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General Information
Symbol
Dmel\Cds1
Species
D. melanogaster
Name
FlyBase ID
FBal0044698
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
CdsA1
Key Links
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference
Insertion components
P{HZ}Cds1
Product class / Tool use(s)
Encoded product / tool
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
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

CdsA1/CdsACB-0128-3 as well as CdsA1/CdsAEY08412 and CdsA1/CdsAUM-8246-3 adult males are fertile, while CdsA1/Df(3L)BSC795 males are sterile.

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.

CdsA1 mutants have ectopic lipid droplets in their salivary glands.

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.

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.

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.

Mutant flies show photoreceptor degeneration when raised in bright light.

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

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).

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.

External Data
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

Phenotype Manifest In
Enhanced by
Suppressed by
Statement
Reference

Cds1 has rhabdomere phenotype, suppressible | partially by PisninaE.PW

Enhancer of
Statement
Reference
NOT Suppressor of
Statement
Reference

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

Additional Comments
Genetic Interactions
Statement
Reference

CdsA1, Seipinnull 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; Seipinnull mutants than in CdsA1 single mutants.

Expression of garzEP2028 under the control of Scer\GAL4GMR.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 garzEP2028 under the control of Scer\GAL4GMR.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 Gap69CScer\UAS.cRa under the control of Scer\GAL4GMR.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.

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

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

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.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
Comments
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.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
References (13)