FlyBase Allele Report: Dmel\kis[1]

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.

(Gervais et al., 2019)

81.5% of heterozygous females have ectopic wing veins.

(Rougeot et al., 2013)

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.

(Terriente-Félix et al., 2011)

One copy of kis¹ is unable to suppress position effect variegation (PEV) at the w locus caused by In(1)w^m4.

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.

(Doheny et al., 2008)

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.

(Daubresse et al., 1999)

brm² shows little if any interaction in double heterozygous combination with kis¹; less than 3% of flies have held-out wings.

(Vazquez et al., 1999)

Mutation does not affect the level of w expression in ph-p^lac+3 flies.

(Fauvarque et al., 1995)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressed by

Statement

Reference

kis¹ has visible | dominant phenotype, suppressible by EloA[+]/EloA^G4930

(Rougeot et al., 2013)

kis¹ has visible | dominant phenotype, suppressible by EloC^SH1520/l(2)SH1520[+]

(Rougeot et al., 2013)

kis¹ has visible | dominant phenotype, suppressible by Elongin-C[+]/EloC^SH1299

(Rougeot et al., 2013)

Enhancer of

Statement

Reference

kis[+]/kis¹ is an enhancer of visible | adult stage phenotype of Marcal1^UAS.cBa, Scer\GAL4^Tub.PU

(Morimoto et al., 2016)

kis[+]/kis¹ is an enhancer of visible | adult stage phenotype of Hsap\SMARCAL1^UAS.cBa, Scer\GAL4^Bx-MS1096

(Morimoto et al., 2016)

kis¹ is an enhancer of visible | dominant phenotype of tna¹

(Gutierrez et al., 2003)

NOT Enhancer of

Statement

Reference

kis¹ is a non-enhancer of visible phenotype of Scer\GAL4^ey.PH, brm^{K804R.UAS.Tag:HA}

(Armstrong et al., 2005)

kis¹ is a non-enhancer of visible phenotype of BEAF-32^UAS.cYa, Scer\GAL4^GMR.PS

(Yamaguchi et al., 2001)

Suppressor of

Statement

Reference

kis¹ is a suppressor of lethal phenotype of Ras85D^V12.sev, sev^S11.Tag:MYC

(Maixner et al., 1998)

NOT Suppressor of

Statement

Reference

kis¹ is a non-suppressor of visible phenotype of Myc^UAS.cZa, Scer\GAL4^GMR.PF

(Secombe et al., 2007)

kis¹ is a non-suppressor of visible phenotype of Scer\GAL4^ey.PH, brm^{K804R.UAS.Tag:HA}

(Armstrong et al., 2005)

kis¹ is a non-suppressor of visible phenotype of BEAF-32^UAS.cYa, Scer\GAL4^GMR.PS

(Yamaguchi et al., 2001)

Other

Statement

Reference

kis[+]/kis¹, mir-965^KO1 has viable phenotype

(Verma and Cohen, 2015)

kis[+]/kis¹, mir-965^KO2 has viable phenotype

(Verma and Cohen, 2015)

Ras85D^V12.sev, kis¹, sev^S11.Tag:MYC has viable phenotype

(Maixner et al., 1998)

Phenotype Manifest In

Suppressed by

Statement

Reference

kis¹ has wing vein | ectopic phenotype, suppressible by EloC^SH1520/l(2)SH1520[+]

(Rougeot et al., 2013)

kis¹ has wing vein | ectopic phenotype, suppressible by Elongin-C[+]/EloC^SH1299

(Rougeot et al., 2013)

kis¹ has wing vein | ectopic phenotype, suppressible by EloA[+]/EloA^G4930

(Rougeot et al., 2013)

Enhancer of

Statement

Reference

kis[+]/kis¹ is an enhancer of wing vein | adult stage phenotype of Marcal1^UAS.cBa, Scer\GAL4^Tub.PU

(Morimoto et al., 2016)

kis[+]/kis¹ is an enhancer of wing vein | adult stage phenotype of Hsap\SMARCAL1^UAS.cBa, Scer\GAL4^Bx-MS1096

(Morimoto et al., 2016)

kis[+]/kis¹ is an enhancer of eye | heat sensitive phenotype of Df(3R)p13/ato¹⁰⁹⁰

(Melicharek et al., 2008)

kis[+]/kis¹ is an enhancer of photoreceptor neuron | heat sensitive phenotype of Df(3R)p13/ato¹⁰⁹⁰

(Melicharek et al., 2008)

kis[+]/kis¹ is an enhancer of wing vein | ectopic phenotype of Snr1^E1

(Marenda et al., 2004)

kis¹ is an enhancer of wing phenotype of tna¹

(Gutierrez et al., 2003)

NOT Enhancer of

Statement

Reference

kis¹ is a non-enhancer of eye phenotype of Scer\GAL4^ey.PH, brm^{K804R.UAS.Tag:HA}

(Armstrong et al., 2005)

kis¹ is a non-enhancer of eye phenotype of CycE^JP

(Brumby et al., 2002)

kis¹ is a non-enhancer of eye phenotype of BEAF-32^UAS.cYa, Scer\GAL4^GMR.PS

(Yamaguchi et al., 2001)

Suppressor of

Statement

Reference

kis¹ is a suppressor of phenotype of Pc⁴

(Kennison and Tamkun, 1988)

NOT Suppressor of

Statement

Reference

kis¹ is a non-suppressor of eye phenotype of Myc^UAS.cZa, Scer\GAL4^GMR.PF

(Secombe et al., 2007)

kis¹ is a non-suppressor of eye phenotype of Scer\GAL4^ey.PH, brm^{K804R.UAS.Tag:HA}

(Armstrong et al., 2005)

kis¹ is a non-suppressor of eye phenotype of CycE^JP

(Brumby et al., 2002)

kis¹ is a non-suppressor of eye phenotype of BEAF-32^UAS.cYa, Scer\GAL4^GMR.PS

(Yamaguchi et al., 2001)

Additional Comments

Genetic Interactions

Statement

Reference

The formation of ectopic wing veins observed in adult flies expressing Marcal1^Scer\UAS.cBa under the control of Scer\GAL4^tub.PU is exacerbated by combination with a single copy of kis¹.

(Morimoto et al., 2016)

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 EloA^G4930 (48.8% penetrance), EloC^SH1520 (17.5%) or EloC^SH1299 (9.2%).

(Rougeot et al., 2013)

A kis¹ heterozygous background gives a dominant mild enhancement to the ato¹⁰⁹⁰/Df(3R)p13 eye phenotype at 25[o]C.

(Melicharek et al., 2008)

Has little or no effect on the phenotype of E2f^GMR.PD Dp^GMR.PD BacA\p35^GMR.PH flies.

(Staehling-Hampton et al., 1999)

The lethality caused by sev^{S11.T:Hsap\MYC} in combination with Ras85D^V12.sev is suppressed by kis¹.

(Maixner et al., 1998)

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.

(Kennison and Tamkun, 1988)

Xenogenetic Interactions

Statement

Reference

The formation of ectopic wing veins observed in adult flies expressing Hsap\SMARCAL1^Scer\UAS.cBa under the control of Scer\GAL4^Bx-MS1096 is exacerbated by combination with a single copy of kis¹.

(Morimoto et al., 2016)

Complementation and Rescue Data

Fails to complement

kis^AO9

(Melicharek et al., 2008)

kis^AS21

(Melicharek et al., 2008)

kis^EC1

(Melicharek et al., 2008)

kis^LM27

(Melicharek et al., 2008)

Rescued by

kis¹ is rescued by kis^{UAS.L.Tag:polyHis,Tag:FLAG}/Scer\GAL4^Tub.PU

(Gervais et al., 2019)

Comments

Expressing kis^{UAS.L.Tag:polyHis,Tag:FLAG} under the control of Scer\GAL4^Tub.PU fully rescues the increased overall number of cells and of intestinal stem cells in somatic clones homozygous for kis¹.

(Gervais et al., 2019)

Images (0)

Mutant

Wild-type

Stocks (2)

Bloomington

431

kis¹ cn¹ bw¹ speck¹/SM6a

Kyoto

105909

kis¹ cn¹ bw¹ speck¹/SM6a

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (4)

Reported As

Symbol Synonym

Kis¹

(Horvath et al., 2016, Secombe et al., 2007)

kis¹

(Genç et al., 2020, Gervais et al., 2019, Verma and Cohen, 2015, Rougeot et al., 2013, Vasanthi et al., 2013, Terriente-Félix et al., 2011, Arancio et al., 2010, Bhatia et al., 2010, Doheny et al., 2008, Melicharek et al., 2008, Vázquez et al., 2008, Chang et al., 2007)

kiss¹

(Bejarano and Busturia, 2004)

Name Synonyms

kismet1

(Verma and Cohen, 2015)

Secondary FlyBase IDs

References (35)

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