Dmel\P{SUPor-P}KG00878 Insertion

General Information
Symbol	Dmel\P{SUPor-P}KG00878	Species	D. melanogaster
Name		FlyBase ID	FBti0127886
Feature type	transposable_element_insertion_site
Description
Inserted element	P{SUPor-P}	Expression data
Affected gene(s)	plexB	Viability / fertility
Causes allele(s)	plexB^KG00878	Stock availability	none publicly available
LINE ID
Genomic Location
Chromosomal location	4	Sequence location
Member of Large Scale Dataset(s)
Dataset	TI_set_P{SUPor-P}.KG A set of transgenic insertion stocks derived by TE mobilization using the P-element construct P{SUPor-P}; created and vetted by the Gene Disruption Project (GDP). The P{SUPor-P} construct carries two visible markers: a w[+mC] mini-white marker flanked by su(Hw)-binding sites, designed to reduce the variablity of the phenotype of the white gene marker due position effects, in addition to the mini-yellow marker y[+mDint2]. (Bellen et al., 2004)
Recent Updates
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FB2013_03	References Bellen et al., 2004, Genetics 167(2): 761--781
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
Orientation
Cytological location (computed by FlyBase)
Cytological location (reported)
Comments concerning location
Sequence Data
Flanking sequence
Inserted Element
Construct	P{SUPor-P}
Location-dependent role
Size	11.467Kb
Associated alleles	gypsy\su(Hw)BR⁴³⁰ w^BR.E.BR y^+mDint2
Molecular map
Affected Gene(s)
Insertion may affect gene	plexB (Ayoob et al., 2006)
Alleles and Phenotypes
Causes alleles	plexB^KG00878 (Ayoob et al., 2006)

Lethality References partially lethal - majority die (Ayoob et al., 2006)
Sterility References
Phenotype Manifest In
	intermediate longitudinal fascicle \| embryonic stage (Wu et al., 2011) intersegmental nerve (Ayoob et al., 2006) medial longitudinal fascicle (Ayoob et al., 2006) MP1 tract (Wu et al., 2011) segmental nerve branch SNa of A1-7 (Ayoob et al., 2006)
Detailed Description
Statement Reference Heterozygosity for plexB[KG00878] has no effect on the mutant ISNb phenotype seen in embryos expressing RhoGAPp190[dsRNA.N.Scer\UAS] under the control of Scer\GAL4[elav.PLu]. (Jeong et al., 2012) The MP1 pathway is often disorganised, defasciculated and discontinuous in homozygous embryos. (Wu et al., 2011) The intermediate Fas2-positive longitudinal tract is severely disorganised in homozygous embryos, with phenotypes including defasciculation, disorganisation and wandering of axon bundles within this intermediate position. 71.0% of hemisegments show disorganisation of the intermediate Fas2-positive longitudinal tract. The medial and lateral Fas2-positive tracts appear normal in the mutant embryos. Chordotonal organ axons extend into the central nervous system but fail to form regular terminal branches in the region of the disrupted intermediate longitudinal tract in mutant embryos, instead remaining stalled, with expanded, splayed out morphologies over the region where they would normally elaborate their synaptic contacts. (Wu et al., 2011) plexB[KG00878] fails to complement Df(4)M101-62f with respect to the plexB[KG00878] lethality phenotype. Expression of plexB[Scer\UAS.cHa] in all neurons in a plexB[KG00878] homozygous background, under the control of Scer\GAL4[elav-C155], significantly rescues the intersegmental nerve b (ISNb) motor axon defects. Restoring plexB to all neurons also rescues the lethality associated with the plexB[KG00878] mutants (16.8% homozygous viable progeny compared to 5.7% of the plexB[KG00878]/+ x Df(4)M101-62f/+ crossing being homozygous viable progeny). Expression of plexB[Scer\UAS.cHa] in all neurons in a plexB[KG00878] homozygous background, under the control of Scer\GAL4[elav-C155], significantly reduces the number of SNa defects by over 50%. Expression of plexB[Scer\UAS.cHa] in all neurons in a plexB[KG00878] homozygous background, under the control of Scer\GAL4[elav-C155] rescues the severe defasciculation of the medial Fas2-stained longitudinal fascicle. (Ayoob et al., 2006) plexB[KG00878] is semi-lethal and yields a small percentage (approximately 5.7%) of homozygous adult flies that are unable to mate successfully. plexB[KG00878] homozygous embryos exhibit highly penetrant defects in axon guidance. Motor axons that contribute to the intersegmental nerve, the segmental nerve, and a subset of longitudinally projecting CNS axons, fail to defasciculate from one another. plexB[KG00878] homozygous embryos do not exhibit defects in overall muscle morphology. Motor axons in the Segmental nerve a (SNa) pathway are affected in plexB[KG00878] mutant embryos. In approximately almost 50% of all plexB[KG00878] hemisegments the anterior of the SNa dorsal branch incorrectly projects between muscles 21 and 22 instead of more posteriorly between muscles 22 and 23. In approximately 33.1% of all hemisegments the anteriorly misprojecting SNa motor axons take the wrong path but subsequently make two turns to reach their proper target. In approximately 14.7% of all plexB[KG00878] hemisegments the anteriorly projecting SNa dorsal branch takes the wrong path and is unable to reach its proper target. plexB[KG00878] homozygous embryos exhibit defects in the innervation of the ventral muscles in most of the segments examined. The medial Fas2-stained longitudinal fascicle in plexB[KG00878] mutants is severely defasciculated along its length. plexB[KG00878]/Df(4)M101-62f double heterozygous embryos exhibit phenotypes that are virtually identical to those observed in homozygous plexB[KG00878] embryos. (Ayoob et al., 2006) Expression of plexA[Scer\UAS.T:Ivir\HA1] in a plexB[KG00878] mutant background rescues the total number of ISNb defasciculation defects by 25%, and the more severe ISNb bypass phenotypes by almost 50%. plexA[Scer\UAS.T:Ivir\HA1] expression does not rescue the \'double turn\' or \'lost\' phenotypes of plexB[KG00878] mutants. plexA[Scer\UAS.T:Ivir\HA1] expression reduces the incidence of plexB[KG00878] SNa \'stall\' phenotypes in plexB[KG00878] mutants by 20%. However, it does not reduce the total fraction of defective SNa pathways and is incapable of rescuing plexB[KG00878] CNS phenotypes. Expression of plexA[Scer\UAS.T:Ivir\HA1] also provides a modest reduction in the lethality observed in plexB[KG00878] mutants. Approximately 58%of Df(3R)swp2[MICAL]/+; plexB[KG00878]/+ double transheterozygous embryonic hemisegments exhibit ISNb defects. This penetrance is equivalent to that seen for the same ISNb defects in plexB[KG00878] homozygous mutants. A plexB[KG00878] background greatly reduces the tranverse nerve phenotype found in Sema-2a[Scer\UAS.cKa]; Scer\GAL4[how-24B] mutants (from aberrant formation in 27.9% to 12.2% of hemisegments). (Ayoob et al., 2006)
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
Origin as a multiple insertion line
Progenitor(s) within the Genome

Related Aberration or Balancer
Aberration
Balancer
Stocks ( 0 )

Linkouts
Synonyms & Secondary IDs
Reported As
Symbol Synonym	P{SUPor-P}KG00878 (FlyBase, 1992-, Ayoob et al., 2006, )
Secondary FlyBase IDs

References ( 7 )
Research paper	Jeong et al., 2012, Neuron 76(4): 721--734 The Control of Semaphorin-1a-Mediated Reverse Signaling by Opposing Pebble and RhoGAPp190 Functions in Drosophila. [FBrf0219982] Wu et al., 2011, Neuron 70(2): 281--298 A combinatorial semaphorin code instructs the initial steps of sensory circuit assembly in the Drosophila CNS. [FBrf0213571] Ayoob et al., 2006, Development 133(11): 2125--2135 Drosophila Plexin B is a Sema-2a receptor required for axon guidance. [FBrf0190270] Bellen et al., 2004, Genetics 167(2): 761--781 The BDGP gene disruption project: single transposon insertions associated with 40% of Drosophila genes. [FBrf0179132]
Supplementary material	Wu et al., 2011, Neuron 70(2): Supplemental Information. [FBrf0217575]
FlyBase analysis	FlyBase Curators, 2013, Members of GDP insertion collections: P{GT1}, P{SUPor-P}, P{EPgy2}, Mi{ET1}, Mi{MIC}. Members of GDP insertion collections: P{GT1}, P{SUPor-P}, P{EPgy2}, Mi{ET1}, Mi{MIC}. [FBrf0220667] FlyBase, 1992-, FlyBase curation. FlyBase curation. [FBrf0105495]