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General Information
Symbol
Df(2L)prd1.7
Species
D. melanogaster
Name
FlyBase ID
FBab0001902
Feature type
Also Known As
Df(2L)prd1.7
Computed Breakpoints include

33B3;34A1-34A2

Deleted Segment
Sequence coordinates
Member of large scale dataset(s)
Nature of Aberration
Cytological Order
Progenitor
Mutagen
Class of aberration (relative to wild type)
Causes alleles
Carries alleles
Transposon Insertions
Formalized genetic data

esc << bk1 << E(var)33AD << pdm2 << bk2

Genetic mapping information
Comments

Breakpoint(s) molecularly mapped

Distal breakpoint mapped to the DNA (Frei et al., 1985).

Comments on Cytology

Ref: Lindsley and Zimm, 1992

Left limit of break 1 from polytene analysis (FBrf0049878) Right limit of break 1 from polytene analysis (FBrf0076124) Limits of break 2 from polytene analysis (FBrf0049878)

Sequence Crossreferences
DNA sequence
Protein sequence
Gene Deletion and Duplication Data
Phenotypic Data
In combination with other aberrations

Df(2L)esc10 is semi-lethal in combination with Df(2L)prd1.7. Surviving males and females are fertile.

Df(2L)esc10/Df(2L)prd1.7 adult survivors lack almost all interommatidial bristles.

No effect on In(1)wm4h position-effect variegation.

NOT in combination with other aberrations

Heterozygous Df(2L)prd1.7 larvae show a reduction in food ingestion rate of about 35% compared to wild-type larvae. Waste excretion rates of heterozygous Df(2L)prd1.7 larvae are reduced compared to wild type.

The Df(2L)prd1.7 chromosome does not act as a dominant suppressor of telomeric silencing (assayed using the effect of the chromosome on the eye colour phenotype of flies carrying "P{wvar}KR3-2", a stable "brown-red" variant of the P{3'WP-2,wvar}2Lt insertion).

Df(2L)prd1.7 in combination with a pair of introgressions from D.simulans spanning 30F1-31E7 to 35D7-36A14 Dsim\Int(2L)S and 21A1 to 22D1--23A2 Dsim\Int(2L)D produces sterile male flies. These flies are female sterile.

Does not cause unconditional lethality in hybrid females when heterozygous with D.simulans chromosome.

No second site non-complementing phenotype with zipEbr and zipmhc-c6.1.

Shows no maternal enhancement of dpphr4.

100% of homozygotes lack cells from the RP2/sib lineage in all remaining hemisegments. Heterozygotes show a weak haploinsufficient phenotype, with approximately 6.5% of embryos having an RP2 lineage defect. All Df(2L)prd1.7/Df(2L)Prl embryos have hemisegments which show RP2/sib lineage defects.

Deficient embryos show an uninterpretable mutant midgut phenotype.

Homozygous embryos do not complete head involution and tracheae are disconnected. The midgut does not constrict and the midgut epithelium shows variable degrees of degeneration.

Heterozygosity for this deletion has no effect on the mutant ovarian phenotype of ovoD2.

eve-positive RP2/sib GMCs are not observed in 7.5hr deficiency embryos.

prd4/Df(2L)prd1.7 transheterozygotes only survive to adulthood in the presence of a copy of P{prd-SN20}. These adults give rise to fertile offspring.

Stocks (3)
Notes on Origin
Discoverer

Nusslein-Volhard.

 
Balancer / Genotype Variants of the Aberration
 
Separable Components
 
Other Comments
 
Synonyms and Secondary IDs (8)
References (57)