Allele Dmel\Adgf-A^Karel.5'

General Information
Symbol	Dmel\Adgf-A^Karel.5'	Species	D. melanogaster
Name		FlyBase ID	FBal0157461
Feature type	allele	Associated gene	Dmel\Adgf-A

Allele class
Mutagen	recombination, SCEI endonuclease, FLPase, ends-in gene targeting
Recent Updates
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FB2013_03
FB2013_02
All updates	Click here to see a list of all updates to this record from FB2010_08 and on.
Nature of the Allele
Allele class
Mutagen	ends-in gene targeting (Dolezal et al., 2003) FLPase (Dolezal et al., 2003) recombination (Dolezal et al., 2003) SCEI endonuclease (Dolezal et al., 2003)
Mutations Mapped to the Genome

Type Location Additional Notes References
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name

UniProtKB/Swiss-Prot
UniProtKB/TrEMBL

Progenitor genotype	Adgf-A^HR.cDa (Dolezal et al., 2003)
Nature of the lesion	Statement Reference Mutant copy of Adgf-A. (Dolezal et al., 2003)
Caused by aberration	Dp(3;3)Karel (Dolezal et al., 2003)
Cytology
Phenotypic Data
Phenotypic Class
	developmental rate defective (with Adgf-A^Karel.3') (Dolezal et al., 2005) lethal (with Adgf-A^Karel.3') (Dolezal et al., 2005) lethal \| larval stage (with Adgf-A^Karel.3') (Dolezal et al., 2003) melanotic mass phenotype (with Adgf-A^Karel.3') (Dolezal et al., 2003, Dolezal et al., 2005)
Phenotype Manifest In
	adult abdomen (with Adgf-A^Karel.3') (Dolezal et al., 2005) crystal cell (with Adgf-A^Karel.3') (Dolezal et al., 2005) embryonic/larval fat body (with Adgf-A^Karel.3') (Dolezal et al., 2003, Dolezal et al., 2005) embryonic/larval hemocyte (with Adgf-A^Karel.3') (Dolezal et al., 2005) embryonic/larval lymph gland (with Adgf-A^Karel.3') (Dolezal et al., 2005) lamellocyte (with Adgf-A^Karel.3') (Dolezal et al., 2005) melanotic mass (with Adgf-A^Karel.3') (Dolezal et al., 2003, Dolezal et al., 2005) pupal abdomen (with Adgf-A^Karel.3') (Dolezal et al., 2005) sessile hemocyte (with Adgf-A^Karel.3') (Dolezal et al., 2005)
Detailed Description
	Statement Reference Under optimal conditions (20-30 isolated homozygous larvae per vial) about 60% of Dp(3;3)Karel homozygous larvae (Dp(3;3)Karel carries the Adgf-A^Karel.3' and Adgf-A^Karel.5' mutant alleles) reach the third instar. Development during the third larval instar is significantly delayed (wandering homozygous larvae appear about 2 days after their heterozygous siblings) and some homozygous third instar larvae can be found alive even after 10 days of development. Dp(3;3)Karel homozygous third instar larvae show fat body disintegration and have multiple melanotic tumours, predominantly in the caudal part of the body and accompanied by disintegration of the fat body. Melanisation of the lymph gland is not seen in these larvae and the imaginal discs and brain appear normal. The overall structure of the ring gland appears unaffected. Less than 30% of Dp(3;3)Karel homozygotes eventually pupate. Homozygous pupae usually die soon after pupariation, in some cases they develop normal head and thorax imaginal structures, but abdominal parts do not usually develop. The pupal abdomen has an abnormal curvature to the right. Less than 2% of Dp(3;3)Karel pupae develop normally and eventually emerge as adults. These adults do not have any obvious abnormalities besides the abdominal curvature, although some are sterile. Dp(3;3)Karel homozygous early third instar larvae contain a much higher number of "sessile hemocytes" (hemocytes attached to the tissues under the integument) than wild-type controls. Dp(3;3)Karel homozygous late third instar larvae contain an average of 7-fold more hemocytes in circulation than wild-type larvae. More than 75% of the mutant hemocytes are strongly adhesive when placed on a substrate (in contrast to wild-type larval plasmatocytes which remain rounded) and after being placed on a drop of hemolymph on a microscope slide, they develop filamentous and membranous extensions. 7% of the mutant hemocytes are lamellocytes (a cell type that is not present in the circulation of wild-type larvae under normal conditions) and the mutant larvae also contain excess crystal cells compared to wild-type. The lymph glands of the mutant larvae appear dispersed in the late third instar (dispersal of the lymph glands normally occurs during metamorphosis). Pupariation frequency in Dp(3;3)Karel mutants is restored to almost wild-type levels by treatment with 20-hydroxyecdysone, and the delay in development is also significantly reduced. (Dolezal et al., 2005) Homozygous Dp(3;3)Karel animals are mostly lethal in the late third larval instar and larval development is significantly delayed. Disintegration of the fat body is seen and most third instar larvae develop melanotic tumours. They rarely pupate, but those that do produce abnormal pupae. This phenotype appears to be due to Adgf-A loss of function (Dp(3;3)Karel carries two mutated copies of Adgf-A - Adgf-A^Karel.5' and Adgf-A^Karel.3') since it can be rescued by overexpression of an Adgf-A transgene. (Dolezal et al., 2003)
External Data
Linkouts
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Statement Reference Adgf-A^Karel.3'/Adgf-A^Karel.5' has developmental rate defective phenotype, suppressible \| partially by AdoR¹ (Dolezal et al., 2005) Adgf-A^Karel.3'/Adgf-A^Karel.5' has lethal phenotype, suppressible \| partially by AdoR¹ (Dolezal et al., 2005) Adgf-A^Karel.3'/Adgf-A^Karel.5' has melanotic mass phenotype phenotype, suppressible \| partially by AdoR¹ (Dolezal et al., 2005) Adgf-A^Karel.3'/Adgf-A^Karel.5' has melanotic mass phenotype phenotype, suppressible \| partially by crq[+]/crq^KG01679 (Dolezal et al., 2005) Adgf-A^Karel.3'/Adgf-A^Karel.5' has melanotic mass phenotype phenotype, suppressible \| partially by l(3)hem¹/l(3)hem¹ (Dolezal et al., 2005) Adgf-A^Karel.3'/Adgf-A^Karel.5' has melanotic mass phenotype phenotype, suppressible by crq^KG01679/crq^KG01679 (Dolezal et al., 2005)
NOT suppressed by
Statement Reference Adgf-A^Karel.3'/Adgf-A^Karel.5' has developmental rate defective phenotype, non-suppressible by l(3)hem¹/l(3)hem¹ (Dolezal et al., 2005)
Phenotype Manifest In
Suppressed by
Statement Reference Adgf-A^Karel.3'/Adgf-A^Karel.5' has crystal cell phenotype, suppressible by AdoR¹ (Dolezal et al., 2005) Adgf-A^Karel.3'/Adgf-A^Karel.5' has crystal cell phenotype, suppressible by crq^KG01679/crq^KG01679 (Dolezal et al., 2005) Adgf-A^Karel.3'/Adgf-A^Karel.5' has embryonic/larval fat body phenotype, suppressible \| partially by crq[+]/crq^KG01679 (Dolezal et al., 2005) Adgf-A^Karel.3'/Adgf-A^Karel.5' has embryonic/larval fat body phenotype, suppressible \| partially by l(3)hem¹/l(3)hem¹ (Dolezal et al., 2005) Adgf-A^Karel.3'/Adgf-A^Karel.5' has embryonic/larval fat body phenotype, suppressible by crq^KG01679/crq^KG01679 (Dolezal et al., 2005) Adgf-A^Karel.3'/Adgf-A^Karel.5' has embryonic/larval hemocyte phenotype, suppressible \| partially by crq^KG01679/crq^KG01679 (Dolezal et al., 2005) Adgf-A^Karel.3'/Adgf-A^Karel.5' has embryonic/larval hemocyte phenotype, suppressible \| partially by l(3)hem¹/l(3)hem¹ (Dolezal et al., 2005) Adgf-A^Karel.3'/Adgf-A^Karel.5' has lamellocyte phenotype, suppressible \| partially by AdoR¹ (Dolezal et al., 2005) Adgf-A^Karel.3'/Adgf-A^Karel.5' has lamellocyte phenotype, suppressible by crq^KG01679/crq^KG01679 (Dolezal et al., 2005) Adgf-A^Karel.3'/Adgf-A^Karel.5' has melanotic mass phenotype, suppressible \| partially by AdoR¹ (Dolezal et al., 2005) Adgf-A^Karel.3'/Adgf-A^Karel.5' has melanotic mass phenotype, suppressible \| partially by crq[+]/crq^KG01679 (Dolezal et al., 2005) Adgf-A^Karel.3'/Adgf-A^Karel.5' has melanotic mass phenotype, suppressible \| partially by l(3)hem¹/l(3)hem¹ (Dolezal et al., 2005) Adgf-A^Karel.3'/Adgf-A^Karel.5' has melanotic mass phenotype, suppressible by crq^KG01679/crq^KG01679 (Dolezal et al., 2005)
NOT suppressed by
Statement Reference Adgf-A^Karel.3'/Adgf-A^Karel.5' has embryonic/larval fat body phenotype, non-suppressible by AdoR¹ (Dolezal et al., 2005) Adgf-A^Karel.3'/Adgf-A^Karel.5' has pupal abdomen phenotype, non-suppressible by l(3)hem¹/l(3)hem¹ (Dolezal et al., 2005)
Additional Comments
Genetic Interactions
Statement Reference l(3)hem¹ suppresses some of the Dp(3;3)Karel mutant phenotypes; the number of circulating hemocytes in late third instar l(3)hem¹ Dp(3;3)Karel double mutant larvae is significantly reduced compared to Dp(3;3)Karel single mutant larvae. In addition, only 40% of the double mutant larvae show disintegration of the fat body compared to 90% of Dp(3;3)Karel single mutants, and only 55% of the double mutant larvae have melanotic tumours compared to more than 83% of Dp(3;3)Karel single mutants. The delay in development, block in pupariation and abnormal shape of Dp(3;3)Karel pupae are not suppressed by l(3)hem¹. Introduction of the AdoR¹ mutation significantly increases pupariation and the adult emerging rate in Dp(3;3)Karel mutants. Developmental delay in the double mutant larvae is much less pronounced than in the Dp(3;3)Karel single mutant, with most of the double mutant larvae pupariating within 1 day after their control siblings. The disintegration of the fat body seen in Dp(3;3)Karel larvae is not altered by introduction of AdoR¹, but the formation of melanotic tumours is significantly reduced. The total number of circulating hemocytes is not significantly changed in the double mutant larvae compared to Dp(3;3)Karel single mutants, but the number of lamellocytes is decreased and the number of crystal cells is normal. crq^KG01679 Dp(3;3)Karel double mutant third instar larvae show a decrease in the total number of circulating hemocytes compared to Dp(3;3)Karel single mutants, although the number is still significantly increased compared to wild-type, and the cells show increased clumping. Lamellocytes are not detected in the double mutant larvae and the number of crystal cells is normal. The disintegration of the fat body and the formation of melanotic tumours seen in Dp(3;3)Karel single mutant larvae is completely suppressed in the double mutant. crq^KG01679/+ Dp(3;3)Karel/Dp(3;3)Karel larvae show significant suppression of the fat body disintegration seen in Dp(3;3)Karel single mutants and rarely have melanotic tumours. (Dolezal et al., 2005)
Xenogenetic Interactions
Statement Reference
Complementation & Rescue Data
Rescued by	Adgf-A^Karel.3'/Adgf-A^Karel.5' is rescued by Scer\GAL4^Act.PU/Adgf-A^{Scer\UAS.T:Hsap\MYC} (Dolezal et al., 2005) Adgf-A^Karel.3'/Adgf-A^Karel.5' is rescued by Scer\GAL4^c564/Adgf-A^{Scer\UAS.T:Hsap\MYC} (Dolezal et al., 2005) Adgf-A^Karel.3'/Adgf-A^Karel.5' is rescued by Scer\GAL4^e33C/Adgf-A^{Scer\UAS.T:Hsap\MYC} (Dolezal et al., 2005)
Partially rescued by	Adgf-A^Karel.3'/Adgf-A^Karel.5' is partially rescued by Adgf-A^hs.PD (Dolezal et al., 2005) Adgf-A^Karel.3'/Adgf-A^Karel.5' is partially rescued by Scer\GAL4⁵⁰¹⁵/Adgf-A^{Scer\UAS.T:Hsap\MYC} (Dolezal et al., 2005) Adgf-A^Karel.3'/Adgf-A^Karel.5' is partially rescued by Scer\GAL4^Cg.PA/Adgf-A^{Scer\UAS.T:Hsap\MYC} (Dolezal et al., 2005) Adgf-A^Karel.3'/Adgf-A^Karel.5' is partially rescued by Scer\GAL4^Dot.PK/Adgf-A^{Scer\UAS.T:Hsap\MYC} (Dolezal et al., 2005)
Not rescued by	Adgf-A^Karel.3'/Adgf-A^Karel.5' is not rescued by Scer\GAL4^Act.PU/Adgf-A^{mut.Scer\UAS.T:Hsap\MYC} (Dolezal et al., 2005) Adgf-A^Karel.3'/Adgf-A^Karel.5' is not rescued by Scer\GAL4^Lsp2.PH/Adgf-A^{Scer\UAS.T:Hsap\MYC} (Dolezal et al., 2005) Adgf-A^Karel.3'/Adgf-A^Karel.5' is not rescued by Scer\GAL4^Mef2.PR/Adgf-A^{Scer\UAS.T:Hsap\MYC} (Dolezal et al., 2005) Adgf-A^Karel.3'/Adgf-A^Karel.5' is not rescued by Scer\GAL4^T110/Adgf-A^{Scer\UAS.T:Hsap\MYC} (Dolezal et al., 2005)
Comments
Stocks ( 0 )

Notes on Origin
Discoverer
	Induced with: Adgf-A^Karel.3'. Induced with: Msi^Karel.5'. Induced with: Msi^Karel.3'. Induced with: Adgf-B^Karel.5'. Induced with: Adgf-B^Karel.3'. Created by a targeted recombination event, using P{TV2.FRT(ADGF-A2^-.-A^-.-B^-.w⁺)} as the donor template. This construct is a donor template for "ends-in" targeted knockout of three genes (Msi, Adgf-A and Adgf-B). The targeted recombination event is expected to result in a duplication of the three genes, with the expected combination of open reading frames being: Msi (wild type), Adgf-A (mutant), Adgf-B (mutant), w (from the donor construct), Msi (mutant), Adgf-A (wild type), Adgf-B (wild type). The actual combination of open reading frames is: Msi (wild type), Adgf-A (mutant), Adgf-B (mutant), w (from the donor construct), Msi (mutant), Adgf-A (mutant), Adgf-B (wild type). This represents a duplication with conversion of wild-type Adgf-A to mutant. (Dolezal et al., 2003)
External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 2 )
Reported As
Symbol Synonym	Adgf-A^Karel.5' adgf-a^karel (Dolezal et al., 2005)
Name Synonym
Secondary FlyBase IDs

References ( 2 )
Research paper	Dolezal et al., 2005, PLoS Biol. 3(7): e201 A role for adenosine deaminase in Drosophila larval development. [FBrf0188209] Dolezal et al., 2003, Genetics 165(2): 653--666 Genetic analysis of the ADGF multigene family by homologous recombination and gene conversion in Drosophila. [FBrf0167663]

Allele Dmel\Adgf-AKarel.5'

Allele Dmel\Adgf-A^Karel.5'