Dmel\P{EP}leaEP2582 Insertion
| General Information | |||
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| Symbol | Dmel\P{EP}leaEP2582 | Species | D. melanogaster |
| Name | FlyBase ID | FBti0011255 | |
| Feature type | transposable_element_insertion_site | ||
| Description | |||
| Inserted element | P{EP} | Expression data | |
| Affected gene(s) | lea | Viability / fertility | |
| Causes allele(s) | leaEP2582 | Stock availability | 1 publicly available |
| LINE ID | EP(2)2582 | ||
| Genomic Location | |||
| Chromosomal location | 2L ( 22A1 ) | Sequence location | 2L:1,420,531..1,420,531 [-] |
Map (
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| Member of Large Scale Dataset(s) | |||
| Dataset |
A set of transgenic insertion stocks derived by TE mobilization using the P-element construct P{EP}. The P{EP} construct construct carries a w[+mC] mini-white visible marker, Scer\UAS binding sites for the Scer\GAL4 transcriptional regulator, and bacterial sequences that allow plasmid rescue. The GAL4-UAS system allows regulated expression
of genes proximate to the site of the insertion: genes properly oriented with respect to the Scer\UAS sequences can be conditionally expressed via transgene-derived Scer\GAL4 activity.
Insertion lines from this collection were mapped and assessed for inclusion in the Gene Disruption Project collection; flanking
sequence data were submitted to GenBank.
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Recent Updates
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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. | ||
Detailed Mapping Data
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| Chromosome (arm) | |||
| Sequence Location |
2L:1,420,531..1,420,531 [-]
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| Orientation | |||
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Cytological location
(computed by FlyBase) |
22A1 ( inferred by FlyBase from sequence location )
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Cytological location
(reported) |
22A1-22A2 (in situ hybridization reported)
22A2-22A2 (reported as inferred from sequence location)
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Comments concerning
location |
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Sequence Data
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| Flanking sequence | |||
Inserted Element
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| Construct | P{EP} | ||
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Location-dependent
role |
mobile activating element (UASG)
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| Size | 7.987Kb | ||
| Associated alleles | |||
| Molecular map | |||
Affected Gene(s)
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Insertion may
affect gene |
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Alleles and Phenotypes
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| Causes alleles | |||
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Lethality
References
lethal
partially lethal - majority die
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Sterility
References
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Phenotype Manifest In
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abdominal lateral pentascolopidial chordotonal organ lch5
abdominal lateral pentascolopidial chordotonal organ lch5 & scolopidial dendrite
abdominal lateral pentascolopidial chordotonal organ lch5 & scolopidial dendritic cap cell
antennal commissure
antennal lobe glomerulus
cell body & serotonin neuron
dMP2 neuron
intersegmental nerve
serotonin neuron & ventral nerve cord
ventral nerve cord commissure
vMP2 neuron
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Detailed Description
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Statement
Reference
In leaEP2582; Scer\GAL4eg-Mz360 embryos, serotonergic axons do not cross the midline. Despite their defects in serotonergic neuronal axon guidance, these
neurons retain their normal ability to take up serotonin. Unlike wild-type serotonergic neurons, the ability of serotonergic
neurons in the ventral nerve cord of stage 16 leaEP2582; Scer\GAL4eg-Mz360 embryos to take up serotonin is not lost when their axonal contacts with the midline are severed. The cell bodies of serotonergic
neurons in the ventral nerve cord of stage 16 leaEP2582; Scer\GAL4eg-Mz360 embryos are shifted laterally compared to wild-type.
Commissure formation and glomerular morphology in the antennal lobes of leaEP2582; Scer\GAL4SG18.1 flies are restored by Df(2R)WMG/+.
Antennal commissure formation is abolished and glomerular morphology is disrupted in the antennal lobes of leaEP2582; Scer\GAL4SG18.1 flies.
The transformation of abdominal lch5 chordotonal organs to a morphology resembling thoracic dch3 chordotonal organs that is
seen in larvae expressing leaEP2582 under the control of Scer\GAL4elav-C155 is still seen if they are also mutant for robo7; 36.4% of abdominal segments have partial or complete transformation of the lch5 organs in the double mutant larvae. The
transformation of abdominal lch5 chordotonal organs to a morphology resembling thoracic dch3 chordotonal organs that is seen
in larvae expressing leaEP2582 under the control of Scer\GAL4elav-C155 is attenuated if the larvae also carry one copy of sli2; only 17.2% of abdominal segments have partial or complete transformation of the lch5 organs in the double mutant larvae
at 25oC.
Abdominal lch5 chordotonal organs are transformed so that they resemble thoracic dch3 chordotonal organs in larvae expressing
leaEP2582 under the control of Scer\GAL4elav-C155. The transformed "lch5" chordotonal organs are displaced dorsally in the ectoderm. They have the usual number of five neurons
per cluster, but their dendrites and support cells show a variety of orientations, which range from the ventral orientation
typical of dch3 organs, through intermediate bent orientations, to orientations similar to those of normal lch5 organs. At
29oC, 44% of abdominal segments have partial or complete transformation of lch5 chordotonal organ morphology. At 25oC, 32% of abdominal segments have partial or complete transformation of lch5 chordotonal organ morphology. Defects indicating
transformation of the lch5 chordotonal organs can be detected as early as stage 14 in embryos expressing leaEP2582 under the control of Scer\GAL4elav-C155. The cap cells of the transformed "lch5" organs always follow the orientation of the transformed neurons. At 29oC, 30.5% of abdominal segments have partial or complete transformation of lch5 chordotonal organ morphology towards that of
the thoracic dch3 chordotonal organs, in larvae expressing leaEP2582 under the control of Scer\GAL4ato.3.6. Some abdominal lch5 chordotonal organs fail to migrate ventrally (as occurs in wild type) in embryos expressing leaEP2582 under the control of Scer\GAL4ato.3.6. Some of these "stalled" abdominal clusters extend projections dorsally. At 29oC, 17% of abdominal segments have partial or complete transformation of lch5 chordotonal organ morphology towards that of
the thoracic dch3 chordotonal organs, in embryos expressing leaEP2582 under the control of Scer\GAL448Y.
ventral nerve cord commissures in stage 17 leaEP2582; Scer\GAL4sca-4512 embryos are missing or fused.
Mutant larvae expressing leaEP2582 under the control of Scer\GAL4elav-C155 have ISN neuron pathfinding defects.
When expression of leaEP2582 is driven by Scer\GAL4elav.PLu, commissures are lost.
Expression of leaEP2582 under the control of Scer\GAL4ap-md544 causes ap-expressing neurons to move laterally (relative to wild type) and extend anteriorly in a specific location between the intermediate
and lateral Fas2-expressing pathways. The ap-expressing axons from neighbouring segments appear to pick the same lateral pathway and to fasciculate together as they extend
anteriorly from segment to segment. Expression of leaEP2582 under the control of Scer\GAL415J2 results in a bimodal phenotype. The dMP2 and vMP2 axons always appear to extend in a Fas2-expressing pathway, but they are now found in either the intermediate or lateral pathways (they normally extend in the medial
pathway). They are usually found in the intermediate pathway and occasionally found in the lateral pathway.
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Expression Data
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| Reporter Expression | |||
| Additional Information | |||
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Statement
Reference
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| Marker for | |||
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Reflects
expression of |
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Reporter construct
used in assay |
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External Images
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| FlyView (LinkOut) | |||
Data on Genetic Line
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| Line ID |
EP(2)2582
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| Origin as a multiple insertion line | |||
Progenitor(s) within the Genome
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Related Aberration or Balancer
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| Aberration | |||
| Balancer | |||
Stocks
( 1 )
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| Bloomington |
17071
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Linkouts
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Comments
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Location 2L:1420530-1420531 determined by FlyBase alignment of dbGSS accession AQ254875 to D. melanogaster arm Release_4 and
heterochromatin Release_3.2b. Insertion orientation revised.
insertion of mobile activating element
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Synonyms & Secondary IDs
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| Reported As | |||
| Symbol Synonym |
EP(2)2582
EP-robo2
P{EP}EP2582
P{EP}leaEP2582
P{EP}robo2EP2582
UAS-robo2
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| Secondary FlyBase IDs | |||
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References
( 19 )
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| Research paper |
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| Supplementary material |
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| Personal communication to FlyBase |
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| FlyBase analysis |
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