Dmel\P{?PZ}dia⁵ Insertion

General Information
Symbol	Dmel\P{?PZ}dia⁵	Species	D. melanogaster
Name		FlyBase ID	FBti0072065
Feature type	transposable_element_insertion_site
Description
Inserted element	P{?PZ}	Expression data
Affected gene(s)	dia	Viability / fertility
Causes allele(s)	dia⁵	Stock availability	none publicly available
LINE ID
Genomic Location
Chromosomal location	2L ( 38E7-38E8 )	Sequence location
Member of Large Scale Dataset(s)
Dataset
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
Orientation
Cytological location (computed by FlyBase)	38E7-38E8 ( near gene of known cytology )
Cytological location (reported)
Comments concerning location
Sequence Data
Flanking sequence
Inserted Element
Construct	P{?PZ}
Location-dependent role
Size
Associated alleles
Molecular map
Affected Gene(s)
Insertion may affect gene	dia (Grosshans et al., 2005)
Alleles and Phenotypes
Causes alleles	dia⁵ (Grosshans et al., 2005)

Lethality References lethal \| embryonic stage \| non-rescuable maternal effect \| recessive (Afshar et al., 2000) lethal \| recessive (Afshar et al., 2000)
Sterility References
Phenotype Manifest In
	actin filament & embryonic/larval tracheal system (Massarwa et al., 2009) amnioserosa \| maternal effect (Homem and Peifer, 2008) blastoderm embryo \| germline clone (Padash Barmchi et al., 2005) bract \| somatic clone (Peng et al., 2012) cortical actin cytoskeleton & syncytial blastoderm embryo \| maternal effect (Webb et al., 2009) cycle 11 embryo \| germline clone (Afshar et al., 2000) denticle belt \| germline clone (Afshar et al., 2000) dorsal closure embryo \| germline clone (Afshar et al., 2000) egg chamber \| somatic clone (Wang and Riechmann, 2007) embryonic/first instar larval cuticle \| germline clone (Afshar et al., 2000) embryonic head \| germline clone (Afshar et al., 2000) epithelium \| somatic clone (Wang and Riechmann, 2007) follicle cell \| somatic clone (Wang and Riechmann, 2007) furrow canal \| germline clone (Grosshans et al., 2005) gastrula embryo \| germline clone (Afshar et al., 2000) morphogenetic furrow \| somatic clone (Corrigall et al., 2007) pole bud \| germline clone (Afshar et al., 2000) pole cell \| germline clone (Afshar et al., 2000) tormogen cell \| somatic clone (Peng et al., 2012) ventral furrow \| non-rescuable maternal effect (Homem and Peifer, 2008)
Detailed Description
Statement Reference Expression of dia[ΔDad.Scer\UAS.P\T.T:Avic\GFP-EGFP] in the sensory organ precursor lineage (using Scer\GAL4[neur-GAL4-A101]) in large homozygous dia[5] clones in the leg restores socket cell protrusions and the formation of associated bract cells in the clones. (Peng et al., 2012) The four cells within mutant sensory organ precursors develop in correct number and position in large homozygous clones in the leg, but the socket cell protrusions which are normally seen in wild type are significantly suppressed and disorganised. Bracts are not induced adjacent to the mutant sensory organs in these large clones. (Peng et al., 2012) Expression of spi[s.Scer\UAS.T:Avic\GFP-EGFP] in the sensory organ precursor lineage (using Scer\GAL4[neur-GAL4-A101]) in large homozygous dia[5] clones in the leg restores bract formation in the clones. (Peng et al., 2012) Embryos lacking both maternal and zygotic dia function which are grown at 18[o]C and then shifted to 25[o]C for analysis during dorsal closure undergo dorsal closure more slowly than normal and have defects in epidermal sheet alignment. The mutant leading edge cells form both filopodia and lamellipodia. Filopodial number is decreased, filopodial length is increased and lamellipodial area is increased. (Homem and Peifer, 2009) Apical F-actin in the trachea disappears in mutant embryos, while residual F-actin is retained in the adherens junctions. (Massarwa et al., 2009) Pupal eye epithelial adherens junctions are unaffected in dia[5] MRCM clones. dia[5] clones that are shifted to the non-permissive temperature for 30 hours before dissection do not exhibit any effect on the adherens junctions. (Warner and Longmore, 2009) Actin pseudocleavage furrow extension is significantly impaired in all embryos maternally mutant for dia[5]. In some cases, most actin remain in caps during metaphase in dia[5] mutants, but more frequently actin is located in weak rings. (Webb et al., 2009) Heterozygotes do not exhibit any gross defects in external bristle morphology. Compared to controls, heterozygous mutants show a reduced response to an auditory stimulus mimicking flies\' courtship song. (Cosetti et al., 2008) Embryos derived from dia[5] homozygous female germline clones and which have a paternally derived copy of dia[+] have defects in ventral furrow formation; first, a subset of cells that should apically constrict fail to do so, and second, as some cells invaginate, they pull on neighbouring cells, which become massively multinucleate, rather than stretching towards the midline as occurs in wild-type embryos. Adherens junctions are normal in these embryos at the end of gastrulation. Adherens junctions form and cortical F-actin and myosin are not grossly disrupted at the end of gastrulation in embryos derived from dia[5] homozygous female germline clones and which are also zygotically mutant for dia (dia[2]/dia[5]). However, although the initial assembly of adherens junctions occurs, maintenance of adherens junctions is defective in these embryos, and adherens junction destabilisation is accompanied by cortical blebbing on the basolateral cortex. Embryos derived from dia[5] homozygous female germline clones which and which are also zygotically mutant for dia (dia[2]/dia[5]) have abnormal cell protrusions that extend from the amnioserosa cells during dorsal closure. Dorsal closure is defective, with cell misalignment as the epidermal sheets meet at the dorsal midline. (Homem and Peifer, 2008) Homozygous cells in the morphogenetic furrow (in clones that encompass the morphogenetic furrow) fail to undergo apical constriction. (Corrigall et al., 2007) dia[5] follicle cell clones exhibit cytokinesis defects in the presence of a normal actin cortex. During early oogenesis, these clones retain a rectangular shape, do not flatten, and the underlying cyst bulges out. Late clones show no outward bulging over the growing oocyte and maintain a normal cell shape, with the exception that the cells are bigger because of the absence of cytokinesis. (Wang and Riechmann, 2007) In mid-cellularisation embryos derived from dia⁵ germline clones, the furrow canals are considerably enlarged compared to wild-type and are filled with large cytoplasmic blebs. Interruptions in the regular F-actin array (a hexagonal array is normally evident in surface views) are seen in these embryos and a variable proportion of the forming cells contain multiple nuclei. (Grosshans et al., 2005) Embryos derived from dia⁵ germ-line clones have severe cellularization defects. (Padash Barmchi et al., 2005) Single cell γ neuron mutant clones in the mushroom body do not show axon growth defects. (Ng and Luo, 2004) dia⁵ causes larval and pupal lethality. Only about 3% of embryos derived from homozygous female germline clones hatch. Defects in these embryos first appear at nuclear cycle 11. Abnormalities in nuclear and actin cytoskeletal organisation affects almost two-thirds of all fertilised embryos at cycles 11-13 and a higher percentage at later stages. The area of the embryo affected varies considerably between embryos. 100% of embryos fail to form pole cells. More than 95% of embryos are grossly defective at gastrulation (despite the fact that half the embryos have received a wild-type copy of dia paternally). A wide range of cuticle defects, including a failure in head involution, loss of head structures, reduction or absence of denticle bands and incomplete formation of the cuticle are seen. Severe structural changes in the actin cytoskeleton compared to wild type are manifested after nuclear cycle 11 in embryos derived from homozygous female germline clones. Formation of the hexagonal actin arrays is disrupted during prophase and metaphase and there is an absence of actin staining between the metaphase nuclei, indicating that the metaphase furrow fails to form. Nuclei in the mutant embryos frequently show abnormal spacing and in some cases fuse in subsequent nuclear cycles. Nuclei are frequently found displaced into the interior of the embryo although the centrosomes remain at the surface. In embryos derived from homozygous female germline clones there is a variable defect in the organisation of both actin- and microtubule-based structures during cellularisation. In the least severe cases, the cellularisation furrow is absent between some nuclei, without any noticeable defect in morphology or positioning of nuclei or microtubule structure. In more severely affected embryos, actin staining is absent at the furrow canals and irregular at some regions of the cortex. Surface regions that lack any organised actin show abnormalities in the positioning of nuclei and microtubule baskets. Centrosomal behaviour is abnormal in these regions. Formation and growth of the cytoplasmic buds occurs normally at the posterior pole of embryos derived from homozygous female germline clones. The buds never cleave to produce pole cells (as occurs in wild-type embryos). Rather, they regress in synchrony with the buds covering the rest of the embryonic cortex. Buds reform at the posterior pole at each nuclear cycle, but do not undergo cytokinesis. In some embryos, the number and size of the somatic buds are abnormal. Unlike the somatic nuclei, the posterior pole nuclei fail to initiate cellularisation. (Afshar et al., 2000)
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
Modified descendant of	P{PZ}dia¹ (Grosshans et al., 2005)
Related Aberration or Balancer
Aberration
Balancer
Stocks ( 0 )

Linkouts
Synonyms & Secondary IDs
Reported As
Symbol Synonym	P{?}dia⁵ (FlyBase, 1992-, Grosshans et al., 2005) P{?PZ}dia⁵ (FlyBase, 1992-)
Secondary FlyBase IDs

References ( 14 )
Research paper	Peng et al., 2012, Dev. Cell 23(3): 507--518 Planar Polarized Protrusions Break the Symmetry of EGFR Signaling during Drosophila Bract Cell Fate Induction. [FBrf0219458] Homem and Peifer, 2009, Mol. Biol. Cell 20(24): 5138--5155 Exploring the Roles of Diaphanous and Enabled Activity in Shaping the Balance between Filopodia and Lamellipodia. [FBrf0209542] Massarwa et al., 2009, Dev. Cell 16(6): 877--888 Apical secretion in epithelial tubes of the Drosophila embryo is directed by the Formin-family protein Diaphanous. [FBrf0208270] Warner and Longmore, 2009, J. Cell Biol. 185(6): 1111--1125 Distinct functions for Rho1 in maintaining adherens junctions and apical tension in remodeling epithelia. [FBrf0208183] Webb et al., 2009, Development 136(8): 1283--1293 A novel role for an APC2-Diaphanous complex in regulating actin organization in Drosophila. [FBrf0207596] Cosetti et al., 2008, Ann. Otol. Rhinol. Laryngol. 117(11): 827--833 Unique transgenic animal model for hereditary hearing loss. [FBrf0206525] Homem and Peifer, 2008, Development 135(6): 1005--1018 Diaphanous regulates myosin and adherens junctions to control cell contractility and protrusive behavior during morphogenesis. [FBrf0204461] Corrigall et al., 2007, Dev. Cell 13(5): 730--742 Hedgehog Signaling Is a Principal Inducer of Myosin-II-Driven Cell Ingression in Drosophila Epithelia. [FBrf0202245] Wang and Riechmann, 2007, Curr. Biol. 17(15): 1349--1355 The role of the actornyosin cytoskeleton in coordination of tissue growth during Drosophila oogenesis. [FBrf0200870] Grosshans et al., 2005, Development 132(5): 1009--1020 RhoGEF2 and the formin Dia control the formation of the furrow canal by directed actin assembly during Drosophila cellularisation. [FBrf0183918] Padash Barmchi et al., 2005, J. Cell Biol. 168(4): 575--585 DRhoGEF2 regulates actin organization and contractility in the Drosophila blastoderm embryo. [FBrf0184065] Ng and Luo, 2004, Neuron 44(5): 779--793 Rho GTPases Regulate Axon Growth through Convergent and Divergent Signaling Pathways. [FBrf0180582] Afshar et al., 2000, Development 127(9): 1887--1897 Functional analysis of the Drosophila Diaphanous FH protein in early embryonic development. [FBrf0126984]
FlyBase analysis	FlyBase, 1992-, FlyBase curation. FlyBase curation. [FBrf0105495]

Dmel\P{?PZ}dia5 Insertion

Dmel\P{?PZ}dia⁵ Insertion