FlyBase Allele Report: Dmel\Cds[1]

General Information

Symbol

Dmel\Cds¹

Species

D. melanogaster

Name

FlyBase ID

FBal0044698

Feature type

allele

Associated gene

Dmel\Cds

Associated Insertion(s)

P{HZ}Cds¹

Carried in Construct

Also Known As

CdsA¹

Key Links

Allele class

Mutagen

P-element activity

Nature of the Allele

Allele class

Mutagen

P-element activity

(Wu et al., 1995)

Progenitor genotype

Associated Insertion(s)

P{HZ}Cds¹

Cytology

Description

Allele components

Component

Use(s)

Inserted element

P{HZ}

enhancer trap

Encoded product / tool

lacZ

reporter enzyme

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

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

exacerbates congenital generalized lipodystrophy

modeled by Seipin^null

(Tian et al., 2011)

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

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

abnormal neurophysiology

(Krause et al., 2008, Wu et al., 1995)

abnormal thermotaxis

(Kwon et al., 2008)

abnormal visual behavior

(Wu et al., 1995)

male sterile (with Df(3L)BSC795)

(Laurinyecz et al., 2016)

viable

(Liu et al., 2014, Wang and Montell, 2006)

Phenotype Manifest In

Detailed Description

Statement

Reference

CdsA¹/CdsA^CB-0128-3 as well as CdsA¹/CdsA^EY08412 and CdsA¹/CdsA^UM-8246-3 adult males are fertile, while CdsA¹/Df(3L)BSC795 males are sterile.

(Laurinyecz et al., 2016)

CdsA¹ mutants exhibit an ectopic lipid storage phenotype in the salivary gland.

CdsA¹ is a weak and viable allele of CdsA and does not cause an obvious small cell size phenotype.

(Liu et al., 2014)

CdsA¹ mutants have ectopic lipid droplets in their salivary glands.

(Tian et al., 2011)

When grown in constant light, mutant photoreceptors show vesiculation and a variable reduction in the size of the rhabdomeres. In addition, the cell body of the photoreceptors show the presence of abnormal expanded endomembranes. In some cases, these structures appear studded with electron-dense structures resembling ribosomes.

Mutant retinal extracts show a significant elevation of a single species of phosphatidic acid (predicted fatty acyl composition 16:0 / 18:2 ) compared to controls. The levels of phosphatidylcholine, diacylglycerol and phosphatidylinositol in the retinal extracts are normal.

(Raghu et al., 2009)

Whole cell patch-clamp recordings of dissociated ommatidia from CdsA¹ mutants raised in the dark show no Shab-mediated light-dependent modulation of the delayed rectifier current when stimulated with light. Increasing the light level by a factor of ten causes an irreversible upregulation by up to 35%. Adding 26 μM di-C[8] PIP[2] into the extracellular solution results in an upregulation of approximately 15% and a return to baseline within 4 minutes.

(Krause et al., 2008)

CdsA¹ mutants do not have the ability to discriminate between 18[o]C and temperatures between 20-24[o]C. The ability to choose 18[o]C over temperatures in the 14-16 and 26-32[o]C ranges is not impaired.

(Kwon et al., 2008)

Mutant flies show photoreceptor degeneration when raised in bright light.

(Garcia-Murillas et al., 2006)

CdsA¹ flies undergo age-dependent loss of the rhabdomeres; almost all the rhabdomeres have degenerated following 5 days under a light/dark cycle.

(Wang and Montell, 2006)

The peak amplitude of the photoreceptors in response to light is reduced by about 50% compared to wild type and the time-to-peaks are slightly delayed. Quantum bumps are indistinguishable from wild type. Mutant photoreceptors exposed to La³⁺ show no recovery after a light stimulus of sufficient intensity and duration to induce complete decay, in contrast to wild type (which recover within about 90 seconds). Relatively dim flashes repeated at 30 second intervals in a Ca²⁺ free solution result in an exponential and irreversible reduction in sensitivity in mutant photoreceptors (in wild type the response recovers fully between flashes).

(Hardie et al., 2001)

Physiological defect, reduced light sensitivity. Morphological defect, photoreceptors undergo severe light-dependent degeneration, UV-sensitive R7 cells are more resistant to degeneration. P{CdsA⁺10} can fully rescue the light-dependent retinal degeneration of CdsA¹ mutants. P{arr-cds} can fully rescue the morphological and physiological defects of CdsA¹ mutants. Double mutants with norpA³⁹ confer protection from light-dependent degeneration. Double mutants with Arr2³ are unable to enter or maintain a prolonged depolarised afterpotential (PDA), even after successive or prolonged blue light stimulation.

(Wu et al., 1995)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

NOT Suppressor of

Statement

Reference

Cds¹ is a non-suppressor of abnormal neurophysiology phenotype of Gαq¹

(Hardie et al., 2002)

Phenotype Manifest In

Enhanced by

Statement

Reference

Cds¹ has salivary gland phenotype, enhanceable by Seipin^null

(Tian et al., 2011)

Cds¹ has lipid droplet | ectopic phenotype, enhanceable by Seipin^null

(Tian et al., 2011)

Cds¹ has eye photoreceptor cell phenotype, enhanceable by ArfGAP1^UAS.cRa/Scer\GAL4^GMR.PF

(Raghu et al., 2009)

Cds¹ has rhabdomere phenotype, enhanceable by garz^EP2028/Scer\GAL4^GMR.PF

(Raghu et al., 2009)

Cds¹ has rhabdomere phenotype, enhanceable by ArfGAP1^UAS.cRa/Scer\GAL4^GMR.PF

(Raghu et al., 2009)

Cds¹ has eye photoreceptor cell phenotype, enhanceable by rdgA³

(Garcia-Murillas et al., 2006)

Suppressed by

Statement

Reference

Cds¹ has rhabdomere phenotype, suppressible by Pis^ninaE.PW

(Wang and Montell, 2006)

Enhancer of

Statement

Reference

Cds¹ is an enhancer of salivary gland phenotype of Seipin^null

(Tian et al., 2011)

Cds¹ is an enhancer of lipid droplet | ectopic phenotype of Seipin^null

(Tian et al., 2011)

Cds¹ is an enhancer of rhabdomere phenotype of Scer\GAL4^GMR.PF, garz^EP2028

(Raghu et al., 2009)

Cds¹ is an enhancer of rhabdomere phenotype of ArfGAP1^UAS.cRa, Scer\GAL4^GMR.PF

(Raghu et al., 2009)

Cds¹ is an enhancer of eye photoreceptor cell phenotype of rdgA³

(Garcia-Murillas et al., 2006)

NOT Suppressor of

Statement

Reference

Cds¹ is a non-suppressor of photoreceptor neuron phenotype of Gαq¹

(Hardie et al., 2002)

Additional Comments

Genetic Interactions

Statement

Reference

CdsA¹, Seipin^null double mutants exhibit a strong synergistic phenotype (compared to either single mutant) with respect to ectopic lipid droplets in the salivary gland.

There is more phosphatidic acid in the salivary glands of CdsA¹; Seipin^null mutants than in CdsA¹ single mutants.

(Tian et al., 2011)

Expression of garz^EP2028 under the control of Scer\GAL4^GMR.PF in a CdsA¹ background under bright light illumination results in significantly worse defects in rhabdomere size and structure compared to CdsA¹ single mutants of flies expressing garz^EP2028 under the control of Scer\GAL4^GMR.PF in a wild-type background. There is no change in the accumulation of membranes in the cell body of the photoreceptors in the double mutant flies.

Expression of Gap69C^Scer\UAS.cRa under the control of Scer\GAL4^GMR.PF in a CdsA¹ background under bright light illumination results in a dramatic increase in the accumulation of whorls of endomembrane within the cell body, accompanied by poorly formed rhabdomeres.

(Raghu et al., 2009)

rdgA³ ; CdsA¹ double mutant flies show a higher rate of photoreceptor degeneration when raised in bright light than either rdgA³ or CdsA¹ single mutants.

(Garcia-Murillas et al., 2006)

Expression of Pis^ninaE.PW partially suppresses the CdsA¹ retinal degeneration phenotype; after 5 days under a light/dark cycle, Pis^ninaE.PW; CdsA¹ flies have ommatidia that contain several rhabdomeres whereas almost all rhabdomeres have degenerated in CdsA¹ flies at this stage.

(Wang and Montell, 2006)

The small amplitude of quantum bumps in Gα49B¹ photoreceptors (seen when ATP is present in the intracellular solution during recordings) is not increased in size if the flies are also mutant for CdsA¹.

(Hardie et al., 2002)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Fails to complement

Cds¹⁵⁰⁸

(Ghabrial et al., 2011)

Cds¹³⁷⁵

(Ghabrial et al., 2011)

Cds¹²²⁷

(Ghabrial et al., 2011)

Cds⁶¹³

(Ghabrial et al., 2011)

Rescued by

Cds¹ is rescued by Cds^Arr2.PH

(Wu et al., 1995)

Cds¹ is rescued by Cds^+t10

(Wu et al., 1995)

Comments

Images (0)

Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

Comments

Hybrid dysgenesis induced excisions of the P-element generate wild type revertants, ERGs demonstrate light sensitivity is normal. A second class show a reduced ERG response, representing imprecise excisions and internal deletions of the P-element. A third class show a much greater response to light, this may represent misregulation of CdsA due to aberrant excision events. A fourth class are homozygous lethals.

(Wu et al., 1995)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (3)

Reported As

Symbol Synonym

Cds¹

CdsA¹

(Laurinyecz et al., 2016, Liu et al., 2014, Ghabrial et al., 2011, Tian et al., 2011)

cds¹

(Raghu et al., 2009, Krause et al., 2008, Kwon et al., 2008, Garcia-Murillas et al., 2006, Wang and Montell, 2006, Lee et al., 2003, Hardie et al., 2002, Hardie et al., 2001, Wu et al., 1995)

Name Synonyms

Secondary FlyBase IDs

References (13)

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