Aberration Dmel\Df(1)NP5
| General Information | |||
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| Symbol | Dmel\Df(1)NP5 | Species | D. melanogaster |
| Name | FlyBase ID | FBab0026716 | |
| Feature type | inversion_derived_deficiency_plus_aneuploid | ||
| Also Known As | NP5 | ||
| Computed Breakpoints include | |||
| Sequence coordinates | |||
| Member of large scale dataset(s) | |||
Recent Updates
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| Description |
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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 Aberration
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| Cytological Order | |||
| Progenitor | |||
| Mutagen | |||
| Class of aberration (relative to progenitor) | |||
| Breakpoints | |||
| Causes alleles | |||
| Carries alleles | |||
| Transposon Insertions | |||
| Formalized genetic data | bk1 << NetA << rut << bk4 | ||
| Genetic mapping information | |||
| Comments | |||
Comments on Cytology
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The recombinant chromosome is deficient for 12E9-12E11;12F2-5 and has the inversion breakpoints 12F2-12F5;17C2. Another inversion, roughly In(1)2;10, is also present. | |||
Sequence Crossreferences
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| DDBJ
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EMBL / GenBank | DNA sequence Protein sequence Name | ||
Gene Deletion & Duplication Data
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Genes Deleted / Disrupted
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| Complementation Data | |||
| Completely deleted / disrupted | |||
| Molecular Data | |||
Genes NOT Deleted / Disrupted
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| Complementation Data | |||
| Molecular Data | |||
Genes Duplicated
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| Complementation Data | |||
| Molecular Data | |||
Genes NOT Duplicated
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| Complementation Data | |||
| Molecular Data | |||
Related Comments
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Phenotypic Data
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| In combination with other aberrations | |||
| NOT in combination with other aberrations | Df(1)NP5 mutants exhibit fragmented commissures and gaps in longitudinal connectives. 90% of Df(1)NP5/Y embryos show defects in axon guidance in the Bolwig's nerve.
Df(1)NP5 embryos show defects in the commissures of the central nervous system; 2% of anterior commissures are absent, 4% of anterior commissures are thin, 8% of posterior commissures are absent and 15% of posterior commissures are thin. 10% of segments fail to separate the anterior and posterior commissures correctly. Df(1)NP5 embryos exhibit salivary gland guidance defects. In wild-type embryos the salivary glands lie parallel to the CNS midline, while 23% of Df(1)NP5 embryos have glands that curve away laterally and 9% have glands that curve medially towards the midline. This phenotype occurs as the glands migrate along the visceral mesoderm, as the invagination of the salivary glands is normal. Gut constriction is not affected in these mutants. The commissures of the ventral nerve cord are abnormally thin or completely absent in Df(1)NP5 embryos. Embryos heterozygous for Df(1)NP5, removing one copy of NetA and NetB exhibit normal commissures, however the longitudinal tracts, when visualized with BP102 antibody, are thinner between segments and thicker within segments. When fascicles are visualized with Fas2, embryos homozygous or heterozygous for Df(1)NP5 reveal irregularities and interruptions in the longitudinal Fas2 bundles. The heterozygote Df(1)NP5 phenotype is not enhanced in embryos also heterozygous for sliunspecified, robounspecified, or scbunspecified. In contrast, the frequency of midline guidance errors is increased in sliunspecified/+ or robounspecified/+, but not scbunspecified embryos also heterozygous for Df(1)NP5. No abnormalities are seen in SNa and SNc projections. Lateral migration of peripheral and exit glia appears normal. In mutant embryos, the there are defects in the posterior commissure and there are breaks in the longitudinal connectives. Homozygous lethal, lethality is rescued by Dp(1;f)LJ9 and Dp(1;f)LJ4. Hemizygous embryos display a range of phenotypes in the CNS, most notably a thinning or absence of the commissures in the ventral nerve cord. This defect can be rescued by restoring midline expression of either NetA or NetB gene. Homozygous lethal. Lethality can be rescued by Dp(1;f)LJ9. Embryo exhibits CNS phenotype: commissures are much thinner and sometimes completely absent, occasional breaks in the longitudinal tracts. Commissural phenotype is rescued by expression of P{slit-NetA} or P{slit-NetB}. There are no segmentation defects, no gross changes in the fate or pattern of midline cells or CNS neurons, no increase in cell death. Embryos exhibit occasional errors in the projection pattern of the motor nerves, including lack if innervation of muscles 6 and 7. Projection of sensory axons into the CNS is almost completely normal. | ||
Stocks
( 2 ) | |||
| Bloomington | |||
| Kyoto | |||
Notes on Origin
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| Discoverer | |||
Balancer / Genotype Variants of the Aberration
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Separable Components
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Other Comments
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Synonyms & Secondary IDs
( 8 ) | |||
| Reported As | |||
| Symbol Synonym | Df(1)NP3 Df(1)NP5 Df(1)NP-5 Df-NP5 In(1)366.2LP363R In(1)N366.2LP363R NetA,BNP5 | ||
| Name Synonym | |||
| Secondary FlyBase IDs | |||
References
( 17 ) | |||
| Research paper |
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| Personal communication to FlyBase |
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| Abstract |
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| Letter |
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Recent Updates