Dmel\P{lacW}jeb^k05644 Insertion

General Information
Symbol	Dmel\P{lacW}jeb^k05644	Species	D. melanogaster
Name		FlyBase ID	FBti0006774
Feature type	transposable_element_insertion_site
Description
Inserted element	P{lacW}	Expression data
Affected gene(s)	Ecol\lacZ, jeb	Viability / fertility
Causes allele(s)	Ecol\lacZ^jeb-k05644, jeb^k05644	Stock availability	2 publicly available
LINE ID	l(2)k05644
Genomic Location
Chromosomal location	2R ( 48E2 )	Sequence location	2R:7,998,884..7,998,884 [+]
Map ( GBrowse )
Member of Large Scale Dataset(s)
Dataset	TI_set_P{lacW}.BDGP A set of mutant stocks derived by insertional mutagenesis using the P-element construct P{lacW}; most lines have a lethal or sterile phenotype. The P{lacW} construct carries a w[+mC] mini-white visible marker, Ecol\lacZ enhancer trap sequences, and bacterial sequences that allow plasmid rescue (FBrf0049800). Insertion lines from this collection were assessed for inclusion in the Gene Disruption Project collection. (Spradling et al., 1999, Bellen et al., 2004)
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.
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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
Chromosome (arm)
Sequence Location	2R:7,998,884..7,998,884 [+] (BDGP Project Members, 1994-1999)
Orientation
Cytological location (computed by FlyBase)	48E2 ( inferred by FlyBase from sequence location )
Cytological location (reported)	48E1-48E2 (in situ hybridization reported) (BDGP Project Members, 1994-1999)
Comments concerning location
Sequence Data
Flanking sequence	AQ034149 (FlyBase, 1992-,
Inserted Element
Construct	P{lacW}
Location-dependent role	lacZ enhancer trap (Bier et al., 1989)
Size	10.691Kb
Associated alleles	Ecol\lacZ^P\T.W w^+mC
Molecular map
Affected Gene(s)
Insertion may affect gene	Ecol\lacZ (BDGP Project Members, 1994-1999) jeb (BDGP Project Members, 1994-1999, Rohrbough and Broadie, 2010)
Alleles and Phenotypes
Causes alleles	Ecol\lacZ^jeb-k05644 (BDGP Project Members, 1994-1999) jeb^k05644 (BDGP Project Members, 1994-1999, Vining et al., 2005, Weiss et al., 2001, Stute et al., 2004, Englund et al., 2003, Spradling et al., 1999, Rohrbough and Broadie, 2010)

Lethality References lethal \| recessive (Spradling et al., 1999, Weiss et al., 2001, BDGP Project Members, 1994-1999)
Sterility References
Phenotype Manifest In
	circular visceral muscle primordium (Vining et al., 2005) embryonic/larval digestive system (Englund et al., 2003) endoderm (Weiss et al., 2001) muscle founder cell & visceral muscle primordium (Englund et al., 2003) presumptive embryonic salivary gland (Vining et al., 2005) visceral mesoderm (Weiss et al., 2001, Englund et al., 2003)
Detailed Description
Statement Reference The central nervous system of jeb[k05644] mutants appears morphologically normal in terms of segmental nerve branching and segmental muscle patterning. Neuropil synaptic differentiation appears normal in these mutants, with comparable labeling intensity, density and distribution of presynaptic and postsynaptic labels. jeb[k05644] mutant neuromuscular junctions appear correctly and stereotypically formed and elaborated, with no examples of muscle innervation failure or synaptic targeting errors. mutant presynaptic active zones appear normally formed and with wild-type size. Homozygous jeb[k05644] mutants exhibit reduced hatching and mutant larval movement is typically sluggish and highly limited. Locomotory movement in jeb[k05644] mutants is decreased to 20% of the control level, characterised by slower contractions and extended pauses. Severely impaired and motionless larvae remain capable of briefly resuming movement when stimulated, suggesting a defect in the central circuit output driving locomotion. jeb[k05644] mutant neuromuscular junctions exhibit visible glutamate-driven muscle contractions, and consistently large and robust postsynaptic current amplitudes compared to controls. jeb[k05644] mutant neuromuscular junctions display excitatory junction currents that are comparable to controls, with amplitudes of greater than 1nA. In jeb[k05644] mutants, no large (exceeding 500pA) or patterned EJCs are recorded. EJCs are absent in 60% of recordings, and overall EJC frequency is below 1Hz in 40% of active cells. (Rohrbough and Broadie, 2010) jeb^k05644 mutants show a salivary gland phenotype. At stage 14, mutant salivary glands remain associated with the inner circular muscle layer, while in wild type, these structures become separate. After stage 15, cells from the distal tips of the jeb^k05644 salivary glands spread into the region of the undifferentiated midgut that forms the gastric caecae in the wild-type embryos. The mutant glands become mispositioned and/or elongated and maintain contact with the area of the midgut immediately adjacent to the proventriculus. (Vining et al., 2005) jeb^k05644 homozygous larvae do not ingest food, and lack discernible intestinal structures. In stage 13 jeb^k05644 homozygous embryos, visceral mesoderm cells are scattered rather than forming an organized band of cells as they would normally do at this stage. At stage 11, the earliest stage at which a mutant phenotype in the visceral mesoderm can clearly be observed, these embryos lack muscle founder cells. However, myoblasts do form in the visceral mesoderm, and go on to contribute to somatic muscle (i.e.- they are fusion competent.) (Englund et al., 2003) Differentiated visceral mesoderm is not seen in mutant embryos, although other mesodermal tissues (somatic muscles, heart, fat body and hemocytes) develop normally. Visceral mesoderm precursor cells are specified but fail to migrate normally. There is an increase in the number of nuclei in positions consistent with an increase in somatic muscle precursors, but there is no major disruption of somatic muscle patterning. The midgut endoderm is specified normally and migrates to form two longitudinal bands. Subsequent dorsal and ventral endoderm migration is abnormal (probably because this migration depends on the visceral mesoderm). (Weiss et al., 2001)
Expression Data
Reporter Expression

Additional Information
Statement Reference

Marker for
Reflects expression of
Reporter construct used in assay
External Images
FlyView (LinkOut)
Data on Genetic Line
Line ID	l(2)k05644 (Gene Disruption Project members, 2001-)
Origin as a multiple insertion line
Progenitor(s) within the Genome

Related Aberration or Balancer
Aberration
Balancer
Stocks ( 2 )
Bloomington	10576 w^67c23; P{lacW}jeb^k05644/CyO, P{sevRas1.V12}FK1
Kyoto	111183 y^d2 w¹¹¹⁸ P{ey-FLP.N}2 P{GMR-lacZ.C(38.1)}TPN1; P{neoFRT}42D P{lacW}jeb^k05644 /CyO y⁺
Linkouts
Comments
	Location 2R:7627286-7627287 confirmed by FlyBase alignment of dbGSS accession AQ034149 to D. melanogaster arm Release_4 and heterochromatin Release_3.2b. (FlyBase, 2005)
Synonyms & Secondary IDs
Reported As
Symbol Synonym	jeb^k05644 (Rohrbough and Broadie, 2010) P{lacW}jeb^k05644 (FlyBase, 2005, FlyBase, 1992-, ) P{lacW}l(2)k05644^k05644 (BDGP Project Members, 1994-1999, FlyBase, 1992-)
Secondary FlyBase IDs

References ( 13 )
Research paper	Rohrbough and Broadie, 2010, Development 137(20): 3523--3533 Anterograde Jelly belly ligand to Alk receptor signaling at developing synapses is regulated by Mind the gap. [FBrf0211915] Vining et al., 2005, Dev. Biol. 287(1): 19--34 Organ positioning in Drosophila requires complex tissue-tissue interactions. [FBrf0190174] Bellen et al., 2004, Genetics 167(2): 761--781 The BDGP gene disruption project: single transposon insertions associated with 40% of Drosophila genes. [FBrf0179132] Stute et al., 2004, Development 131(4): 743--754 Myoblast determination in the somatic and visceral mesoderm depends on Notch signalling as well as on milliways (mili[Alk]) as receptor for Jeb signalling. [FBrf0174588] Englund et al., 2003, Nature 425(6957): 512--516 Jeb signals through the Alk receptor tyrosine kinase to drive visceral muscle fusion. [FBrf0167923] Weiss et al., 2001, Cell 107(3): 387--398 Jelly belly: a Drosophila LDL receptor repeat-containing signal required for mesoderm migration and differentiation. [FBrf0141412] 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] Bier et al., 1989, Genes Dev. 3: 1273--1287 Searching for pattern and mutation in the Drosophila genome with a P-lacZ vector. [FBrf0049800]
Personal communication to FlyBase	Gene Disruption Project members, 2001-, (Computer file) (Computer file) [FBrf0132177] BDGP Project Members, 1994-1999, BDGP Project Members, 1994-1999, Berkeley Drosophila Genome Project. (Computer file) BDGP Project Members, 1994-1999, Berkeley Drosophila Genome Project. (Computer file) [FBrf0067338]
FlyBase analysis	FlyBase Curators, 2013, Members of BDGP/GDP insertion collections: P{hsneo}, P{PZ}, P{lacW}. Members of BDGP/GDP insertion collections: P{hsneo}, P{PZ}, P{lacW}. [FBrf0220600] FlyBase, 2005, Assessment of transgenic construct insertion sites. Assessment of transgenic construct insertion sites. [FBrf0184339] FlyBase, 1992-, FlyBase curation. FlyBase curation. [FBrf0105495]

Dmel\P{lacW}jebk05644 Insertion

Dmel\P{lacW}jeb^k05644 Insertion