Dmel\P{lacW}pAbp^k10109 Insertion

General Information
Symbol	Dmel\P{lacW}pAbp^k10109	Species	D. melanogaster
Name		FlyBase ID	FBti0006528
Feature type	transposable_element_insertion_site
Description
Inserted element	P{lacW}	Expression data
Affected gene(s)	Ecol\lacZ, pAbp	Viability / fertility
Causes allele(s)	Ecol\lacZ^pAbp-k10109, pAbp^k10109	Stock availability	2 publicly available
LINE ID	l(2)k10109
Genomic Location
Chromosomal location	2R ( 55B8 )	Sequence location	2R:14,028,914..14,028,914 [+]
Map ( GBrowse )
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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FB2012_01
FB2011_10	Controlled Vocabulary Terms germline clone oogenesis stage S6 oocyte oogenesis stage S5 female sterile References Vazquez-Pianzola et al., 2011, Dev. Biol. 357(2): 404--418
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:14,028,914..14,028,914 [+] (BDGP Project Members, 1994-1999)
Orientation
Cytological location (computed by FlyBase)	55B8 ( inferred by FlyBase from sequence location )
Cytological location (reported)	55B5-55B6 (in situ hybridization reported) (BDGP Project Members, 1994-1999)
Comments concerning location
Sequence Data
Flanking sequence	AQ034024 (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) pAbp (BDGP Project Members, 1994-1999, Blagden et al., 2009, Pertceva et al., 2010, Vazquez-Pianzola et al., 2011)
Alleles and Phenotypes
Causes alleles	Ecol\lacZ^pAbp-k10109 (BDGP Project Members, 1994-1999) pAbp^k10109 (BDGP Project Members, 1994-1999, Sigrist et al., 2003, Spradling et al., 1999, Sigrist et al., 2000, Blagden et al., 2009, Pertceva et al., 2010, Vazquez-Pianzola et al., 2011)

Lethality References lethal \| embryonic stage (Sigrist et al., 2000, Blagden et al., 2009) lethal \| recessive (BDGP Project Members, 1994-1999, Spradling et al., 1999, Vazquez-Pianzola et al., 2011)
Sterility References female sterile \| germline clone (Vazquez-Pianzola et al., 2011) male sterile (Blagden et al., 2009)
Phenotype Manifest In
	bouton (Sigrist et al., 2000) bouton \| supernumerary (Reiff et al., 2002) elongation stage spermatid (Pertceva et al., 2010) embryonic/larval neuromuscular junction (Reiff et al., 2002, Sigrist et al., 2003) NMJ bouton \| larval stage (Sigrist et al., 2002) onion stage spermatid (Blagden et al., 2009, Pertceva et al., 2010) oocyte \| germline clone \| oogenesis stage S5 (Vazquez-Pianzola et al., 2011) oocyte \| germline clone \| oogenesis stage S6 (Vazquez-Pianzola et al., 2011) spindle & spermatocyte (Blagden et al., 2009) wing (Roy et al., 2004)
Detailed Description
Statement Reference pAbp[+t7.8] rescues the germline clone phenotypes and the zygotic lethality of pAbp[k10109]. (Vazquez-Pianzola et al., 2011) Homo- or hemizygous pAbp[k10109] is zygotic lethal. In pAbp[k10109] mutant germline clones oogenesis does not proceed further than stages 5-6. pAbp[k10109] mutant germline clones show a variety of phenotypes in stages 5-6. These include small oocytes, mispositioned oocytes, packaging defects producing egg chambers with supernumerary nurse cells and two oocytes, polytene nurse cells and multilayered follicle cells. Some of these phenotypes may also be due to lack of pAbp in the follicle cells. (Vazquez-Pianzola et al., 2011) The BicD[1]/+ mutant embryonic phenotypes are suppressed by pAbp[k10109]/+. The suppression of the BicD[1]/+ embryonic phenotypes by pAbp[k10109]/+ is partially reverted by one copy of pAbp[+t7.8]. (Vazquez-Pianzola et al., 2011) pAbp[k10109]/pAbp[EY11561] heterozygotes exhibit abnormalities in spermatogenesis. these include absence of meiotic cytokinesis (in 5% of cases), resulting in formation of polyploid spermatids and defects in spermatid elongation (in approximately 100% of cases). Nuclei fail to elongate, keep a round shape and are dispersed along the cyst instead of grouping at the head of the cyst. Nebenkern DAPi staining (for DNA) appears to be non-uniform in these mutants, reflecting the effect of the trans-heterozygous mutants on mitochondrial DNA organization in at least 60% of cases. There appears to be no difference between the trans-heterozygous mutant and controls, showing that mutant mitochondrial membranes keep their integrity, but in the mutant, the onion-stage Nebenkern looks larger than in controls, and its morphology differs from a perfect sphere. Examination with an electron microscope reveals abnormal mitochondrial membranes at onion-stage spermatids in the trans-heterozygous mutant. These mitochondria also exhibit defective attachment to axonemes in the elongating spermatids. (Pertceva et al., 2010) pAbp[k10109]/hyd[15] trans-heterozygous double mutants exhibit spermatogenesis defects. The morphology of nuclei in the sperm head bundle are indistinguishable from the control but the nuclei are frequently scattered abnormally. Cytokinetic abnormalities are also increased in these double mutants. pAbp[k10109]/hyd[hs1] trans-heterozygous double mutants exhibit spermatogenesis defects. Approximately 30% of head bundles in the sperm contain both round- and needle-shaped nuclei. Abnormal nuclei scattering occurs at low frequency. Cytokinetic abnormalities are also increased in these double mutants. (Pertceva et al., 2010) pAbp[5-SZ-4029]/pAbp[k10109] cysts in the testis sometimes contain spermatids with nuclei and Nebenkern that are twice the size of the surrounding spermatids. Cytokinesis is also affected, resulting in spermatids with a 2:1 and 3:1 ratio of nuclei:Nebenkern (in contrast to the wild-type ratio of 1:1). 18% of pAbp[EP310]/pAbp[k10109] spermatocytes show defects in meiosis, with the most common phenotype being detachment of the meiotic spindles from astral microtubules. (Blagden et al., 2009) The rough eye phenotype observed in Fmr1[sev.PW] flies is suppressed in a pAbp[k10109]/+ background. (Cziko et al., 2009) Files heterozygous for pAbp^k10109 show wing size reduction. (Roy et al., 2004) pAbp^k10109 mutant larvae have significantly larger NMJs than wild type with more boutons. This effect becomes more prominent when larvae are raised at 25 or 29^oC. At 18^oC, pAbp^k10109 mutants show increased stride-frequency and locomotor speed compared to wild type, but unaltered stride-length and crawling distance. However, at 29^oC, the mutants exhibit similar locomotor parameters to wild type. There is also a greater increase in the amount of large subsynaptic eIF-4E aggregates at 29^oC, compared to wild type. (Sigrist et al., 2003) Scer\GAL4^elav-PG159-mediated expression of Ocun\Mlck2::Xlae\Cam^{2.1.Scer\UAS.T:Avic\GFP-ECFP,T:Avic\GFP-EYFP} does not affect the phenotype of pAbp^k10109/+ mutant larvae: these mutants still have larger evoked postsynaptic currents and significantly more boutons compared to wild type. (Reiff et al., 2002) pAbp^k10109/+ mutants have larger evoked postsynaptic currents and significantly more boutons compared to wild type. These mutants also have proportionally larger NMJs, as is typical in animals with genetically strengthened signal transmission and unaltered muscle input resistance. As the boutons of these mutants show normal levels of Ca²⁺ signalling, it appears that the raised levels of released presynaptic vesicles may be due to the large numbers of contributing boutons. The large NMJs, which contain a larger total number of T-bars than wild-type boutons, continue to transmit without significant derepression at stimulation frequencies that cause considerable depression of signal transmission in wild-type NMJs. (Reiff et al., 2002) The elimination of one copy of GluRIIA in pAbp^k10109/+, GluRIIA^AD9/+ mutants results in an almost complete suppression of enhanced junctional signal transmission and in a corresponding suppression of junctional growth, indicating that animals with genetically restricted GluRIIA expression are incapable of developing a strengthened larval stage neuromuscular junction. (Sigrist et al., 2002) pAbp^k10109/+ mutants exhibit a significant elevation in the junctional GluRIIA immunoreactivity that is primarily attributable to an increase in the number of GluRIIA-positive synapses (similar to a GluRIIA^Scer\UAS.cPa Scer\GAL4^Mhc.PW mutant) and strengthened junctional signal transmission. Neuromuscular junctions (NMJs) of pAbp^k10109/+ animals exhibit unaltered postsynaptic sensitivity compared with wild-type NMJs, but significantly larger evoked responses. Thus, the junctional quantal content is significantly larger at pAbp^k10109/+ NMJs compared to wild-type and is associated with an elevated frequency of spontaneous vesicle fusion events. pAbp^k10109/+ animals exhibit enlarged larval stage neuromuscular junctions (NMJs). This larger size of NMJ is evident in a significant increase in the number of synaptic boutons, which are wild-type in shape and size. (Sigrist et al., 2002) The mean amplitude of miniature postsynaptic currents (mEJCs) at the neuromuscular junction is indistinguishable from wild type in heterozygotes. Evoked postsynaptic currents (eEJCs) in heterozygotes are significantly larger than in wild-type. The number of junctional boutons per neuromuscular junction is increased compared to wild type. (Sigrist et al., 2000)
Expression Data
Reporter Expression

Additional Information
Statement Reference

Marker for
Reflects expression of
External Images
FlyView (LinkOut)
Data on Genetic Line
Line ID	l(2)k10109 (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	10970 y¹ w^67c23; P{lacW}pAbp^k10109/CyO
Kyoto	111280 y^d2 w¹¹¹⁸ P{ey-FLP.N}2 P{GMR-lacZ.C(38.1)}TPN1; P{neoFRT}42D P{lacW}pAbp^k10109 /CyO y⁺
Linkouts
Comments
	Location 2R:13656272-13656273 confirmed by FlyBase alignment of dbGSS accession AQ034024 to D. melanogaster arm Release_4 and heterochromatin Release_3.2b. Insertion orientation confirmed. (FlyBase, 2005)
Synonyms & Secondary IDs
Reported As
Symbol Synonym	P{lacW}l(2)k10109^k10109 (BDGP Project Members, 1994-1999, FlyBase, 1992-) P{lacW}pAbp^k10109 (FlyBase, 2005, FlyBase, 1992-, Blagden et al., 2009, Pertceva et al., 2010) pabp^K10109 (Vazquez-Pianzola et al., 2011)
Secondary FlyBase IDs

References ( 16 )
Research paper	Vazquez-Pianzola et al., 2011, Dev. Biol. 357(2): 404--418 Pabp binds to the osk 3'UTR and specifically contributes to osk mRNA stability and oocyte accumulation. [FBrf0214798] Pertceva et al., 2010, Cell Biol. Int. 34(10): 991--996 The role of Drosophila hyperplastic discs gene in spermatogenesis. [FBrf0211767] Blagden et al., 2009, Dev. Biol. 334(1): 186--197 Drosophila Larp associates with poly(A)-binding protein and is required for male fertility and syncytial embryo development. [FBrf0208825] Cziko et al., 2009, Genetics 182(4): 1051--1060 Genetic Modifiers of dFMR1 Encode RNA Granule Components in Drosophila. [FBrf0208636] Bellen et al., 2004, Genetics 167(2): 761--781 The BDGP gene disruption project: single transposon insertions associated with 40% of Drosophila genes. [FBrf0179132] Roy et al., 2004, Molec. Cell. Biol. 24(3): 1143--1154 The Drosophila poly(A) binding protein-interacting protein, dPaip2, is a novel effector of cell growth. [FBrf0167891] Sigrist et al., 2003, J. Neurosci. 23(16): 6546--6556 Experience-dependent strengthening of Drosophila neuromuscular junctions. [FBrf0160953] Reiff et al., 2002, J. Neurosci. 22(21): 9399--9409 Differential regulation of active zone density during long-term strengthening of Drosophila neuromuscular junctions. [FBrf0152148] Sigrist et al., 2002, J. Neurosci. 22(17): 7362--7372 The postsynaptic glutamate receptor subunit DGluR-IIA mediates long-term plasticity in Drosophila. [FBrf0152143] Sigrist et al., 2000, Nature 405(6790): 1062--1065 Postsynaptic translation affects the efficacy and morphology of neuromuscular junctions. [FBrf0128816] 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]
FlyBase analysis	FlyBase, 2005, Assessment of transgenic construct insertion sites. Assessment of transgenic construct insertion sites. [FBrf0184339] 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]

Dmel\P{lacW}pAbpk10109 Insertion

Dmel\P{lacW}pAbp^k10109 Insertion