
Complementation and Rescue Data
Comments
Expressing kisUAS.L.Tag:polyHis,Tag:FLAG under the control of Scer\GAL4Tub.PU fully rescues the increased overall number of cells and of intestinal stem cells in somatic clones homozygous for kis1.
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
References (31)