A Database of Drosophila Genes & Genomes

FB2012_01, released January 20th, 2012
 

Dmel\P{PZ}sar105712 Insertion

General Information
Symbol Dmel\P{PZ}sar105712 Species D. melanogaster
Name FlyBase ID FBti0005541
Feature type transposable_element_insertion_site
Description
Inserted element P{PZ} Expression data lacZ reporter
Affected gene(s) Ecol\lacZ, sar1 Viability / fertility
Causes allele(s) Ecol\lacZsar1-05712, sar105712 Stock availability 1 publicly available
LINE ID l(3)05712
Genomic Location
Chromosomal location 3R ( 94A5-94A6 ) Sequence location
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Description
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FB2012_01
FB2011_10
All updates Click here to see a list of all updates to this record from FB2010_08 and on.
hide Detailed Mapping Data
Chromosome (arm)
Sequence Location
Orientation
Cytological location
(computed by FlyBase)
94A5-94A6 ( near gene of known cytology )
Cytological location
(reported)
Comments concerning
location
hide Sequence Data
Flanking sequence
 
hide Inserted Element
Construct P{PZ}
Location-dependent
role
lacZ enhancer trap
Size 14.545Kb
Associated alleles
Molecular map
hide Affected Gene(s)
Insertion may
affect gene
hide Alleles and Phenotypes
Causes alleles
Lethality
References
Sterility
References
hide Phenotype Manifest In
cardioblast
embryonic pericardial cell
hide Detailed Description
Statement
Reference
The lethality of sar1[05712]/Df(3R)ED6085 animals is rescued if they are carrying the P{FlyFos-045685} construct (which contains D. pseudoobscura pseudoobscura fosmid sequence that includes the region orthologous to sar1); a few adults survivors are recovered, and they can fly.
Transepithelial barrier function in the trachea is normal in mutant embryos.
Homozygous stage 17 embryos show a "broken hearted" phenotype; the pericardial cells are dissociated from cardioblasts in the dorsal vessel.
sar105712 mutants have major defects in cuticular development; the larval cuticles are smaller (on average only 40-50% the length of wild-type) and weaker than the cuticles of their wild-type siblings, the mouthparts and filzkorper are poorly formed, and sar105712 mutants frequently have large holes in the dorsal cuticle. In addition, there appears to be a general defect in patterning of the cuticle, with dorsal and ventral structures appearing more lateralized. The ventral cuticle exhibits a loss of denticles and the denticles that are present have a very light pigmentation, more consistent with the pigmentation found in more lateral denticles of wild-type larvae. The dorsal surfaces of the mutant larvae consist of thin hairs and naked cuticle, an arrangement more typical of dorsal-lateral reiogns of wild-type cuticles.
hide Expression Data
Reporter Expression
distribution deduced from reporter
Stage
Tissue/Position (including subcellular localization)
Reference
Additional Information
Statement
Reference
Marker for
Reflects
expression of
hide External Images
FlyView (LinkOut)
hide Data on Genetic Line
Line ID
Origin as a multiple insertion line
hide Progenitor(s) within the Genome
hide Related Aberration or Balancer
Aberration
Balancer
hide Stocks ( 1 )
Bloomington
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hide Synonyms & Secondary IDs
Reported As
Symbol Synonym
P{PZ}sar105712
P{ry+t7.2=PZ}l(3)0571205712
Secondary FlyBase IDs
  • FBti0000595
hide References ( 16 )
Research paper
Langer et al., 2010, PLoS ONE 5(1): e8928
In Vivo RNAi Rescue in Drosophila melanogaster with Genomic Transgenes from Drosophila pseudoobscura. [FBrf0209864]
Jayaram et al., 2008, PLoS ONE 3(4): e1964
COPI vesicle transport is a common requirement for tube expansion in Drosophila. [FBrf0210260]
Yi et al., 2006, Science 313(5791): 1301--1303
The mevalonate pathway controls heart formation in Drosophila by isoprenylation of G gamma 1. [FBrf0194083]
Abrams and Andrew, 2005, Development 132(12): 2743--2758
CrebA regulates secretory activity in the Drosophila salivary gland and epidermis. [FBrf0187447]
Bellen et al., 2004, Genetics 167(2): 761--781
The BDGP gene disruption project: single transposon insertions associated with 40% of Drosophila genes. [FBrf0179132]
Spradling et al., 1999, Genetics 153(1): 135--177
The Berkeley Drosophila genome project gene disruption project. Single P-element insertions mutating 25% of vital Drosophila genes. [FBrf0111489]
Harvie et al., 1998, Genetics 149(1): 217--231
Genes expressed in the ring gland, the major endocrine organ of Drosophila melanogaster. [FBrf0102844]
Russell et al., 1998, Genome 41(1): 7--13
Lethal P-lacZ insertion lines expressed during pattern respecification in the imaginal discs of Drosophila. [FBrf0102000]
Mlodzik and Hiromi, 1992, Conn, 1992: 397--414
Enhancer trap method in Drosophila: its application to neurobiology. [FBrf0066714]
Supplementary material
Yi, 2006, Science 313(5791):
[FBrf0195927]
Personal communication to FlyBase
Levis, 2002.10.8, l(3)05712 is an allele of sar1.
l(3)05712 is an allele of sar1. [FBrf0151674]
Vosshall, 1998.8.10, Patterns of lacZ expression.
Patterns of lacZ expression. [FBrf0103142]
Meister and Braun, 1995.10, lacZ expression patterns for P{} insertions at Bloomington.
lacZ expression patterns for P{} insertions at Bloomington. [FBrf0083714]
FlyBase analysis
FlyBase, 1992-, FlyBase curation
FlyBase curation. [FBrf0105495]
Computer file
Gene Disruption Project members, 2001-, [title not yet available]
[title not yet available] [FBrf0132177]
BDGP Project Members, 1994-1999, Berkeley Drosophila Genome Project.
Berkeley Drosophila Genome Project. [FBrf0067338]