A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Allele Dmel\kis1

General Information
SymbolDmel\kis1SpeciesD. melanogaster
NameFlyBase IDFBal0005693
Feature typealleleAssociated geneDmel\kis
Allele classloss of function allele
Mutagenethyl methanesulfonate
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Description
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FB2013_03
FB2013_02
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Cytology
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Clones of kis[1] 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 kis[1] 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 kis[1] mutant cells in the posterior compartment engender the formation of ectopic wing veins of normal thickness and dorso-ventral characteristics. kis[1] mutant clones located adjacent or in longitudinal wing vein 3 (L3) cause the duplication of this vein. kis[1] mutant cells contribute to L3 when the size of the clone is very small, but in most cases kis[1] mutant cells differentiate as intervein, and the ectopic L3 vein is composed of wild-type cells surrounding the mutant clone. kis[1] 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 kis[1] mutant cells occupying the L3-L4 intervein.
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.
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kis1 is an enhancer of visible | dominant phenotype of tna1
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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
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kis1 is a non-enhancer of eye phenotype of CycEJP
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kis1 is a suppressor of phenotype of Pc4
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kis1 is a non-suppressor of eye phenotype of BEAF-32Scer\UAS.cYa, Scer\GAL4GMR.PS
kis1 is a non-suppressor of eye phenotype of CycEJP
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A kis[1] heterozygous background gives a dominant mild enhancement to the ato[1090]/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.
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Fails to complement
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Bloomington
Kyoto
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hide Recent research papers ( 1 )
Terriente-Félix et al., 2011, Dev. Biol. 350(2): 382--392
A conserved function of the chromatin ATPase Kismet in the regulation of hedgehog expression. [FBrf0212899]