FlyBase Allele Report: Dmel\Dark[CD4]

The wings of Ark^CD4 flies that survive to adulthood gradually melanize within 5 days after eclosion. Necrotic cells are also observed in the wings of 5-day-old flies.

Ark^CD4 flies are hypersusceptible to starvation stress compared to wild type.

(Obata et al., 2014)

2.1 +/- 1.1 surviving EW3-sib cells are seen in homozygous larvae (these cells die during embryogenesis in wild type).

Surviving EW3-sib cells are seen in Ark^CD4/Ark⁸² larvae (these cells die during embryogenesis in wild type) and the average number of surviving cells is increased if the female parent is homozygous for Ark^CD4.

(Lee et al., 2013)

The programmed cell death of bursCCAP neurons seen in the adult ventral nerve cord of wild type flies after eclosion is partially suppressed in Ark^CD4 mutant homozygotes. Between 0 and two bursCCAP neurons are seen at 3-5 days.

The programmed cell death of bursCCAP neurons seen in the adult ventral nerve cord of wild type flies after eclosion is partially suppressed in Ark^CD4/Ark⁸² mutants. On average 3.9 bursCCAP neurons are seen at 3-5 days.

(Lee et al., 2013)

Homozygous debcl^E26 mutant larvae do not display any NMJ degeneration or changes in NMJ morphology.

(Keller et al., 2011)

Flies develop melanized blemishes in the wing in a progressive manner - wings are normal at eclosion, but blemishes are evident by day 14.

(Galindo et al., 2009)

Homozygous adult Ark^CD4 mutants exhibit wing blemishes.

On the first day of eclosion, the dorsal and ventral wing cuticles of wild-type animals become tightly merged, with no intervening tissue evident between the dorsal and ventral cuticles. However, even 14 days after eclosion, cells and cell remnants remain situated between the dorsal and ventral cuticles in Ark^CD4 mutants. There is evidence of intact cells soon after eclosion and ectopic cellular material 24 hours after eclosion.

(Link et al., 2007)

The apoptotic response to irradiation is significantly decreased in mutant embryos compared to wild type.

(Sevrioukov et al., 2007)

Ark^CD4 mutants exhibit a delay in programmed cell death in Crz-expressing neurons in the ventral nerve cord during pupation.

(Choi et al., 2006)

Flies homozygous for Ark^CD4 exhibit suppression of dendritic branch removal.

(Williams et al., 2006)

Adults homozygous for Ark^CD4 develop melanized spots on their wings as they age.

(Chew et al., 2004)

Homozygous mutants have normal aristae.

(Cullen and McCall, 2004)

A few neuroblasts ectopically survive in the abdominal neuromeres of homozygous larvae, in contrast to wild type where most of these neuroblasts undergo apoptosis by the end of embryogenesis.

(Peterson et al., 2002)

There is a significant increase in the number of midline glia (~8 cells/segment) in mutants. On exposure to ionising radiation, mutant stage 9 embryos show very few sparsely distributed apoptotic cells, compared to wild-type embryos at the same stage where widespread cell death. No evidence is seen for extra photoreceptor cells in mutant pupal eyes.

(Rodriguez et al., 2002)

Most homozygotes survive to adulthood, although at a lower frequency than heterozygous siblings. Many homozygotes derived from heterozygous parents have melanotic tumours and abnormalities affecting the wings and/or bristles. Most affected flies have severe wing defects similar to a 'gnarled' or 'wrinkled' phenotype, while others have wing blisters or burnt 'notched' wings. 3% of flies have melanotic tumours inside the body, while in 7% of flies, melanotic tumours are seen protruding from the body next to the haltere. Among flies with extra bristles, most have one extra anterior scutellar bristle, while a few have two extra anterior scutellar bristles and/or an extra posterior scutellar bristle. Homozygotes derived from homozygous parents have impaired viability and fecundity and have an increased penetrance and expression of similar defects to those seen in homozygotes derived from heterozygous parents. Most homozygous larvae have a significantly overgrown central nervous system (CNS) compared to wild type. Occasionally, hyperplasia of the CNS is seen in the brain lobes only, while in other cases the ventral nerve cord is abnormally extended. Homozygous embryos show markedly reduced levels of apoptosis compared to wild type. The reduction in number of apoptotic cells is most noticeable in the CNS and epidermis.

(Rodriguez et al., 1999)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

Dark^CD4 has abnormal starvation stress response phenotype, enhanceable by Gnmt^MI04290

(Obata et al., 2014)

Suppressed by

Statement

Reference

Dark^CD4 has abnormal starvation stress response phenotype, suppressible by foxo[+]/foxo^Δ94

(Obata et al., 2014)

Enhancer of

Statement

Reference

Dark^CD4 is an enhancer of abnormal starvation stress response phenotype of Gnmt^MI04290

(Obata et al., 2014)

Suppressor of

Statement

Reference

Dark^CD4 is a suppressor | partially of abnormal neuroanatomy phenotype of Ank2^f02001

(Keller et al., 2011)

Dark^CD4/Ark[+] is a suppressor of visible phenotype of E2f1^UAS.cNa, Scer\GAL4^Act88F.PD

(Morris et al., 2006)

Dark^CD4/Ark[+] is a suppressor of increased cell death phenotype of Scer\GAL4^GMR.PF, egr^UAS.cMa

(Moreno et al., 2002)

Dark^CD4 is a suppressor | partially of female sterile phenotype of Diap1^6B/Diap1⁸

(Rodriguez et al., 2002)

Dark^CD4 is a suppressor of increased cell death phenotype of Diap1⁵

(Rodriguez et al., 2002)

Dark^CD4 is a suppressor of increased cell death phenotype of Diap1⁵/th[+], grim^GMR.PC

(Rodriguez et al., 2002)

Dark^CD4 is a suppressor of increased cell death phenotype of Diap1⁵/th[+], hid^GMR.PG

(Rodriguez et al., 2002)

Dark^CD4 is a suppressor of visible phenotype of Dronc^UAS.EGFP, Scer\GAL4^GMR.PF

(Quinn et al., 2000)

Dark^CD4 is a suppressor of visible phenotype of hid^GMR.PG

(Rodriguez et al., 1999)

Dark^CD4 is a suppressor of visible phenotype of grim^GMR.PC

(Rodriguez et al., 1999)

Dark^CD4 is a suppressor of visible phenotype of rpr^GMR.PW

(Rodriguez et al., 1999)

NOT Suppressor of

Statement

Reference

Dark^CD4/Dark^CD4 is a non-suppressor of visible phenotype of AIF^{ΔN.UAS.Tag:MYC}, Scer\GAL4^ey.PH

(Joza et al., 2008)

Phenotype Manifest In

Enhanced by

Statement

Reference

Dark^CD4 has wing | progressive phenotype, enhanceable by Debcl²²

(Galindo et al., 2009)

Dark^CD4 has wing | progressive phenotype, enhanceable by Debcl⁵⁹

(Galindo et al., 2009)

Dark^CD4 has wing phenotype, enhanceable by Dronc⁵¹/Nc[+]

(Chew et al., 2004)

Suppressor of

Statement

Reference

Dark^CD4 is a suppressor | partially of embryonic/larval neuromuscular junction phenotype of Ank2^f02001

(Keller et al., 2011)

Dark^CD4/Ark[+] is a suppressor of wing blade phenotype of E2f1^UAS.cNa, Scer\GAL4^Act88F.PD

(Morris et al., 2006)

Dark^CD4/Ark[+] is a suppressor of wing disc | wandering third instar larval stage phenotype of Dp^a4/Dp^a2

(Moon et al., 2005)

Dark^CD4 is a suppressor of arista phenotype of Diap1^th-1

(Cullen and McCall, 2004)

Dark^CD4 is a suppressor of arista lateral phenotype of Diap1^th-1

(Cullen and McCall, 2004)

Dark^CD4/Ark[+] is a suppressor | partially of border follicle cell phenotype of Rac1^N17.UAS, Scer\GAL4^slbo.2.6

(Geisbrecht and Montell, 2004)

Dark^CD4/Dark^CD4 is a suppressor | partially of border follicle cell phenotype of Rac1^N17.UAS, Scer\GAL4^slbo.2.6

(Geisbrecht and Montell, 2004)

Dark^CD4/Dark^CD8 is a suppressor | partially of border follicle cell phenotype of Rac1^N17.UAS, Scer\GAL4^slbo.2.6

(Geisbrecht and Montell, 2004)

Dark^CD4/Dark^CD4 is a suppressor of eye phenotype of Scer\GAL4^GMR.PF, egr^UAS.cMa

(Moreno et al., 2002)

Dark^CD4 is a suppressor | partially of egg chamber phenotype of Diap1^6B/Diap1⁸

(Rodriguez et al., 2002)

Dark^CD4 is a suppressor | partially of ovary phenotype of Diap1^6B/Diap1⁸

(Rodriguez et al., 2002)

Dark^CD4 is a suppressor of eye phenotype of Dronc^UAS.EGFP, Scer\GAL4^GMR.PF

(Quinn et al., 2000)

Dark^CD4 is a suppressor of ommatidium phenotype of hid^GMR.PG

(Rodriguez et al., 1999)

Dark^CD4 is a suppressor of eye phenotype of hid^GMR.PG

(Rodriguez et al., 1999)

Dark^CD4 is a suppressor of ommatidium phenotype of grim^GMR.PC

(Rodriguez et al., 1999)

Dark^CD4 is a suppressor of eye phenotype of grim^GMR.PC

(Rodriguez et al., 1999)

Dark^CD4 is a suppressor of ommatidium phenotype of rpr^GMR.PW

(Rodriguez et al., 1999)

Dark^CD4 is a suppressor of eye phenotype of rpr^GMR.PW

(Rodriguez et al., 1999)

NOT Suppressor of

Statement

Reference

Dark^CD4/Dark^CD4 is a non-suppressor of eye phenotype of AIF^{ΔN.UAS.Tag:MYC}, Scer\GAL4^ey.PH

(Joza et al., 2008)

Additional Comments

Genetic Interactions

Statement

Reference

foxo^Δ94/+ partially rescues the starvation stress phenotype of Ark^CD4 flies.

Ark^CD4 Gnmt^MI04290 double mutants show a starvation stress phenotype that is more severe than in either single mutant.

(Obata et al., 2014)

Homozygous Ark^CD4 partially suppresses the NMJ degeneration seen in Ank2^f02001 mutants.

(Keller et al., 2011)

The incidence and severity of melanized wing blemishing is exacerbated in debcl²², Ark^CD4 or debcl⁵⁹, Ark^CD4 double mutants compared to Ark^CD4 alone.

(Galindo et al., 2009)

The mutant eye phenotype caused by expression of AIF^{ΔN.Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^ey.PH is not ameliorated by Ark^CD4/Ark^CD4.

(Joza et al., 2008)

The melanized wing spot phenotype of Ark^CD4 homozygotes is enhanced by Nc⁵¹/+.

(Chew et al., 2004)

The border follicle cell migration defect seen in egg chambers expressing Rac1^N17.Scer\UAS under the control of Scer\GAL4^slbo.2.6 is partially suppressed by Ark^CD4/+, Ark^CD4/Ark^CD4 or Ark^CD4/Ark^CD8.

(Geisbrecht and Montell, 2004)

Homozygosity for Ark^CD4 partially supresses the eye ablation phenotype seen in egr^Scer\UAS.cMa; Scer\GAL4^GMR.PF flies.

(Moreno et al., 2002)

The addition of th⁵ to grim^GMR.PC heterozygotes leads to an enhancement of retinal apoptosis. The subsequent addition of Ark^CD4/Ark^CD4 suppresses that enhancement. The addition of W^GMR.PG to th⁵ heterozygotes leads to an enhancement of cell killing. The subsequent addition of Ark^CD4/Ark^CD4 suppresses that enhancement. The addition of Ark^CD4/Ark^CD4 or Ark^CD4/+ to suppresses the sterility of th^6B/th⁸ females, leading to 47% and 69% of females laying eggs respectively. Ovaries are considerably larger and generally wild-type in appearance. Most egg chambers are normal in morphology and number.

(Rodriguez et al., 2002)

Suppresses the eye ablation phenotypes caused by grim^GMR.PC, W^GMR.PG or rpr^GMR.PW.

(Rodriguez et al., 1999)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Fails to complement

Dark⁸²

(Akdemir et al., 2006)

Dark^CD8

(Rodriguez et al., 1999)

Rescued by

Dark^CD4 is rescued by Dark^+t20

(Obata et al., 2014)

Comments

One copy of Ark^+t20 completely rescues the wing melanization phenotype of Ark^CD4 flies.

(Obata et al., 2014)

Images (0)

Mutant

Wild-type

Stocks (1)

Bloomington

9926

y¹ w^*; P{lacW}Dark^CD4/CyO; TM3, Sb¹/Df(3L)H99, kni^ri-1 p^p

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (7)

Reported As

Symbol Synonym

Ark^CD4

(Sevrioukov et al., 2007)

DARK^CD4

(Moreno et al., 2002)

Dark^CD4

ark^CD4

(Srivastava et al., 2007)

dArk^CD4

(Morris et al., 2006)

dark^CD4

(Lee et al., 2013, Lee et al., 2013, Keller et al., 2011, Galindo et al., 2009, Joza et al., 2008, Link et al., 2007, Akdemir et al., 2006, Choi et al., 2006, Williams et al., 2006, Moon et al., 2005, Chew et al., 2004, Cullen and McCall, 2004, Geisbrecht and Montell, 2004, Peterson et al., 2002, Rodriguez et al., 2002, Quinn et al., 2000)

dark^cd4

(Obata et al., 2014)

Name Synonyms

Secondary FlyBase IDs

References (23)

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