A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Aberration Dmel\Df(3L)ri-XT1

General Information
SymbolDmel\Df(3L)ri-XT1SpeciesD. melanogaster
NameFlyBase IDFBab0000008
Feature typechromosomal_deletion
Also Known AsDf(3L)riXT1, Df(3L)riXT1
Computed Breakpoints include 77E2;[>78A4]
Deleted segment77E2--78A4
Sequence coordinates
Member of large scale dataset(s)
hide Recent Updates
Description
What does this section display?
This section contains items that were added to this record for each release. It currently only tracks new links between this FlyBase report and other FlyBase data classes (e.g. genes, references, stocks) or controlled vocabulary terms (e.g. GO, anatomy terms).
What does this section not display?
This section does not currently display links that were removed or gene model changes.
Update Feed
Click the icon below to subscribe to this FlyBase record and receive updates automatically through your feed reader.
FB2013_03
FB2013_02
All updates Click here to see a list of all updates to this record from FB2010_08 and on.
hide Nature of the Aberration
Cytological Order
Progenitor
Mutagen
Class of aberration (relative to progenitor)
Breakpoints
77E2-77E4;78A2-78A4
Causes alleles
Carries alleles
Transposon Insertions
Formalized genetic data bk1 << knrl << fng << bk2
Genetic mapping information
Comments
hide Comments on Cytology
The 77E1-4 quadruplet is attenuated, but a distal portion is still present. The 78A5,6 doublet is present, but the 78A1,2 doublet is absent.
Left limit of break 1 from polytene analysis (citation unavailable) Right limit of break 1 from inclusion of kni (FBrf0045941) Left limit of break 2 from inclusion of fng (FBrf0076041)
 
hide Sequence Crossreferences
DDBJ /
EMBL /
GenBank
DNA sequence
Protein sequence
Name
 
hide Gene Deletion & Duplication Data
hide Genes Deleted / Disrupted
Complementation Data
Completely deleted / disrupted
Molecular Data
hide Genes NOT Deleted / Disrupted
Complementation Data
Molecular Data
hide Genes Duplicated
Complementation Data
Molecular Data
hide Genes NOT Duplicated
Complementation Data
Molecular Data
hide Related Comments
hide Phenotypic Data
In combination with other aberrations
Homozygous lethal. Lethal in combination with fng80 and fng13 semi-viable in combination with fngM69 (at 18oC), fng52 and fng2, with 5.0%, 3.3%, and 2.3% of animals surviving to adulthood.
In Df(3L)ri-XT1 mutant embryos, the developing small intestine and the rectum epithelia in the hindgut and the esophagus epithelium in the foregut start to lose integrity in mutants leading to a disconnection is seen of the hindgut and the midgut. Larger nuclei and larger cells are seen in the hindgut epithelial cells of mutant embryos.
NOT in combination with other aberrations
The Df(3L)ri-XT1 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).
Mutant embryos have defects in the visceral branch of the tracheal system. Only five tracheal metameres develop, and the tracheal cells do not migrate. When partially rescued with knitRa, segmentation is restored, but dorsal and ventral branches have breaks in the dorsal trunk. Embryos usually lack the visceral branches and if present they are very rudimentary.
Tracheal metameres in remaining 5 abdominal segments of homozygotes show much more disrupted phenotype than kni8. Rudimentary tracheal metameres invaginate but lack primary branching and interconnections. When combined with knitRa, dorsal trunk formation is similar to wild type, though dorsal outgrowth fails and lateral trunk fusion is only partial. Visceral and ganglionic tracheal branches fail to reach the gut and nervous system. Lack of tracheal branch formation is caused by failure of cell migration.
Homozygous embryos display abdominal segmentation defect. One copy of Res1r1 lacks the rescued abdominal segments.
Deletion of abdominal segments, severe head defect and absence of SNS. SNS defect can be rescued by expression of either the knitRa or knrlkni.PR construct. Phenotypic rescue with the knrl transgene is dose dependent, three copies provides an almost normal head as strong as that observed with two copies of kni transgene.
Mutant abdominal phenotype of Df(3L)ri-XT1 embryos can be rescued by P{kniSH} but only weak rescue of head defects.
hide Stocks ( 2 )
Bloomington
Kyoto
hide Notes on Origin
Discoverer
hide Balancer / Genotype Variants of the Aberration
hide Separable Components
hide Other Comments
hide Synonyms & Secondary IDs ( 10 )
Reported As
Symbol Synonym
Df(3L)ri-XT1
Df(3l)ri-XT1
Name Synonym
Secondary FlyBase IDs
hide References ( 28 )
Generate a list of
List References by type
hide Recent research papers ( 2 )
Munoz-Soriano et al., 2012, J. Mol. Neurosci. 48(1): 136--143
Septin 4, the Drosophila Ortholog of Human CDCrel-1, Accumulates in parkin Mutant Brains and is Functionally Related to the Nedd4 E3 Ubiquitin Ligase. [FBrf0219099]
Nakayama et al., 2011, PLoS ONE 6(8): e22984
Drosophila carrying pex3 or pex16 mutations are models of zellweger syndrome that reflect its symptoms associated with the absence of peroxisomes. [FBrf0214614]
hide Recent reviews (0)
All reviews listed in FlyBase were published before 2011