Dmel\P{lacW}shg^k03401 Insertion

General Information
Symbol	Dmel\P{lacW}shg^k03401	Species	D. melanogaster
Name		FlyBase ID	FBti0004007
Feature type	transposable_element_insertion_site
Description
Inserted element	P{lacW}	Expression data
Affected gene(s)	Ecol\lacZ, shg	Viability / fertility
Causes allele(s)	Ecol\lacZ^shg-k03401, shg^k03401	Stock availability	2 publicly available
LINE ID	l(2)k03401
Genomic Location
Chromosomal location	2R ( 57B16 )	Sequence location	2R:16,944,296..16,944,296 [-]
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
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Detailed Mapping Data
Chromosome (arm)
Sequence Location	2R:16,944,296..16,944,296 [-] (Tepass et al., 1996)
Orientation
Cytological location (computed by FlyBase)	57B16 ( inferred by FlyBase from sequence location )
Cytological location (reported)	57B13-57B14 (in situ hybridization reported) (BDGP Project Members, 1994-1999)
Comments concerning location
Sequence Data
Flanking sequence
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 (Jaiswal et al., 2006, Brown et al., 2006, BDGP Project Members, 1994-1999, Dumstrei et al., 2003, Niewiadomska et al., 1999, Godt and Tepass, 1998, Mathews et al., 2006, Becam et al., 2005, Genevet et al., 2009) shg (Tepass et al., 1996, Igaki et al., 2006, Igaki et al., 2006, Abreu-Blanco et al., 2011, Tepass et al., 1996)
Alleles and Phenotypes
Causes alleles	Ecol\lacZ^shg-k03401 (BDGP Project Members, 1994-1999, Dumstrei et al., 2003, Jaiswal et al., 2006, Niewiadomska et al., 1999, Godt and Tepass, 1998, Mathews et al., 2006, Brown et al., 2006, Becam et al., 2005, Genevet et al., 2009) shg^k03401 (Tepass et al., 1996, BDGP Project Members, 1994-1999, Dumstrei et al., 2003, Le Borgne et al., 2002, Silver and Montell, 2001, Niewiadomska et al., 1999, Godt and Tepass, 1998, Brown and Freeman, 2003, Spradling et al., 1999, Igaki et al., 2006, Igaki et al., 2006, Abreu-Blanco et al., 2011)

Lethality References lethal \| embryonic stage \| recessive (Tepass et al., 1996) lethal \| recessive (Spradling et al., 1999)
Sterility References
Phenotype Manifest In
	border follicle cell (Niewiadomska et al., 1999) cardioblast (Haag et al., 1999) cardioblast & adherens junction (Haag et al., 1999) embryonic/first instar larval cuticle (Dumstrei et al., 2002) embryonic/first instar larval cuticle \| ventral (Tepass et al., 1996) embryonic head (Dumstrei et al., 2002) embryonic head & embryonic/first instar larval cuticle (Tepass et al., 1996) ommatidial precursor cluster \| cell non-autonomous \| somatic clone (Mirkovic and Mlodzik, 2006) ommatidium (Mirkovic and Mlodzik, 2006) oocyte (Godt and Tepass, 1998, Gonzalez-Reyes and St. Johnston, 1998) sensory mother cell \| somatic clone (Le Borgne et al., 2002)
Detailed Description
Statement Reference Embryos that are maternally mutant for shg[k03401] display impaired wound repair. In comparison with wild-type controls, these embryos show excessive expansion upon ablation, as well as defects in actin ring assembly. Nevertheless, these embryos heal eventually. (Abreu-Blanco et al., 2011) RhoL[10-161];shg[k03401] double homozygous mutant embryos display the normal number of haemocytes migrating into the tail region of the embryo. (Siekhaus et al., 2010) p130CAS[1] homozygotes in combination with heterozygous shg[k03401] severely reduce viability. shg[k03401]; p130CAS[1] double homozygotes arrest in late embryogenesis (and thereby do not hatch) and are considered semi-lethal. Athough most of the embryos form at least partial cuticles, absence of p130CAS[1] significantly enhances shg[k03401] single mutant cuticle defects, with shg[k03401]; p130CAS[1] mutant embryos showing severe defects that essentially eliminate head and ventral cuticle, while incomplete dorsal closure is reflected by the presence of holes in the dorsal cuticle. (Tikhmyanova et al., 2010) shg[k03401] mutant larval brain cells expressing Ras85D[V12.Scer\UAS] under the control of Scer\GAL4[Act5C.PI] exhibit a weak invasive phenotype and can invade the ventral nerve cord (this phenotype occurs with 20% penetrance). shg[k03401] mutant larval brain cells expressing both Ras85D[V12.Scer\UAS] and egr[Scer\UAS.cIa] under the control of Scer\GAL4[Act5C.PI] generate into invasive tumours that can invade the ventral nerve cord (this phenotype occurs with 88% penetrance). Expression of Ras85D[V12.Scer\UAS], egr[Scer\UAS.cIa] and bsk[DN.Scer\UAS], under the control of Scer\GAL4[Act5C.PI] in shg[k03401] mutant larval cephalic complexes (brain, eye and antennal discs) induces tumor invasion of the ventral nerve cord. Overexpression of hep[CA.Scer\UAS] in shg[k03401] mutant cephalic cells (i.e. cells in the larval brain and eye-antennal discs) expressing Ras85D[V12.Scer\UAS] results in neither enhanced tumour growth nor metastatic behaviour. (Igaki et al., 2006) In late 3rd instar larval discs, at the stage of ommatidial rotation, clones of shg^k03401 show robust rotation defects. Within mutant tissue, about 50% of ommatidia do not initiate rotation and several others rotate less in comparison with wild-type clusters of the same stage. Rotation defects are apparent in both in small and large shg^k03401 clones. There is no significant evidence for apicobasal polarity defects in the clones. Mosaic ommatidia containing shg^k03401 clones do not have a higher probability of rotating correctly when both R3 and R4 are wild type. Wild-type preclusters that are directly adjacent to shg^k03401 interommatidial cells can also fail to rotate correctly. The ommatidial under-rotation of Scer\GAL4^hs.2sev>shg^{dCR3h.Scer\UAS.T:Avic\GFP-rs} eyes is enhanced in Scer\GAL4^hs.2sev>shg^{dCR3h.Scer\UAS.T:Avic\GFP-rs}; shg^k03401/+ flies. Expression of shg^Scer\UAS.cSa under the control of Scer\GAL4^hs.2sev increases the number of ommatidial clusters that initiate rotation correctly in shg^k03401 clones. (Mirkovic and Mlodzik, 2006) Heterozygous shg^k03401, significantly enhances the ommatidial misrotation phenotype seen S⁰⁵⁶⁷¹/+ animals. (Brown and Freeman, 2003) The proportion of shg^k03401 embryos showing the severe ventral cuticle phenotype is completely suppressed by rho⁹ and is enhanced by expression of btl::Egfr^{Scer\UAS.T:λ\cI-DD} under the control of Scer\GAL4^da.G32. (Dumstrei et al., 2002) The head cuticle is missing in homozygous embryos, although most embryos only show minor defects in the ventral trunk cuticle. 12% of embryos have a more severe phenotype in which the entire ventral cuticle is missing. (Dumstrei et al., 2002) When homozygous somatic clones are made in the thoracic epithelium the orientation of division of pIIa relative to the pI division axis is significantly more variable than wild-type. 39% of pIIa cells divide at an α angle of more than 20^o (compared to 2% for wild-type). (Le Borgne et al., 2002) Cardioblasts remain rounded in homozygous embryos, in contrast to wild type where they adopt a crescent shape. There is no lumen between the cardioblasts and no adherens junctions between them. Amnioserosa cells are still attached to the ventral surface of the cardioblasts, in contrast to wild type. (Haag et al., 1999) shg^k03401/shg^R6 flies are semi-viable. Border follicle cell migration is substantially delayed in many cases in shg^k03401/shg^R6 follicles. Approximately 65% of the border cell clusters that have not reached the oocyte at stage 10 are located between nurse cells and only 35% of border cell clusters do not penetrate between nurse cells. (Niewiadomska et al., 1999) The oocyte is mislocalised in 29.5% of stage 7-9 shg^k03401/shg^R6 follicles. (Godt and Tepass, 1998) Homozygous female germ line clones give rise to egg chambers with misplaced oocytes in 18% of cases. (Gonzalez-Reyes and St. Johnston, 1998) Class II allele: lacks most of the head cuticle and has small holes in the ventral cuticle. Germ line clones give rise to only a few eggs, giving rise to embryos with Class III and class IV phenotypes. (Tepass et al., 1996)
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)k03401 (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	10377 y¹ w^67c23; P{lacW}shg^k03401/CyO
Kyoto	111074 y^d2 w¹¹¹⁸ P{ey-FLP.N}2 P{GMR-lacZ.C(38.1)}TPN1; P{neoFRT}42D P{lacW}shg^k03401 /CyO y⁺
Linkouts
Comments
	P{lacW}shg^k03401 insertion site reported as behind nucleotide 368 of GB:D28749 in the 5' UTR of shg. This was interpreted by the curator as meaning inserted after base 368. The insertion orientation was not reported. (Tepass et al., 1996) This insertion was listed in the BDGP database as a lethal or sterile line during the period 1994-1999, but was not verified as such prior to the summary publication (FBrf0111489). Reasons for excluding lines from the collection described in FBrf0111489 include presence of more than one P insertion on the mutant chromosome, separation of lethality (or sterility) from the location of the insertion, and loss of lethality (or sterility) from the stock. Further information is available from http://www.fruitfly.org/bfd/ and from Dr. Allan Spradling (spradling@mail1.ciwemb.edu). (FlyBase, 1992-)
Synonyms & Secondary IDs
Reported As
Symbol Synonym	DE-Cad-lacZ (Jaiswal et al., 2006) hg^k03401 (Igaki et al., 2006) P{lacW}shg^k03401 (FlyBase, 1992-, Tepass et al., 1996, ) P^lacWshg^k03401 (Genevet et al., 2009) shg^k03401 (Igaki et al., 2006, Abreu-Blanco et al., 2011) shg^P34-1 (Becam et al., 2005) shg^P34-lacZ (Dumstrei et al., 2003) shg^P341 (Dumstrei et al., 2003) shg-lacZ (Brown et al., 2006, Genevet et al., 2009)
Secondary FlyBase IDs

References ( 29 )

Generate a list of	All references relating to this insertion ( 29 )

List References by type	Research paper ( 24 ) Supplementary material ( 1 ) Personal communication to FlyBase ( 2 ) FlyBase analysis ( 2 )
Recent research papers ( 1 )
	Abreu-Blanco et al., 2011, J. Cell Biol. 193(3): 455--464 Cell wound repair in Drosophila occurs through three distinct phases of membrane and cytoskeletal remodeling. [FBrf0213583] Show all research papers ...

Dmel\P{lacW}shgk03401 Insertion

Dmel\P{lacW}shg^k03401 Insertion