A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Aberration Dmel\Df(1)N-54l9

General Information
SymbolDmel\Df(1)N-54l9SpeciesD. melanogaster
NameDeficiency (1) NotchFlyBase IDFBab0000564
Feature typechromosomal_deletion
Also Known AsN54l9, N5419, Df(1)N54l9, N54/9, Notch54l9, Df(1)N5419
Computed Breakpoints include 3C6;3C11
Deleted segment3C6--3C11
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No matching regions found.

Sequence coordinates
X:3,134,959..3,136,127 [-] (Df(1)N-54l9:bk2)
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
3C5-3C6;3C11-3C12
3C6;3C11
Causes alleles
Carries alleles
Transposon Insertions
Formalized genetic data rst << bk1 << vt << ng2 << bk2 << ng1
Genetic mapping information
Comments
Lacks Sgs-4 sequences (McGinnis et al., 1980).
 
hide Comments on Cytology
Left limit of break 1 from polytene analysis (FBrf0023492) Right limit of break 1 from inclusion of vt (FBrf0023492) Left limit of break 2 from inclusion of ng2 (FBrf0058951) Right limit of break 2 from polytene analysis (FBrf0063630)
 
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DDBJ /
EMBL /
GenBank
DNA sequence
Protein sequence
Name
 
hide Gene Deletion & Duplication Data
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
Lethal in male double hemizygous combination with Df(1)w67c3.
Viable in combination with Df(1)w67k30, producing flies which have a strong vt phenotype, but are not rough eyed.
Df(1)N-54l9/Df(1)w67k30 viable Df(1)N-54l9/Df(1)w67k30 vt phenotype
 
NOT in combination with other aberrations
Df(1)N-54l9/+ females display a relatively weak notch-wing phenotype, characterised by wing vein thickening (preferentially L3 and L5) and by delta formation at the contact between wing veins and the wing edge. One or more notches is present in 75% of Df(1)N-54l9/+ wings.
55% of Df(1)N-54l9/+ flies have a notched wing phenotype.
The number of cap cells and germline stem cells in the ovaries of 2 day old heterozygous females is significantly reduced compared to wild type.
Df(1)N-54l9 heterozygotes exhibit notches at the wing margin. Df(1)N-54l9 Mer4; exe1 triple transheterozygous mutants suppress the Df(1)N-54l9 heterozygous wing notch phenotype.
Clones of Df(1)N-54l9 mutant cells in the eye disc show a cell-autonomous block of mitosis and DNA synthesis in the position of the second mitotic wave (SMW). However, a small number of mutant cells do incorporate BrdU (a marker of S phase) in the most posterior regions of clones, significantly behind the SMW. Cell proliferation ahead of the morphogenetic furrow is not detectably impaired in Df(1)N-54l9 mutant cells.
Df(1)N-54l9 third instar nota clones exhibit at least eight sensory organ precursors (SOPs) in approximately 44.5% of SOP positions scored. Approximately 26% of SOP positions display between four and eight ectopic SOPs, while approximately 26% exhibit between one and four SOPs, with only 3.5% exhibiting one SOP, as in wild-type. Df(1)N-54l9 third instar nota clones exhibit a partially penetrant growth defect.
Large Df(1)N-54l9 mutant clones in the eye disc (generated in a Minute/+ background) have very few or no neurons. Small clones (generated in a wild-type background) have extra neuronal cells. Basally located nuclei are found along the posterior margin of small clones.
Neuronal development is impaired in when Df(1)N-54l9 is expressed in clones within the eye-antennal disc.
Visceral mesoderm is reduced in mutant embryos.
Non-muscle defects are seen in mutants.
Heterozygous Df(1)N-54l9 flies exhibit a weakly-penetrant wing nicking phenotype.
Notches at the distal wing margin.
No R8 cells or photoreceptor neurons develop in a N clone on the eye-disc.
Notching of the distal wing margin can be suppressed by osa308.
Abnormal epidermal and muscle development. Presence of Scer\GAL4twi.PBa can normalise some but no all aspects of myogenesis in Df(1)N-54l9 mutants.
No effect on the faf eye phenotype.
Suppression of the lethal SerBd-3 Ser+r83k combination, escapers exhibit phenotypically normal eyes and legs but lack halteres and had wing blades one half normal size.
Dominant enhancer of the scaMSKF mutant phenotype.
A few flies of the genotype Df(1)N-54l9,dxENU/+,dxENU;Su(dx)1/+ escape the lethality of their dead Df(1)N-54l9,dxENU/+,dxENU siblings. However they have the same, small, rough eye defect as their dead siblings.
Heterozygotes show lethal interaction with gain of function Su(H) alleles.
The wing-notching phenotype of Df(1)N-54l9 heterozygotes is more severe in flies which also carry one or two copies of EgfrE3 or EgfrE1.
cosP{479BE} construct rescues the embryonic lethality and therefore the neurogenic phenotype of homozygotes and the dominant wing notching phenotype of heterozygous females.
Puff formation at 3C11 during intermoult period.
Homozygous males are lethal.
Weak Notch. Deltas of long veins reliable in classification when wing tips not notched.
 
hide Stocks ( 1 )
Bloomington
hide Notes on Origin
Discoverer
Mohler, 9th Dec. 1954.
 
hide Balancer / Genotype Variants of the Aberration
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hide Synonyms & Secondary IDs ( 10 )
Reported As
Symbol Synonym
Df(1)N-54l9
 
Df(1)N-5419
Name Synonym
Deficiency (1) Notch
 
Secondary FlyBase IDs
  • FBab0023986
  • FBal0038924
hide References ( 68 )
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hide Recent research papers ( 3 )
Weber et al., 2012, Genetics 191(1): 145--162
Novel regulators of planar cell polarity: a genetic analysis in Drosophila. [FBrf0218210]
Cho and Fischer, 2011, Development 138(7): 1349--1359
Ral GTPase promotes asymmetric Notch activation in the Drosophila eye in response to Frizzled/PCP signaling by repressing ligand-independent receptor activation. [FBrf0213208]
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]
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All reviews listed in FlyBase were published before 2011