A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Aberration Dmel\Df(1)N-8

General Information
SymbolDmel\Df(1)N-8SpeciesD. melanogaster
NameDeficiency (1) NotchFlyBase IDFBab0000579
Feature typechromosomal_deletion
Also Known AsDf(1)N8, Df(1)N8, N8, N8
Computed Breakpoints include 3C1;3D6
Deleted segment3C1--3D6
Sequence coordinates
Member of large scale dataset(s)
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Description
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FB2013_03
FB2013_02
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hide Nature of the Aberration
Cytological Order
Progenitor
Mutagen
Class of aberration (relative to progenitor)
Breakpoints
3B4-3C1;3D6-3E1
3C1-3C2;3D5-3D6
3C1-3C2;3E2-3E3
Causes alleles
Carries alleles
Transposon Insertions
Formalized genetic data l(1)3Bf << bk1 << crm << l(1)EA65 << bk2 << l(1)3Eb
Genetic mapping information
Comments
hide Comments on Cytology
Deletion of 17/19 bands.
Left limit of break 1 from polytene analysis (FBrf0004288) Right limit of break 1 from inclusion of crm (FBrf0038033) Left limit of break 2 from polytene analysis (FBrf0040178) Right limit of break 2 from polytene analysis (FBrf0004288)
 
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DDBJ /
EMBL /
GenBank
DNA sequence
Protein sequence
Name
 
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hide Genes Deleted / Disrupted
Complementation Data
Completely deleted / disrupted
Molecular Data
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Complementation Data
Molecular Data
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Complementation Data
Molecular Data
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Complementation Data
Molecular Data
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In combination with other aberrations
Does not complement Df(1)w67k30.
NOT in combination with other aberrations
Df(1)N-8 heterozygotes exhibit a dominant wing notching phenotype.
Heterozygotes show loss of wing margin and wing vein thickening.
Flies bearing Df(1)N-8 are generally smaller than wild-type flies and have a transient, slightly brown, eye phenotype shortly after eclosion.
Df(1)N-8 flies exhibit a weak loss of wing margin.
Shows dominant wing nicking which is enhanced by PsnW11 and PsnW6.
Does not cause unconditional lethality in hybrid females when heterozygous with D.simulans chromosome.
Heterozygotes of Df(1)N-8 or N55e11 with Abl1,NrtM54 or In(3L)std11 show defects in eye development leading to rough eyes with high penetrance.
No second site non-complementing phenotype with zipEbr and zipmhc-c6.1.
Shows no maternal enhancement of dpphr4.
Single cells from Df(1)N-8 embryos transplanted into the ventral neurogenic region of wild-type host embryos can give rise to both neural and epidermal cells.
Dominantly causes tergite defects in less than 50% of run3 heterozygotes.
Deficient embryos show an uninterpretable mutant midgut phenotype.
Homozygous embryos are very abnormal compared to wild-type. Midgut primordia do not fuse, and Malpighian tubules branch.
Heterozygosity for this deletion has no effect on the mutant ovarian phenotype of ovoD2.
Reveals antimorphic alleles of P{en1}wgen11.
Hyperplasia of replicating sensory precursors: due to an increased number of ectodermal cells being recruited as sensory precursor cells. Extra precursor cells are recruited beyond the normal time window for neurogenesis in the PNS.
Heterozygous females exhibit reduced viability and fertility.
hide Stocks ( 2 )
Bloomington
Kyoto
hide Notes on Origin
Discoverer
Mohr, 7 Oct. 1918.
 
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hide Synonyms & Secondary IDs ( 13 )
Reported As
Symbol Synonym
DelNotch8
Df(1)Notch-8
N-8 Mohr
Name Synonym
Deficiency (1) Notch
 
Secondary FlyBase IDs
  • FBal0029936
  • FBal0058507
hide References ( 81 )
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hide Recent research papers ( 2 )
Leonardi et al., 2011, Development 138(16): 3569--3578
Multiple O-glucosylation sites on Notch function as a buffer against temperature-dependent loss of signaling. [FBrf0214548]
Tsubota et al., 2011, Fly 5(4): 275--284
Interactions between enhancer of rudimentary and Notch and deltex reveal a regulatory function of enhancer of rudimentary in the Notch signaling pathway in Drosophila melanogaster. [FBrf0217950]
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All reviews listed in FlyBase were published before 2011